****** 8252957
----K E
----T Modification of exercise performance by sharp reduction of blood pressure. A study in patients with uncomplicated hypertension.
----A We evaluated exercise performance in 14 patients with uncomplicated essential hypertension 1 h after the administration of a single dose of placebo, nifedipine (20 mg), captopril (50 mg), and propranolol (80 mg). Drugs were administered at the same time of day following a randomized, double-blind protocol. Mean resting blood pressure (+/- SE) was 135 +/- 3 mm Hg with placebo administration, 118 +/- 4 with captopril, 110 +/- 4 with nifedipine, and 115 +/- 5 with propranolol and increased with exercise to 163 +/- 4, 146 +/- 3, 136 +/- 4, 136 +/- 4, respectively. Oxygen consumption at peak exercise and at ventilatory anaerobic threshold (VAT) was 25.2 +/- 1.1 and 18.1 +/- 1.0 ml/min/kg with placebo. Only propranolol (-2.3 ml/min/kg) decreased peak exercise oxygen consumption. Oxygen consumption at VAT was reduced by nifedipine and propranolol but unaffected by captopril. The effects on exercise capacity of blood pressure reduction in hypertensive patients are dependent on the drug utilized and are not related to the amount of blood pressure reduction. The lowered oxygen consumption at VAT observed with nifedipine and propranolol, and not with captopril, might be due to an excessive downward shift of the muscle perfusion pressure--oxygen consumption relationship which might take place during exercise.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Anaerobic_Threshold_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Double-Blind_Method_MeSH P_Exercise_Tolerance_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Oxygen_Consumption_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH 
****** 8259746
----K E
----T Comparison of outcome of labetalol or hydralazine therapy during hypertension in pregnancy in very low birth weight infants.
----A Ninety-seven women with moderate to severe preeclampsia (PE) were allocated at random to labetalol or hydralazine treatment. Of these, 22 women with severe PE gave birth to neonates with VLBW (very low birth weight < or = 1500 g). Seven were allocated to labetalol treatment (Group A), eight to hydralazine treatment (Group B) and seven women received both drugs due to poor blood pressure control with a single drug therapy (Group C). No difference in cesarean section rate or in the indication for operative delivery could be seen. Gestational age was 29.9 weeks (25.4-32.5) in Group A, 28.6 weeks (26.6-33.4) in Group B and 27.3 weeks (26.7-31.1) in Group C (median and range). Birth weight did not differ between groups and 13 of the 22 infants weighed below 1000 g. There was a tendency to lower Apgar scores at five minutes in the hydralazine group. Time spent in the neonatal intensive care unit did not differ between groups. Five of the 11 neonates with gestational age (GA) < or = 28 weeks and three of the seven neonates in GA 29-30 weeks died. Neither the number of infants requiring intermittent positive pressure ventilation or duration of O2- treatment, nor number of infants with respiratory distress syndrome differed between groups. We did not find any difference in the outcome of the VLBW infants when the hypertensive mother had been treated with either hydralazine or labetalol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hydralazine_MeSH S_adverse_effects_MeSH Hydralazine_adverse_effects_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH P_Infant__Low_Birth_Weight_MeSH M_Infant__Newborn_MeSH M_Labetalol_MeSH S_adverse_effects_MeSH Labetalol_adverse_effects_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Pre-Eclampsia_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Outcome_MeSH 
****** 7903213
----K E
----T The effects of tertatolol on lipid profile.
----A Tertatolol is a noncardioselective beta-blocker without intrinsic sympathomimetic activity. In a preliminary 3-month open study, it was shown that T was devoid of any atherogenic effect since HDL-cholesterol (HDL-C) and apoprotein levels did not change for 3 months of therapy. To investigate the long-term effects of tertatolol on the lipid profile and its safety in hypertensive patients with peripheral arterial disease (PAD), a 9-month, randomized, double-blind, parallel group study was carried out in 40 patients. Tertatolol 5 mg once daily was compared with metoprolol 200 mg once daily. If BP was not controlled after 2 months, a vasodilatator agent, dihydralazine, was added at the lowest dose required to control BP (diastolic BP < 90 mm Hg). Lipoprotein fractions and apoproteins were assayed before (M0) and after 2, 6 and 9 months of therapy. At the same occasions, peripheral arterial disease (PAD) was evaluated on exercise tests carried out on a treadmill and on the regional blood flow measured in the ankle arteries by the Doppler technique. Four patients were not eligible for analysis. In the tertatolol group, 1 patient with a normal BP, and 2 patients who dropped out, 1 because of persistent nausea and 1 because of personal reasons. In the metoprolol group, 1 patient refused to take dihydralazine. In the 35 fully documented patients, BP control was achieved in both groups. The mean reductions in supine systolic/diastolic BP were 31.4/14.6 and 34.7/17.1 mm Hg in the tertatolol and metoprolol groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dihydralazine_MeSH S_therapeutic_use_MeSH Dihydralazine_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Intermittent_Claudication_MeSH S_physiopathology_MeSH Intermittent_Claudication_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH P_Thiophenes_MeSH M_Time_Factors_MeSH 
****** 7903214
----K E
----T Overview of clinical safety and efficacy of tertatolol.
----A Tertalolol is a noncardioselective beta-blocker, devoid of intrinsic sympathomimetic activity. Its renal vasodilating properties have been demonstrated both in animals and in man. The beta-blocking activity of tertatolol was assessed on the reduction of heart rate at submaximal exercise. The oral dose of 5 mg was optimal, leading to a significant reduction of diastolic blood pressure throughout 24 h. The efficacy was confirmed in mid- and long-term studies. In mid-term, randomized controlled studies, versus beta-blockers, the antihypertensive efficacy of tertatolol 5 mg was comparable to that of acebutolol 400 mg but of earlier onset, and comparable to that of atenolol 100 mg. Its efficacy was confirmed in 3 long-term studies. In the first study, tertatolol 5 mg alone or combined with a diuretic and, if necessary, dihydralazine, controlled 93.6% of patients (supine DBP < 90 mm Hg). 72.7% of patients were controlled with tertatolol alone, 16.4% with tertatolol plus diuretic, and 4.5% with tertatolol plus diuretic and dihydralazine. In a second study, 88.5% of patients were controlled, 56.3% with tertatolol alone and 32.2% with tertatolol plus diuretic. In the third study, 88.8% of patients were controlled after 1 year treatment, 66.1% with tertatolol alone and 22.7% with tertatolol plus diuretic. The overall clinical safety was excellent: only 6.6% of the 2,706 patients treated for 1 year withdrew from the study because of side effects. In patients followed for 1 year, side effects were rare, transient and mostly of mild severity. Biochemical surveillance did not show any adverse metabolic effects of tertatolol. Conversely, in two long-term studies, creatinine and cholesterol levels decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH P_Thiophenes_MeSH M_Time_Factors_MeSH 
****** 7903218
----K E
----T Overview of novel renal properties of tertatolol.
----A The renal vasodilatating properties of tertatolol demonstrated in animals have been confirmed in man. In a first study [Paillard et al., 1986], tertatolol (T) 5 mg and propranolol (Pr) 160 mg (SR) were given orally for 15 days to 2 groups of 9 patients with essential hypertension. Glomerular filtration rate (GFR), measured by inulin clearance and renal plasma flow (RPF) measured by PAH clearance increased in T group (+8.9%, p = 0.038 and + 13.0%, p = 0.007, respectively) and decreased in Pr group (-2.8%, NS and -13.4%, p < 0.001, respectively). Two clinical pharmacology studies [Leeman et al., 1986; Nitenberg et al., 1990] have shown specific and selective effects of tertatolol on the renal vasculature. In 8 hypertensive patients with chronic renal failure, the effects of tertatolol 5 mg were evaluated before and after 3 months of treatment on GFR using inulin clearance, and RPF, using PAH clearance [Hannedouche et al., 1991]. After 3 months of treatment, GFR and effective RPF increased significantly by 10 and 13%, respectively, whereas RVR decreased by 16% and the filtration fraction was unchanged. In summary, tertatolol 5 mg, contrasting with other beta-blockers, possesses a selective effect on the renal circulation beneficial to hypertensive patients. The mechanisms of this renal vasodilatation are not fully understood but might involve renal 5-HT1A receptor stimulation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Kidney_Failure_MeSH S_complications_MeSH Kidney_Failure_complications_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Renal_Circulation_MeSH S_drug_effects_MeSH Renal_Circulation_drug_effects_MeSH P_Thiophenes_MeSH 
****** 8262084
----K I
----T Atenolol versus the fixed combination of atenolol and nifedipine in stable angina pectoris.
----A One hundred and fourteen patients (94 male) with chronic stable angina who had a positive exercise test after 4 weeks on atenolol alone were randomized to receive either atenolol alone or the fixed combination of atenolol and nifedipine slow release formulation for 4 weeks in a double-blind cross-over manner. Exercise stress testing (Bruce protocol) at the end of each treatment period demonstrated that the time to the onset of pain and occurrence of 1 mm ST segment depression improved significantly (P < 0.05 and P < 0.001 respectively) whilst on the fixed combination compared to atenolol alone. In order to achieve sufficient sensitivity in the analysis of the exercise times, novel statistical methods based on survival analysis were used. Maximum ST segment depression was 0.13 mm less (P < 0.04) while on the fixed combination. The incidence of withdrawals and adverse effects was similar on both treatments.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Delayed-Action_Preparations_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH 
****** 8263885
----K E
----T Randomised double-blind comparative study of efficacy and safety of hydroflumethiazide and reserpine and chlortalidone and atenolol in the treatment of mild to moderate hypertension in black patients.
----A This randomised, double-blind study compared the efficacy and safety of a fixed combination of hydroflumethiazide 50 mg and reserpine 0.125 mg (H-R) and chlortalidone 12.5 mg and atenolol 50 mg (C-A) in adult black patients with mild to moderate hypertension (a resting supine diastolic blood pressure (DBP) between 95 and 115 mmHg after a two week placebo washout period). If the DBP did not reach 90 mmHg after four weeks, the dosage was doubled. There were 27 patients in the H-R group and 22 in the C-A group who completed the study. In the H-R group, supine systolic and diastolic BP were reduced from 156.5 (95% confidence intervals 150.1-162.9) and 102.0 (97.5-106.5) mmHg to 137.0 (130.6-143.4) and 87.4 (83.0-91.9) mmHg, respectively. The corresponding values in the C-A group were 154.1 (147.0-161.2) and 103.4 (98.5-108.4) mmHg to 136.4 (129.3-143.5) and 91.2 (86.2-96.1) mmHg, respectively. Normalisation, response and control of DBP was achieved in 88.9, 92.6 and 100% of patients, respectively, in the H-R group, and in 81.8, 95.5 and 95.5% of patients in the C-A group, respectively. The dose was doubled in 14.8% of patients on H-R and 40.1% on C-A. No clinically significant abnormalities in laboratory variables and no serious adverse effects were encountered. Both drugs have been shown to be efficacious and safe in the treatment of mild to moderate hypertension in black patients.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Human_MeSH M_Hydroflumethiazide_MeSH S_adverse_effects_MeSH Hydroflumethiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydroflumethiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Reserpine_MeSH S_adverse_effects_MeSH Reserpine_adverse_effects_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8269444
----K E
----T Low-dose bisoprolol/hydrochlorothiazide: an option in first-line, antihypertensive treatment.
----A Two recent, multicenter, double-blind, placebo-controlled studies established the efficacy and safety of low-dose bisoprolol/hydrochlorothiazide (HCTZ) in patients with mild to moderate essential hypertension. Bisoprolol, a cardioselective beta-blocker, was used in a dose of 2.5 mg, 5 mg, or 10 mg. HCTZ was used at a dose of 6.25 mg. This low-dose compound was developed to minimize dose-related adverse effects. The addition of HCTZ to each of the doses of bisoprolol was compared with monotherapy and placebo. Results of both studies demonstrated that this once-a-day, low-dose option effectively reduced sitting diastolic and systolic blood pressure measured at the end of the 24-hour dosing period. Drug-related adverse effects, including those generally associated with traditional beta-blocker therapy, were infrequent in individuals who received the low-dose bisoprolol/HCTZ regimen. Dose-related side effects were minimized because of the low doses of the two agents used together. There were no significant changes in mean total cholesterol, triglycerides, or serum glucose with bisoprolol/HCTZ 6.25 mg therapy versus placebo (analysis of variance statistical methods). The incidence of treatment-induced hypokalemia with bisoprolol/HCTZ 6.25 mg was not significant; uric acid elevations were minimized, and the incidence of hyperuricemia was significantly (P < 0.01) less with bisoprolol/HCTZ 6.25 mg than with 25 mg of HCTZ. Once-a-day dosing with the low-dose agent controlled (defined as a sitting diastolic blood pressure < or = 90 mmHg and/or a decrease from baseline > or = 10 mmHg) blood pressure in up to 80% of patients for a full 24 hours after dosing.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8276050
----K E
----T The pharmacokinetic and pharmacodynamic interactions of ramipril with propranolol.
----A We have studied the pharmacodynamic effects of ramipril, propranolol, and their combination, as well as the effect of propranolol on the pharmacokinetics of ramipril in 12 healthy men (age 24 (SD 6) y, weight 72 (7) kg). Propranolol and placebo, ramipril and placebo, or propranolol and ramipril were given orally for four days in a crossover, double-blind fashion. The pharmacokinetics of ramipril and ramiprilat were investigated on day 4. Effects on plasma renin activity, ACE activity, and heart rate and blood pressure both before and after a standardized exercise test were measured on days 1 and 4. On day 4 the combination reduced the mean arterial pressure by 2.8 mmHg compared with propranolol alone and by 3.7 mmHg compared with ramipril alone. Ramipril had no effect on the bradycardia induced by propranolol. Propranolol reduced exercise mean arterial pressure by 9 mmHg (day 4) and heart rate by 7 beats.min-1 (day 4) compared with ramipril; this was not affected by co-administration of ramipril. On day 4 the average plasma renin activity was not significantly higher than after the combination. ACE activity was not affected by propranolol. The pharmacokinetics of ramipril and ramiprilat were not influenced by propranolol. The combination of ramipril and propranolol has additive pharmacodynamic effects that may be useful in the treatment of hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Propranolol_MeSH S_pharmacokinetics_MeSH Propranolol_pharmacokinetics_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Ramipril_MeSH S_pharmacokinetics_MeSH Ramipril_pharmacokinetics_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7506322
----K E
----T Systemic and renal hemodynamic responses to carvedilol and metoprolol in hypertensive renal transplant patients.
----A According to a randomized double-blind cross-over design, the short-term (8 weeks, n = 12) and acute (2 h, n = 6) systemic and renal hemodynamic effects of carvedilol (25-50 mg o.d.) and metoprolol (100-200 mg o.d.) were compared in kidney allograft recipients with mild transplant dysfunction and arterial hypertension chronically treated with metoprolol. Cardiac output (Q) was measured by Doppler echography and renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by constant infusion techniques using [123I]iodohippurate and [51Cr]EDTA, respectively. After 8 weeks, mean blood pressure (101 +/- 3 vs. 103 +/- mm Hg) and RBF (318 +/- 14 vs. 316 +/- 14 ml/min) were comparable for the two drugs, whereas heart rate (HR), Q, and GFR (39 +/- 2 vs. 42 +/- 2 ml/min, p < 0.05) were slightly lower and the RBF/Q ratio (6.4 +/- 0.4 vs. 5.8 +/- 0.4%, p < 0.05) was higher with carvedilol than with metoprolol. During short-term treatment, a single dose of metoprolol acutely decreased HR and Q, carvedilol increased RBF, and both carvedilol and metoprolol enhanced the RBF/Q ratio and decreased renal vascular resistance (by 23 and 7%, p < 0.01 carvedilol vs. metoprolol). These data suggest that carvedilol has beneficial acute renal hemodynamic effects in hypertensive kidney allograft recipients with mild transplant dysfunction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH P_Kidney_Transplantation_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8279372
----K I
----T Comparison of nifedipine gastrointestinal therapeutic system and atenolol on antianginal efficacies and exercise hemodynamic responses in stable angina pectoris.
----A A gastrointestinal therapeutic system (GITS) of nifedipine has been developed to provide a once-daily dosing, and predictable, relatively constant plasma concentrations. This study compared the antianginal efficacy of nifedipine GITS with a once-a-day beta-receptor blocker, atenolol. Seventeen patients with documented coronary artery disease and stable stress-induced angina pectoris were studied during a 2-week, single-blind, placebo baseline phase and a 12-week randomized, double-blind, active drug crossover efficacy phase, using the bicycle exercise test and ambulatory electrocardiographic recordings. Patients exercised significantly longer with nifedipine GITS (883 +/- 47 seconds) and atenolol (908 +/- 44 seconds) than with placebo (794 +/- 41 seconds). Nifedipine GITS reduced systolic blood pressure at all stages of exercise compared with placebo but, because heart rate tended to increase more during nifedipine therapy, there was no difference in rate-pressure products between the placebo and nifedipine GITS periods. In contrast, atenolol reduced heart rate, systolic blood pressure and rate-pressure product during exercise compared with placebo. Whereas left ventricular ejection fractions (by radionuclide angiocardiography) increased with exercise, the maximal increase was smaller with atenolol than with placebo and nifedipine. The net increase in left ventricular ejection fraction at the end of exercise was greater with nifedipine than with placebo or atenolol. Ambulatory electrocardiograms showed only a small number of ischemic events. Neither nifedipine GITS nor atenolol reduced the number of ischemic events or total duration of ST-segment deviations significantly. It is concluded that nifedipine GITS is as effective an antianginal agent as atenolol, but the hemodynamic effects of the 2 agents differ.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_radionuclide_imaging_MeSH Angina_Pectoris_radionuclide_imaging_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH P_Drug_Delivery_Systems_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Radionuclide_Angiography_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8279377
----K E
----T Characteristics and radiofrequency ablation therapy of intermediate septal accessory pathway.
----A Fourteen patients (5%) with an intermediate septal accessory pathway were identified among 283 consecutive patients with the Wolff-Parkinson-White syndrome who had electrophysiologic study and radiofrequency ablation therapy. Nine were women and 5 were men (mean age 33 +/- 13 years). The resting electrocardiogram showed ventricular preexcitation in 8 patients and normal PR interval in 6. Anterograde and retrograde mapping studies revealed that the accessory pathway was para-Hisian in 11 patients and paranodal in 3. The accessory pathway was successfully ablated in 10 patients (9 para-Hisian and 1 paranodal) and damaged in 1 (para-Hisian). Treatment of 3 patients was complicated by transient atrioventricular (AV) block, of 1 by intermittent second-degree AV block, and of another by permanent complete AV block requiring implantation of a permanent pacemaker. Six patients underwent a follow-up electrophysiologic study 84 +/- 55 days after ablation; none had induction of tachycardia even after isoproterenol infusion. It is concluded that radiofrequency ablation therapy for intermediate septal accessory pathway is feasible. However, the success rate is only modest (71%), whereas complications with heart block (36%) or complete right bundle branch block (29%) are high. Thus, the procedure should be reserved for patients with life-threatening or troublesome symptomatic tachyarrhythmias.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH P_Catheter_Ablation_MeSH S_adverse_effects_MeSH Catheter_Ablation_adverse_effects_MeSH M_Electrocardiography_MeSH M_Electrophysiology_MeSH M_Female_MeSH M_Heart_Block_MeSH S_etiology_MeSH Heart_Block_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Wolff-Parkinson-White_Syndrome_MeSH S_physiopathology_MeSH Wolff-Parkinson-White_Syndrome_physiopathology_MeSH S_surgery_MeSH Wolff-Parkinson-White_Syndrome_surgery_MeSH 
****** 8281538
----K E
----T The effect of sulfinpyrazone on treadmill exercise-induced angina pectoris.
----A Suspecting that platelet thromboemboli could play a role in the pathogenesis of myocardial ischemia, we have done a random-order, double-blind, crossover study of the effect of the platelet-active drug sulfinpyrazone on treadmill exercise-induced angina pectoris in 30 men with coronary artery disease. The mean duration of exercise before onset of angina was 43 s longer after taking sulfinpyrazone than before and 11 s shorter after taking placebo than before. Analysis of variance for crossover design showed that the mean difference between the values obtained before and after sulfinpyrazone was significantly different (p < 0.01) from the mean difference between the values before and after placebo. Sulfinpyrazone had no effect on the mean heart rate-blood pressure product at onset of angina, change in ST segment during exercise, or preexercise platelet aggregate ratio and bleeding time. Exercise until angina occurred did not affect the platelet aggregate ratio.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Sulfinpyrazone_MeSH S_pharmacology_MeSH Sulfinpyrazone_pharmacology_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 8282334
----K E
----T Effects of a beta-blocker or a converting enzyme inhibitor on resistance arteries in essential hypertension.
----A Seventeen male untreated mild essential hypertensive patients aged 41 +/- 2 years agreed to participate in a double-blind randomized trial to test the effects of antihypertensive treatment on the structure and function of subcutaneous resistance arteries. Patients were treated with either 50 to 100 mg/d atenolol or 2.5 to 5 mg/d cilazapril. Blood pressure before treatment was 148 +/- 6/99 +/- 1 and 147 +/- 2/99 +/- 1 mm Hg, respectively. At 1 year of treatment blood pressure was 131 +/- 4/85 +/- 2 and 132 +/- 2/87 +/- 1 mm Hg, respectively. Resistance arteries (200 to 400 microns lumen diameter) dissected from subcutaneous gluteal biopsies obtained before treatment and at 1 year showed that the media-lumen ratio of arteries from patients treated with cilazapril was reduced to 6.31 +/- 0.21% from 7.54 +/- 0.31% before treatment (P < .05), still slightly but significantly larger (P < .05) than the media-lumen ratio of resistance arteries of normotensive control subjects (5.15 +/- 0.30%). In contrast, in arteries from patients treated with atenolol there was no significant change with treatment (7.97 +/- 0.60% before and 8.07 +/- 0.45% after 1 year of treatment). Active wall tension responses to endothelin-1 were blunted in hypertensive patients and normalized in the cilazapril-treated patients. Depressed active media stress responses to norepinephrine, arginine vasopressin, and endothelin-1 were accordingly normalized in the patients receiving cilazapril as the media width became thinner but were unchanged in those taking atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8288408
----K E
----T Effect of metoprolol and diltiazem on the total ischaemic burden in patients with chronic stable angina: a randomized controlled trial.
----A We conducted a randomised controlled trial to study the effects of metoprolol and diltiazem on the total ischaemic burden--sum of symptomatic and silent myocardial ischaemia, in 146 patients with stable angina pectoris. One-hundred thirty-four completed the study protocol. Sixty-eight patients received metoprolol (100 mg twice daily, n = 52, 50 mg twice daily, n = 16) while 66 received diltiazem (90 mg three times daily, n = 50, 60 mg three times daily, n = 16). The drugs were given for 4 weeks. The primary outcome variables were frequency and duration of total ischaemic burden, silent and symptomatic myocardial ischaemia. These were measured on 48 h of Holter monitoring. The reductions in duration and frequency of total ischaemic burden by metoprolol, 76% and 40%, respectively, were significantly higher than by diltiazem, 43% and 24%, respectively (P < 0.01 and P < 0.02). The frequency and duration of silent myocardial ischaemia, which constituted more than 80% of the total ischaemic burden in the two groups showed similar results. However, the reduction in frequency of symptomatic myocardial ischaemia only was significantly greater by metoprolol (63% than diltiazem (24%) as the difference in reduction of duration of symptomatic ischaemia was insignificant (85% vs. 75%; P > 0.05). Whether a greater reduction of total ischaemic burden by metoprolol as compared to diltiazem has any implications for prognosis in patients with chronic stable angina remains to be established.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7507638
----K I
----T Effects of diltiazem, metoprolol, enalapril and hydrochlorothiazide on frequency of ventricular premature complexes.
----A Ventricular arrhythmias occur frequently in patients with hypertensive left ventricular (LV) hypertrophy and have been associated with increased incidence of sudden death. In this study, the effect of various antihypertensive medications on ventricular arrhythmias was evaluated in 31 hypertensive patients with moderate to severe LV hypertrophy. Patients were assessed at baseline (after 3 weeks of placebo treatment) and after treatment with each of 4 monotherapies: diltiazem 120 or 240 mg/day, metoprolol 100 or 200 mg/day, enalapril 10 or 20 mg/day and hydrochlorothiazide 50 or 100 mg/day. Each drug therapy was administered for 4 weeks. The sequence of each treatment was determined at random. Echocardiographic measurements and electrocardiograms were obtained only at baseline. Biochemical measurements and 48-hour Holter monitoring were obtained at baseline and at the end of each treatment. All treatments resulted in a significant but similar decrease in blood pressure. In the group as a whole diltiazem decreased ventricular premature complexes (VPCs) by 65% (p < 0.05) and metoprolol by 52% (p = 0.07). Enalapril and hydrochlorothiazide had no effect. In 12 patients with > or = 5 VPCs/hour at baseline, diltiazem and metoprolol decreased VPCs by 66% (p < 0.05). It is concluded that in hypertensive patients with moderate to severe LV hypertrophy, both diltiazem and metoprolol significantly reduce VPCs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiac_Complexes__Premature_MeSH S_etiology_MeSH Cardiac_Complexes__Premature_etiology_MeSH S_prevention_&_control_MeSH Cardiac_Complexes__Premature_prevention_&_control_MeSH S_ultrasonography_MeSH Cardiac_Complexes__Premature_ultrasonography_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Echocardiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8299527
----K 3
----T [The effect of angiotensin-converting enzyme inhibitors on proteinuria in chronic glomerulonephritis]
----A The effect of two angiotensin-converting enzyme (ACE) inhibitors, lisinopril and captopril, on proteinuria and renal haemodynamics was investigated in 11 hypertensives (9 men, 2 women; mean age 46 +/- 16 years) with proteinuria (> 1.5 g/24 h) due to chronic glomerulonephritis and impaired renal function (glomerular filtration rate < 75 ml/min). In a randomized and double-blind cross-over trial the patients received, each time for six weeks, either lisinopril (5 mg/d, sometimes increased to 10 mg/d after 3 weeks) or captopril (twice daily 12.5 mg, sometimes increased to twice 25 mg after 3 weeks). Initially and between the individual treatment phases they were on a placebo phase for 4 weeks. The following were measured: protein excretion, including fractional clearance of albumin and IgG, plasma-renin activity and renal haemodynamics. Protein excretion was not significantly reduced by either drug (placebo: 7.1 +/- 4.0 g/d; lisinopril: 5.1 +/- 2.8 g/d; captopril: 5.4 +/- 3.0 g/d). Albumin excretion and fractional albumin clearance were significantly decreased only by lisinopril (P < 0.05), not by captopril. Plasma-renin activity was increased more by lisinopril than captopril (Placebo: 1.0 +/- 0.9 ng/ml.h; lisinopril: 5.2 +/- 2.8 ng/ml.h [P < 0.05]; captopril: 1.8 +/- 1.3 ng/ml.h [P < 0.05]). The renal haemodynamics was only slightly influenced by either drug, but captopril significantly decreased the filtration fraction in the presence of chronic glomerulonephritis and renal failure. - Resulting from their influence on the renin-angiotensin-aldosterone system, ACE inhibitors have, in addition to their known action on renal haemodynamics, an independent effect on the loading barrier of the basal membrane of the kidney.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Glomerulonephritis_MeSH S_complications_MeSH Glomerulonephritis_complications_MeSH S_drug_therapy_MeSH Glomerulonephritis_drug_therapy_MeSH M_Human_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH 
****** 8300464
----K E
----T Effect of atenolol and labetalol on serum lipids.
----A Adverse alterations in lipid profile suggesting higher atherogenicity were observed following 12 weeks treatment with atenolol in patients of hypertension. No significant alterations in lipid profile were observed with labetalol therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_chemically_induced_MeSH Hyperlipidemia_chemically_induced_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Labetalol_MeSH S_adverse_effects_MeSH Labetalol_adverse_effects_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH 
****** 8301064
----K E
----T A prospective randomized study to evaluate propranolol in patients undergoing long-term endoscopic sclerotherapy.
----A A prospective randomized double-blind study was conducted to evaluate the efficacy of propranolol in patients with portal hypertension undergoing long-term endoscopic sclerotherapy (EST) for recurrent variceal bleeding. Consecutive patients with portal hypertension (Child's class A or B) due to cirrhosis (n = 72), non-cirrhotic portal fibrosis (n = 29) and extrahepatic portal venous obstruction (n = 13) attending the liver clinic of a tertiary care center were included in the study. All patients had had at least one documented episode of variceal bleed in the previous 4 weeks. Fifty-eight patients received propranolol and 56 received placebo in addition to weekly EST. Rebleeding occurred in 12 (21%) patients in the placebo group and 10 (17%) patients in the propranolol group during a mean follow-up period of 24.4 +/- 10.4 months in the former and 23.8 +/- 9.2 months in the latter group (P > 0.1). The number of episodes of rebleeding (14 in the placebo and 12 in the propranolol group) were also similar (P > 0.1). The median bleeding-free period was more than 40 months in both treatment groups (P > 0.1). The mean transfusion requirements and the number of hospital admissions for rebleeding were also similar in the two treatment groups (P > 0.1). Complete obliteration of varices was achieved in 44 (78.9%) patients in the placebo group and 43 (75.5%) patients in the propranolol group (P > 0.1). Recurrence of new varices was seen in two patients in the placebo and in three of those in the propranolol group. Seven patients in the placebo group and five in the propranolol group died (P > 0.1). Complications related to EST were similar in the two treatment groups but additional adverse effects were observed in the propranolol group. The cumulative incidence of rebleeding in the placebo group was 12.7 and in the propranolol group it was 11.2 per 100 patient years of follow-up. It is concluded that the addition of propranolol in patients with portal hypertension and fair hepatic function on long-term EST does not confer any additional benefit.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Combined_Modality_Therapy_MeSH M_Double-Blind_Method_MeSH M_Endoscopy_MeSH S_methods_MeSH Endoscopy_methods_MeSH M_Female_MeSH M_Hemorrhage_MeSH S_complications_MeSH Hemorrhage_complications_MeSH S_drug_therapy_MeSH Hemorrhage_drug_therapy_MeSH S_therapy_MeSH Hemorrhage_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_epidemiology_MeSH Hypertension__Portal_epidemiology_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Liver_MeSH S_drug_effects_MeSH Liver_drug_effects_MeSH S_physiology_MeSH Liver_physiology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_therapy_MeSH Liver_Cirrhosis_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_standards_MeSH Propranolol_standards_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH M_Time_Factors_MeSH M_Varicose_Veins_MeSH S_complications_MeSH Varicose_Veins_complications_MeSH S_drug_therapy_MeSH Varicose_Veins_drug_therapy_MeSH S_therapy_MeSH Varicose_Veins_therapy_MeSH 
****** 8301065
----K 3
----T Propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing endoscopic sclerotherapy. A randomized controlled trial.
----A The purpose of this study was to investigate the possible value of continuous administration of propranolol in the prevention of recurrent upper gastrointestinal bleeding in patients with cirrhosis undergoing chronic endoscopic sclerotherapy. Among 239 patients admitted for acute variceal bleeding, 85 with cirrhosis were randomized to receive sclerotherapy either alone (40) or in combination with propranolol (45). Sclerotherapy was carried out with an intravariceal injection of 5% ethanolamine oleate through a fiberoptic endoscope. The procedure was performed every week, until the esophageal varices at the gastroesophageal junction were too small for any further injections. Varices were reinjected if they recurred. Propranolol was given orally twice a day until heart rate was reduced by 25% in the resting position. The mean follow-up period was 23.2 and 24.2 months for sclerotherapy and the sclerotherapy plus propranolol groups, respectively. During this period a significant (P = 0.001) reduction in the recurrence of esophageal varices was observed in patients treated with the combination of sclerotherapy plus propranolol compared with those treated with sclerotherapy alone. However, the time of rebleeding from any source or from esophageal varices did not differ significantly between the two groups. In the sclerotherapy group 21 patients rebled (35 bleeding episodes) compared with 14 (22 episodes) in the combination therapy group. Patients in the sclerotherapy group were more prone to bleed from gastric varices and congestive gastropathy than patients treated with the combination of sclerotherapy plus propranolol (P = 0.012). Twenty-five patients in the endoscopic sclerotherapy group developed complications attributed to sclerotherapy compared with 23 patients in the sclerotherapy plus propranolol group. Complications directly attributable to propranolol were observed in 11 patients. Three of these patients stopped taking the drug due to heart failure (1) and flapping tremor (2). Eight patients (17.8%) died in the latter group while the corresponding figure in the sclerotherapy group was nine (22.5%). It is concluded that the continuous administration of propranolol may reduce incidences of recurrent upper gastrointestinal hemorrhage from gastric sources in patients with cirrhosis undergoing chronic sclerotherapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Combined_Modality_Therapy_MeSH M_Endoscopy_MeSH S_methods_MeSH Endoscopy_methods_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_complications_MeSH Gastrointestinal_Hemorrhage_complications_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_epidemiology_MeSH Liver_Cirrhosis_epidemiology_MeSH S_therapy_MeSH Liver_Cirrhosis_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Propranolol_MeSH S_standards_MeSH Propranolol_standards_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8303108
----K 1
----T [Prevention of digestive hemorrhage recurrence in hepatic cirrhosis with propranolol. A 4 years' follow-up study]
----A The aim of this study was to assess the effect of propranolol treatment on the recurrence of variceal bleeding and mortality in patients with hepatic cirrhosis. Fifty seven patients were studied; they were recruited within 15 days of an episode of variceal bleeding, assigned randomly to receive propranolol (n = 29) placebo (n = 28) and followed during 4 years. Three patients were lost from follow up and in 3 propranolol was discontinued due to secondary effects. Bleeding recurrence was less frequent in the treated patients (Kaplan Meier analysis p < 0.01). Ten patients on placebo and 1 receiving the active drug died. Life table analysis showed a significantly better survival in the group of patients treated with propranolol. It is concluded that propranolol decreases the recurrence of variceal bleeding and improves survival in patients with hepatic cirrhosis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8304366
----K I
----T Efficacy and safety of atenolol, enalapril, and isradipine in elderly hypertensive women.
----A PURPOSE: This trial was designed to evaluate the efficacy and safety of three different classes of antihypertensive agents in elderly women. PATIENTS AND METHODS: The trial had three phases: 4 to 8 weeks of placebo, 6 weeks of titration, and 16 weeks of maintenance. White women between 60 and 80 years old with sitting diastolic blood pressures (DBPs) from 95 through 114 mm Hg treated with placebo were evaluated by history, physical examination, laboratory studies, and quality-of-life interview. After double-blind randomization with low-dose atenolol, enalapril, or isradipine, the dose was increased stepwise and hydrochlorothiazide added as needed to achieve goal DBP (less than 90 mm Hg and greater than 10 mm Hg below baseline). During maintenance, patients not at goal were "stepped up," and patients with uncontrolled DBP at maximum dosage were removed from the study. The pretreatment (baseline) blood pressure of the 315 randomized participants averaged 161/100 mm Hg; 92% had been treated previously for hypertension, 15% had diabetes mellitus, 11% smoked, and 38% consumed alcohol. RESULTS: For 245 patients completing the trial, the average decrease in blood pressure during treatment was 18.2/15.6 mm Hg. Antihypertensive efficacy was similar for the monotherapy drug regimens, with 84%, 71%, and 80% of patients receiving atenolol, enalapril, and isradipine, respectively, achieving DBP goal. Of the 70 patients who did not complete the trial, 42 left because of symptoms and 19 because of uncontrolled DBP. No important, unexpected drug-induced changes in symptoms or blood chemistries were noted. Symptom frequency differed little among the three dosage levels, becoming maximal by the second visit at the same dosage level. CONCLUSION: All three drugs lowered DBP comparably, and none produced alarming effects. Thirteen percent of patients left the study because of symptoms.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isradipine_MeSH S_adverse_effects_MeSH Isradipine_adverse_effects_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8306902
----K E
----T Comparative study of the efficacy and tolerability of hydroflumethiazide versus propranolol in Africans with mild to moderate hypertension.
----A Sixty patients with Diastolic Blood Pressure (DBP) of 100-110mmHg matched for age, sex and Bp levels were randomly assigned to propranolol 80mg daily or Hydroflumethiazide (HFM) 50mg daily. HFM causes a significant reduction in systolic blood pressure (SBP) and DBP within 4 weeks compared both with baseline and propranolol (SBP 143.7 +/- 12.3 vs 158.1 +/- 10.9mmHg, P < 0.05; DBP 92.0 +/- 4.5 vs 102.4 +/- 5.1mmHg, P < 0.05), (SBP 143.7 +/- 12.2 vs 152 +/- 11.0mmHg P < 0.05; DBP 92.0 +/- 4.5 vs 101.1 +/- 6.1mmHg, P < 0.05), respectively. Propranolol produced no significant difference from the baseline at 4 weeks (SBP 152.0 +/- H.0 vs 154.1 +/- 11.5mmHg NS; DBP 101.1 +/- 6.1 vs 102.2 +/- 5.6mmHg, NS). Reduction in BP by HFM was maintained after 8 and 12 weeks with further reduction but which did not achieve statistical significance. Increased dose of propranolol (160mg daily) after 4 weeks caused significant reduction in BP by 8 week (SBP 146.8 +/- 11.8 vs 152.0 +/- 11.0mmHg, P < 0.05; DBP 95.9 +/- 4.4 vs 101.1 +/- 6.1mmHg P < 0.05), which was maintained upto 12 weeks. The values however remained higher than in the HFM group. More patients in the HFM group achieved target BP (< 140/90), SBP 53.8% vs 29.6% P < 0.05, DBP 69.2% vs 14.8% P < 0.01. Incidence of side effects was similar and will be discussed. Thiazides are superior to B'blockers as initial monotherapy in black hypertensives.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH M_Female_MeSH M_Human_MeSH M_Hydroflumethiazide_MeSH S_pharmacology_MeSH Hydroflumethiazide_pharmacology_MeSH S_therapeutic_use_MeSH Hydroflumethiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_classification_MeSH Hypertension_classification_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kenya_MeSH M_Male_MeSH M_Matched-Pair_Analysis_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Severity_of_Illness_Index_MeSH M_Time_Factors_MeSH 
****** 8307623
----K E
----T Hypertension in the spontaneously hypertensive rat and the sex chromosomes.
----A We investigated the involvement of loci on the sex chromosomes in the hypertension of the spontaneously hypertensive rat (SHR) by studying male F1 and F2 generation rats derived from reciprocal crosses of SHR with Wistar-Kyoto (WKY) rats (cross 1: WKY female x SHR male; cross 2: SHR female x WKY male). At 16 weeks of age there was no significant difference in the blood pressures of F1 animals derived from the two crosses. Similarly, in the F2 generation there was no significant difference in either indirect blood pressures measured at 12, 16, or 20 weeks of age or in direct systolic and diastolic blood pressures measured at 25 weeks of age between animals derived from the two crosses maintained on a normal salt diet. In a second study, cohorts of F2 rats from the two crosses were given 1% salt in their drinking water for 10 weeks from 16 weeks of age with indirect blood pressure measurements at 16 (presalt), 18, and 20 weeks and direct blood pressure measurements at 26 weeks. Although overall these animals had significantly higher blood pressures at both 20 and 26 weeks than animals of the first study, again there was no difference in blood pressures of animals derived from the two crosses, apart from a marginally significantly higher blood pressure at 18 weeks in animals from cross 1 (with SHR grandfather). The findings indicate that the sex chromosomes of the SHR and WKY rat used in these crosses do not contain loci where alleles differentially influence blood pressure under the genetic milieu provided by the cross.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Journal_Article 
----M M_Animals_MeSH M_Blood_Pressure_MeSH M_Chromosome_Mapping_MeSH M_Female_MeSH M_Hypertension_MeSH S_genetics_MeSH Hypertension_genetics_MeSH M_Male_MeSH M_Rats_MeSH M_Rats__Inbred_SHR_MeSH M_Rats__Inbred_WKY_MeSH P_Sex_Chromosomes_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8106700
----K E
----T Beneficial effects of metoprolol in heart failure associated with coronary artery disease: a randomized trial.
----A OBJECTIVES. This clinical trial was performed to determine the safety and clinical impact of titrated metoprolol therapy in patients with heart failure, documented coronary artery disease and a low ejection fraction. BACKGROUND. Despite known cardiodepressant effects, long-term use of beta-adrenergic antagonists appears to be beneficial in patients with idiopathic dilated cardiomyopathy. However, this therapy has not been critically evaluated in patients with heart failure and coronary artery disease. METHODS. In 50 patients with heart failure, known coronary artery disease and an ejection fraction < or = 0.40, we examined the impact of metoprolol therapy in a 6-month double-blind, placebo-controlled randomized trial, assessing the frequency of heart failure exacerbations and changes in symptoms (New York Heart Association functional class), ejection fraction and exercise duration. Placebo-treated patients who completed 6-month follow-up studies then underwent a trial with metoprolol therapy (crossover group). RESULTS. Metoprolol was titrated to a mean maximal dose of 87 mg/day (range 25 to 100) without serious adverse reactions. During double-blind therapy, use of a beta-blocker was associated with a significant reduction in the number of hospital admissions (4% vs. 32%, p < 0.05), overall improved functional class (p = 0.02), increased ejection fraction (4 +/- 7% [mean +/- SD] compared with 0 +/- 6%, p < 0.05) and a greater increase in exercise duration (193 +/- 276 vs. 38 +/- 213 s with placebo, p < 0.01). Crossover outcome paralleled the favorable impact seen during randomized metoprolol therapy. CONCLUSIONS. Cautious use of titrated metoprolol appears to be safe and beneficial when added to standard heart failure therapy in patients with dilated cardiomyopathy associated with coronary artery disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 8107184
----K E
----T Duplex Doppler ultrasonographic comparison of the effects of propranolol and isosorbide-5-mononitrate on portal hemodynamics.
----A Eighteen cirrhotic patients with esophageal varices at risk for bleeding took part in a double-blind study. The variations in PFV induced by either 40 mg of propranolol or 60 mg of sustained-release isosorbide-5-mononitrate on two consecutive days were evaluated with a duplex Doppler device. Both drugs caused a significant decrease in maximum (propranolol, P = 0.002; isosorbide-5-mononitrate, P = 0.021). Four patients responded to propranolol, three to isosorbide-5-mononitrate, and eight to both drugs; three did not show any change. Duplex Doppler sonography may be of use in the selection of the right pharmacologic treatment for the individual patient for the prevention of a bleeding esophageal varix.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Monitoring_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH S_ultrasonography_MeSH Hypertension__Portal_ultrasonography_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH 
****** 8111817
----K E
----T The safety and efficacy of once-daily nifedipine coat-core in combination with atenolol in hypertensive patients. Adalat CC Cooperative Study Group.
----A The efficacy and safety of once-daily nifedipine coat-core when added to a regimen of atenolol (ATN; 50 mg/day) were compared with ATN and placebo in 251 patients with essential hypertension in this 12-week, multicenter, randomized, double-blind, placebo-controlled, parallel-group study. Mean net reductions (ATN effect subtracted) in supine diastolic blood pressure at endpoint were 7.9 mmHg, 9.4 mmHg, and 9.9 mmHg at 30, 60, and 90 mg/day of nifedipine coat-core, respectively, and 4.1 mmHg on ATN+placebo. Beyond the first week of double-blind therapy, all reductions produced by nifedipine coat-core combined with ATN were statistically significant (P < 0.05) compared with ATN+placebo. On ambulatory blood pressure monitoring, trough-to-peak ratios of the change in diastolic blood pressure for the 30, 60, and 90 mg/day doses were 41%, 68%, and 78%, respectively. Adverse events were generally mild or moderate and most reflected the vasodilatory properties of nifedipine (eg, edema, headache). Nifedipine coat-core, when combined with ATN in patients not controlled by ATN alone, had significant antihypertensive activity for the entire 24-hour dosing interval and was well tolerated by the majority of patients in the study.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_blood_MeSH Nifedipine_blood_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tablets_MeSH 
****** 7509894
----K E
----T Bisoprolol and atenolol in essential hypertension: effects on systemic and renal hemodynamics and on ambulatory blood pressure.
----A The acute and short-term responses to bisoprolol and to atenolol on systemic and renal hemodynamics and on ambulatory blood pressure (BP) were compared in a randomized double-blind cross-over study including 14 patients with mild to moderate essential hypertension. After a 4-week placebo period, the patients received either bisoprolol (10 mg once daily, o.d.) or atenolol (100 mg o.d.) for 4 weeks and were switched to the other drug after a new 4-week placebo period. Cardiac output (CO) was measured by Doppler echography, and renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by constant infusion techniques using [123I]iodohippurate and [51Cr]EDTA, respectively. Bisoprolol and atenolol decreased diurnal and nocturnal blood pressure (BP). Both drugs decreased heart rate (HR) and BP both acutely and after 4 weeks. During short-term treatment, CO was maintained with bisoprolol but reduced by atenolol (by 17%). RBF decreased after the first drug intake (by 9 and 12%, respectively) but returned to its baseline value after 4 weeks, so that calculated renal vascular resistance (RVR) was reduced (by 12 and 15%, respectively). Overall, GFR was not affected by treatment. Bisoprolol and atenolol are effective antihypertensive agents that preserve renal hemodynamics during short-term treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_blood_supply_MeSH Kidney_blood_supply_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Monitoring__Physiologic_MeSH M_Renal_Circulation_MeSH S_drug_effects_MeSH Renal_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 8136096
----K E
----T Effect of withdrawal of antihypertensive drug on depressive mood.
----A To evaluate the effects on depressive mood of withdrawal of antihypertensive medication, we conducted a randomized, multi-center study with clinical centers at the Albert Einstein College of Medicine, Bronx, NY, University of Alabama School of Medicine, Birmingham, and the University of Mississippi School of Medicine in Jackson. Patients were formerly active participants in the Hypertension Detection and Follow-Up Program (HDFP) whose blood pressure was controlled with drugs for a period of 5 years. Of 496 patients, 431 had both baseline and "1-year" mood scores. Patients, stratified by obesity, were randomized to one of three groups: continue the HDFP medication; discontinue medication with no dietary intervention, or with sodium restriction and potassium increase; or, for those overweight, to a weight reduction intervention. Depression was assessed using the CES-D scale (Center for Epidemiological Studies--Depressed Mood), administered at baseline and again approximately 1 year after randomization. Of the seven treatment groups, only those who continued their HDFP medication showed significant improvement in mood from baseline. The overweight continue-medication group showed significantly greater improvement compared to the no-drugs, no-diet intervention groups, and to the overweight sodium-restriction group. Patients who had their blood pressure successfully controlled with weight reduction had a significant improvement in mood from 11.0 scale points to 8.0, P = .006. Comparisons between those withdrawn from diuretic alone and those withdrawn from both diuretic plus reserpine were inconclusive. Dietary Intervention Study of Hypertension (DISH) shows no evidence that continued use of chlorthalidone has a negative impact on quality of life, while our results concerning reserpine were inconclusive.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Affect_MeSH S_drug_effects_MeSH Affect_drug_effects_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH S_psychology_MeSH Depression_psychology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diet_therapy_MeSH Hypertension_diet_therapy_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Psychiatric_Status_Rating_Scales_MeSH M_Questionnaires_MeSH M_Reserpine_MeSH S_adverse_effects_MeSH Reserpine_adverse_effects_MeSH M_Substance_Withdrawal_Syndrome_MeSH S_psychology_MeSH Substance_Withdrawal_Syndrome_psychology_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8142192
----K I
----T Ten year mortality in relation to original size of myocardial infarct: results from the Gothenburg metoprolol study.
----A OBJECTIVE--To describe the relation between the extent of a myocardial infarct, measured according to maximum serum enzyme activity of lactate dehydrogenase, and mortality at 10 years. PATIENTS--In 759 patients with acute myocardial infarction in whom serum activity of heat stable lactate dehydrogenase had been determined every 12 hours for 108 hours after randomisation in an early intervention trial with metoprolol. MAIN OUTCOME MEASURE--Mortality at 10 years in relation to quartile of maximum serum lactate dehydrogenase activity and history of cardiovascular disease. RESULTS--Among all patients mortality at 10 years was 39% in the lowest quartile, 51% in the second quartile, 50% in the third, and 59% in the fourth (p < 0.001 for relation between infarct size and 10 year mortality). Among patients without a history of myocardial infarction, angina pectoris, diabetes mellitus, or hypertension the mortality in each quartile was 29%, 32%, 41%, and 56%, respectively (p < 0.001 for relation between infarct size and 10 year mortality). Among patients with any of these risk indicators the association between the estimated infarct size and mortality at 10 years was weak (p < 0.05). CONCLUSION--Estimated size of a myocardial infarct and mortality over 10 years seem to be related but mainly in patients without a history of cardiovascular disease.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_L-Lactate_Dehydrogenase_MeSH S_metabolism_MeSH L-Lactate_Dehydrogenase_metabolism_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_enzymology_MeSH Myocardial_Infarction_enzymology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH 
****** 8144799
----K E
----T A pilot trial of recombinant desulfatohirudin compared with heparin in conjunction with tissue-type plasminogen activator and aspirin for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 5 trial.
----A OBJECTIVES. The purpose of this study was to assess the value of recombinant desulfatohirudin (hirudin) as adjunctive therapy to thrombolysis in acute myocardial infarction. BACKGROUND. Failure to achieve initial reperfusion and reocclusion of the infarct-related artery remain major limitations of thrombolytic therapy despite aggressive regimens of heparin and aspirin. Hirudin, a direct thrombin inhibitor, has been shown in experimental models to enhance thrombolysis and reduce reocclusion. METHODS. The Thrombolysis in Myocardial Infarction (TIMI) 5 trial was a randomized, dose-ranging, pilot trial of hirudin versus heparin, given with front-loaded tissue-type plasminogen activator and aspirin to 246 patients with acute myocardial infarction. Patients received either intravenous heparin or hirudin at one of four ascending doses for 5 days. Patients underwent coronary angiography at 90 min and at 18 to 36 h, unless rescue angioplasty was performed. RESULTS. The primary end point, TIMI grade 3 flow in the infarct-related artery at 90 min and 18 to 36 h without death or reinfarction before the 18- to 36-h catheterization was achieved in 97 (61.8%) of 157 evaluable hirudin-treated patients compared with 39 (49.4%) of 79 evaluable heparin-treated patients (p = 0.07). All four doses of hirudin led to similar findings in the angiographic and clinical end points. At 90 min, TIMI grade 3 flow was present in 105 (64.8%) of 162 hirudin-treated patients compared with 48 (57.1%) of 84 heparin-treated patients (p = NS). Infarct-related artery patency (TIMI grade 2 or 3 flow) was similar in the two groups (82.1% and 78.6%, respectively). At 18 to 36 h, 129 (97.8%) of 132 hirudin-treated patients had a patent infarct-related artery compared with 58 (89.2%) of 65 heparin-treated patients (p = 0.01). Reocclusion by 18 to 36 h occurred in 2 (1.6%) of 123 hirudin-treated patients versus 4 (6.7%) of 60 heparin-treated patients (p = 0.07). Death or reinfarction occurred during the hospital period in 11 (6.8%) of 162 hirudin-treated patients compared with 14 (16.7%) of 84 heparin-treated patients (p = 0.02). Major spontaneous hemorrhage occurred in 1.2% of hirudin-treated patients versus 4.7% of heparin-treated patients (p = 0.09), and major hemorrhage at an instrumented site occurred in 16.3% and 18.6%, respectively (p = NS). CONCLUSIONS. Hirudin is a promising agent compared with heparin as adjunctive therapy with thrombolysis for acute myocardial infarction, and its evaluation in larger trials is warranted.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adjuvants__Pharmaceutic_MeSH S_therapeutic_use_MeSH Adjuvants__Pharmaceutic_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Hirudin_MeSH S_analogs_&_derivatives_MeSH Hirudin_analogs_&_derivatives_MeSH M_Hirudin_Therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH M_Partial_Thromboplastin_Time_MeSH M_Pilot_Projects_MeSH M_Recombinant_Proteins_MeSH S_therapeutic_use_MeSH Recombinant_Proteins_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Thrombolytic_Therapy_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vascular_Patency_MeSH 
****** 8147676
----K E
----T Sexual dysfunction with antihypertensive drugs.
----A The relationship of antihypertensive drugs have a long history of association with sexual dysfunction; however, this relationship is poorly documented. There appears to be a higher rate of sexual dysfunction in untreated hypertensive men compared with normotensive men. Sexual dysfunction increases with age and is associated with physical and emotional symptoms. There are few studies assessing sexual dysfunction with female and African-American hypertensive patients. Sexual dysfunction is associated with impairment of quality of life and noncompliance. Since group data may hide individual drug effects, baseline data should be collected on all patients before initiating therapy with any antihypertensive agent. Although questionnaires may not provide objective information on sexual dysfunction, the response rate to direct questioning may be less than the response rate on a questionnaire and may be affected by the gender or race of the interviewer. Research protocols using a double-blind, placebo-controlled design should assess sexual dysfunction in men and women in a standardized fashion.
----P Journal_Article Review Review__Tutorial 
----M M_Age_Factors_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Clinical_Trials_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Patient_Compliance_MeSH M_Quality_of_Life_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH 
****** 8148217
----K E
----T An assessment of lacidipine and atenolol in mild to moderate hypertension.
----A 1. The aim of this randomised, double-blind four way crossover study was to assess the interaction between the new calcium antagonist, lacidipine and atenolol, in patients with mild to moderate hypertension. 2. Sitting blood pressure at 4 h post-dosing with lacidipine (4 mg) and atenolol (100 mg) alone was significantly lower compared with placebo (137/89 +/- 3/3 mmHg; 142/89 +/- 5/3 mmHg; and 154/98 +/- 5/3 mmHg respectively; P < 0.001). Co-administration of both drugs produced a significant additive effect compared with atenolol and lacidipine alone (124/80 +/- 4/2 mmHg; P < 0.002). 3. Heart rate on treatment with lacidipine alone was significantly greater at 4 h compared with placebo (86 +/- 1 beats min-1 and 74 +/- 2 beats min-1 respectively; P < 0.001). When both drugs were used in combination, there was a significant decrease in pulse rate compared with lacidipine alone (58 +/- 1 beats min-1 and 86 +/- 1 beats min-1 respectively; P < 0.001). 4. Home blood pressure recordings confirmed the statistically significant reduction in blood pressure on co-dosing (120/82 +/- 10/2 mmHg) compared with lacidipine (140/92 +/- 5/3 mmHg) and atenolol (146/90 +/- 6/3 mmHg) given alone (P < 0.05). 5. Lacidipine alone produced a significant exercise tachycardia compared with atenolol alone and the atenolol/lacidipine combination (97 +/- 8 beats min-1; 65 +/- 4 beats min-1 and 75 +/- 7 beats min-1 respectively; P < 0.001). Exercise tolerance was not adversely affected by the co-administration of both lacidipine and atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Dihydropyridines_MeSH S_adverse_effects_MeSH Dihydropyridines_adverse_effects_MeSH S_pharmacology_MeSH Dihydropyridines_pharmacology_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Exercise_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pulse_MeSH S_drug_effects_MeSH Pulse_drug_effects_MeSH 
****** 7908532
----K E
----T Beta-adrenoceptor blockers in atrial fibrillation: the importance of partial agonist activity.
----A 1. The ideal drug treatment for atrial fibrillation will control resting heart rate, blunt exercise induced tachycardia whilst not exacerbating nocturnal bradycardia. Monotherapy with digoxin may not be ideal. We have compared the effect of combining digoxin (0.25 mg daily) with atenolol 50 mg and 100 mg or pindolol 5 mg twice daily and 15 mg twice daily in a cross-over randomised single-blind trial in eight symptomatic patients (six male; mean age 62 years) with poorly controlled atrial fibrillation. 2. Heart rate control was measured by 24 h ECG at baseline on digoxin therapy and after 2 weeks with each treatment. Symptom scores for breathlessness and palpitation were measured using visual analogue scales. 3. The addition of both beta-adrenoceptor blockers significantly reduced mean diurnal maximum heart rate from baseline (all P < 0.001 ANOVA). Atenolol at both doses caused a greater reduction than either dose of pindolol (P < 0.001 ANOVA). Nocturnal maximum heart rate was not significantly reduced from baseline by either beta-adrenoceptor blocker, but both doses of pindolol caused increases in nocturnal maximum heart rate compared with atenolol (P < 0.001 ANOVA). 4. Atenolol caused a reduction in diurnal minimum heart rate compared with baseline and caused a reduction in nocturnal minimum heart rate whereas pindolol caused an increase (P < 0.001 ANOVA). 5. Atenolol 100 mg caused longer nocturnal pauses compared with baseline but pindolol 15 mg twice daily reduced the number of nocturnal pauses > 1.5 s (P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Bradycardia_MeSH S_drug_therapy_MeSH Bradycardia_drug_therapy_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH S_pharmacology_MeSH Digoxin_pharmacology_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_pharmacology_MeSH Pindolol_pharmacology_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Single-Blind_Method_MeSH 
****** 8149521
----K E
----T Recombinant hirudin for unstable angina pectoris. A multicenter, randomized angiographic trial.
----A BACKGROUND: Coronary artery thrombosis plays an important pathophysiological role in unstable angina and non-Q-wave myocardial infarction. To date, heparin and thrombolytic therapy has not provided complete or consistent benefit. We hypothesized that recombinant hirudin, a direct thrombin inhibitor, would prevent accumulation of coronary artery thrombus in a manner superior to heparin. METHODS AND RESULTS: Patients with rest ischemic pain, abnormal ECG, and baseline angiogram indicating a > or = 60% stenosis of a culprit coronary artery or saphenous vein graft with visual appearance of thrombus were randomized to one of two different doses of heparin (either a target activated partial thromboplastin time [aPTT] of 65 to 90 or 90 to 110 seconds) or one of four doses of hirudin (0.05, 0.10, 0.20, or 0.30 mg.kg-1.h-1 infusion) in a dose-escalating protocol. After 72 to 120 hours of study drug, a repeat coronary angiogram was obtained, and the paired studies underwent quantitative analysis. The primary end point was change in the average cross-sectional area of the culprit lesion. Other efficacy end points also involved changes in culprit lesion dimensions and TIMI flow grade. Recombinant hirudin led to a dose-dependent elevation of aPTT that appeared to plateau at the 0.2-mg/kg dose. A higher proportion of hirudin-treated patients had their aPTT within a 40-second range (16% heparin versus 71% hirudin, P < .001). Overall, the 116 patients treated with hirudin tended to show more improvement than the 50 patients receiving heparin relative to the primary efficacy variable--the average cross-sectional area (P = .08)--as well as minimal cross-sectional area (P = .028), minimal luminal diameter (P = .029), and percent diameter stenosis (P = .07). CONCLUSIONS: Recombinant hirudin appears to be a promising antithrombotic intervention compared with heparin for inhibition of coronary artery thrombus. Large-scale comparative trials are warranted.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angina__Unstable_MeSH S_blood_MeSH Angina__Unstable_blood_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH S_radiography_MeSH Angina__Unstable_radiography_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Thrombosis_MeSH S_blood_MeSH Coronary_Thrombosis_blood_MeSH S_prevention_&_control_MeSH Coronary_Thrombosis_prevention_&_control_MeSH S_radiography_MeSH Coronary_Thrombosis_radiography_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_administration_&_dosage_MeSH Fibrinolytic_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heparin_MeSH S_administration_&_dosage_MeSH Heparin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Hirudin_MeSH S_administration_&_dosage_MeSH Hirudin_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Hirudin_analogs_&_derivatives_MeSH M_Hirudin_Therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Partial_Thromboplastin_Time_MeSH M_Recombinant_Proteins_MeSH S_administration_&_dosage_MeSH Recombinant_Proteins_administration_&_dosage_MeSH S_therapeutic_use_MeSH Recombinant_Proteins_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8150546
----K E
----T Long-term open evaluation of amlodipine vs hydrochlorothiazide in patients with essential hypertension.
----A The long-term efficacy and safety of amlodipine (2.5 to 10 mg) once daily was compared with that of hydrochlorothiazide (HCTZ) (25 to 100 mg) daily in 139 patients with mild-to-moderate hypertension. The study was a randomized, open-label, parallel comparison of 50 weeks' duration. Patients were randomized in a 2:1 ratio (amlodipine n = 92: HCTZ n = 47). Atenolol was added at week 12 if monotherapy was inadequate. At week 12, the mean reductions for supine and standing systolic and diastolic blood pressure values with amlodipine were found to be -15.2/-12.3 mmHg and -14.0/-11.6 mmHg respectively, as compared to -15.5/-11.1 mmHg and -16.1/-10.1 mmHg after treatment with HCTZ. The percentage of patients responding to treatment at week 12 was 74% on amlodipine and 70% on HCTZ. The addition of atenolol in those patients not adequately controlled on monotherapy produced additional mean reductions in supine and standing systolic and diastolic pressures in both the amlodipine-atenolol group and in the HCTZ-atenolol group. The incidence of adverse effects was 47% with amlodipine and 26% with HCTZ at 12 weeks. Overall, six patients were discontinued because of side effects while receiving amlodipine monotherapy and one from the HCTZ monotherapy group; none were discontinued because of side effects on combination therapy. Laboratory test abnormalities were reported by 16% of amlodipine-treated patients compared with 63% of patients on HCTZ. The antihypertensive effects of amlodipine and hydrochlorothiazide appeared to be comparable and were maintained during long-term therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8151265
----K E
----T Metformin and metoprolol CR treatment in non-obese men.
----A OBJECTIVE. To study the effect of metformin and metoprolol CR on insulin sensitivity, blood lipids, fibrinolytic activity and blood pressure. DESIGN. A double-blind, placebo controlled, triple cross-over study with randomization to either metformin, 850 mg b.i.d., or metoprolol CR 100 mg o.d., or placebo for a period of 18 weeks. The glucose uptake was measured with the euglycaemic clamp technique after every 6 weeks' treatment period. Blood pressure and blood samples were taken every 3rd week. SUBJECTS. Eighteen non-obese men (53 +/- 6 years of age). RESULTS. Metformin decreased C-peptide (P < 0.02), FFA (P < 0.003), total and low-density lipoprotein cholesterol, tissue plasminogen activator antigen and the urinary potassium excretion (P < 0.05 for all), but not blood pressure compared to placebo. Metoprolol CR reduced diastolic blood pressure and pulse rate; fasting free fatty acids and the urinary potassium increased (P < 0.05 for all). No effect of metformin or metoprolol CR was seen on the glucose disposal rate, blood glucose, plasma insulin, triglycerides, high-density lipoprotein cholesterol, lipoprotein(a), uric acid or plasminogen activator inhibitor 1 activity or antigen. The glucose uptake was not particularly decreased in these subjects. CONCLUSION. The study shows that metformin has some favourable effects on metabolism and that metoprolol CR is fairly neutral in this regard. The lack of effect of metformin on glucose disposal rate and blood pressure can be explained by the fact that the individuals studied were neither insulin resistant nor hypertensive. The data does not preclude an antihypertensive effect by treating a concomitant insulin resistance.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Analysis_of_Variance_MeSH M_Anthropometry_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH S_physiology_MeSH Body_Weight_physiology_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Fibrinolysis_MeSH S_drug_effects_MeSH Fibrinolysis_drug_effects_MeSH M_Glucose_Clamp_Technique_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metformin_MeSH S_therapeutic_use_MeSH Metformin_therapeutic_use_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8152445
----K E
----T Progression of aortic dilatation and the benefit of long-term beta-adrenergic blockade in Marfan's syndrome.
----A BACKGROUND. The aortic root enlarges progressively in Marfan's syndrome, and this enlargement is associated with aortic regurgitation and dissection. Long-term treatment with beta-adrenergic blockade, by reducing the impulse (i.e., the rate of pressure change in the aortic root) of left ventricular ejection and the heart rate, may protect the aortic root. METHODS. We conducted an open-label, randomized trial of propranolol in adolescent and adult patients with classic Marfan's syndrome (32 treated and 38 untreated [control] patients). Aortic-root dimensions and clinical end points (aortic regurgitation, aortic dissection, cardiovascular surgery, congestive heart failure, and death) were monitored for an average of 9.3 years in the control group and 10.7 years in the treatment group. All 70 patients were included in the analysis according to the intention-to-treat principle. RESULTS. The dose of propranolol was individualized; the mean (+/- SE) dose was 212 +/- 68 mg per day. The mean slope of the regression line for the aortic-root dimensions, which reflect the rate of dilatation, was significantly lower in the treatment group than in the control group (0.023 vs. 0.084 per year, P < 0.001). Clinical end points were reached in five patients in the treatment group and nine in the control group. The Kaplan-Meier survival curve for the treatment group differed significantly from that for the control group during the middle years of the trial and remained better for the treatment group throughout the study. CONCLUSIONS. Prophylactic beta-adrenergic blockade is effective in slowing the rate of aortic dilatation and reducing the development of aortic complications in some patients with Marfan's syndrome.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aneurysm__Dissecting_MeSH S_etiology_MeSH Aneurysm__Dissecting_etiology_MeSH M_Aorta_MeSH S_pathology_MeSH Aorta_pathology_MeSH M_Aortic_Aneurysm_MeSH S_etiology_MeSH Aortic_Aneurysm_etiology_MeSH S_pathology_MeSH Aortic_Aneurysm_pathology_MeSH M_Aortic_Valve_Insufficiency_MeSH S_etiology_MeSH Aortic_Valve_Insufficiency_etiology_MeSH M_Dilatation__Pathologic_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Marfan_Syndrome_MeSH S_complications_MeSH Marfan_Syndrome_complications_MeSH S_drug_therapy_MeSH Marfan_Syndrome_drug_therapy_MeSH S_mortality_MeSH Marfan_Syndrome_mortality_MeSH M_Morbidity_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8154413
----K E
----T Effects of metoprolol on early infarct expansion after acute myocardial infarction.
----A The effects of metoprolol on early infarct expansion after acute myocardial infarction were studied in rats (n = 54) that underwent either left coronary artery ligation (MI) or sham operation. Immediately after surgery, the rats received either metoprolol (M) by mouth, which had been dissolved in drinking water, for 72 hours supplemented with three intraperitoneal doses over the first 24 hours or no treatment (H2O). Three days after the initial surgery, hemodynamic measurements were made before and after volume loading. The rats were killed, the hearts were removed, and passive pressure-volume curves were obtained. The hearts were then fixed at a constant pressure and analyzed morphometrically. Infarct size was nonsignificantly lower in the metoprolol-treated group compared with the untreated group (38% +/- 5% MI-M vs 48% +/- 3% MI-H2O, p = 0.10) Compared with infarcted untreated rats, infarcted metoprolol-treated rats had a lower heart rate (322 +/- 13 beats/min MI-M vs 452 +/- 19 beats/min MI-H2O, p < 0.001), lower left ventricular systolic pressure (63 +/- 4 mm Hg MI-M vs 90 +/- 6 mm Hg MI-H2O, p = 0.004), and lower +dp/dt (1340 +/- 169 mm Hg/sec MI-M vs 2872 +/- 273 mm Hg/sec MI-H2O, p < 0.001), but left ventricular end-diastolic pressure and cardiac index did not differ between the two groups. Left ventricular weight corrected for body weight was higher in infarcted rats treated with metoprolol compared with infarcted untreated rats (2.76 +/- 0.07 gm/kg MI-M vs 2.41 +/- 0.09 gm/kg MI-H2O, p < 0.05). The initial slope of the pressure-volume relationship Ki, an index of operative volume stiffness, was lower in infarcted rats treated with metoprolol compared with infarcted untreated rats (p = 0.03). There were, however, no significant differences in the expansion index, thinning ratio, or left ventricular volume between the two infarcted groups. Thus metoprolol therapy begun in the immediate postinfarction period promotes an increase in left ventricular weight and reduces operative volume stiffness but has no significant effect on indexes of early infarct expansion.
----P Journal_Article 
----M M_Animals_MeSH M_Cardiac_Volume_MeSH S_drug_effects_MeSH Cardiac_Volume_drug_effects_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_pathology_MeSH Myocardial_Infarction_pathology_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Random_Allocation_MeSH M_Rats_MeSH M_Rats__Sprague-Dawley_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Ventricular_Pressure_MeSH S_drug_effects_MeSH Ventricular_Pressure_drug_effects_MeSH 
****** 8155010
----K E
----T Predictive value of clinical history and electrocardiogram in patients with transient ischemic attack or minor ischemic stroke for subsequent cardiac and cerebral ischemic events. The Dutch TIA Trial Study Group.
----A OBJECTIVE: Patients with cerebral ischemia have a high mortality rate. The most common cause of death is myocardial infarction. We attempted to identify risk factors for subsequent cardiac events in patients with cerebral ischemia by means of the history and electrocardiography performed with the patient at rest. DESIGN: The original inception cohort was entered in a multicenter randomized clinical trial (30 or 283 mg/d of aspirin) and followed up prospectively for a mean period of 2.6 years. SETTING: Patients were admitted to the hospital or seen in outpatient clinics. PATIENTS: Patients with one or more transient ischemic attacks (symptoms completely reversible within 24 hours) and patients with minor ischemic stroke (symptoms persisting for longer than 24 hours) were randomized, provided they were independent in most activities of daily living. Patients with a definite or probable source of embolism in the heart were excluded. A total of 3021 patients were included in the study. Follow-up was performed at 4-month intervals. MAIN OUTCOME MEASURES: Primary cardiac outcome events were defined as nonfatal myocardial infarction and cardiac death. Cardiac death included sudden death, fatal myocardial infarction, or death due to congestive heart failure; 189 patients suffered a cardiac death--82 of which were sudden deaths--or nonfatal myocardial infarction. RESULTS: By means of multivariate analysis, the following independent predictors for cardiac events were identified (hazards ratio/95% confidence limits): age older than 65 years (1.6/1.2 to 2.2), male sex (1.5/1.1 to 2.1), angina pectoris (1.5/1.0 to 2.3), diabetes (1.6/1.1 to 2.5), anterior infarction noted on electrocardiography (1.7/1.1 to 2.7), inverted T wave noted on the electrocardiogram (1.6/1.1 to 2.4), and left ventricular hypertrophy noted on electrocardiography (3.2/2.0 to 4.9). CONCLUSIONS: The history and the electrocardiogram obtained with the patient at rest are valuable tools for cardiac risk assessment in patients with recent cerebral ischemia.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Brain_Ischemia_MeSH S_complications_MeSH Brain_Ischemia_complications_MeSH S_etiology_MeSH Brain_Ischemia_etiology_MeSH S_mortality_MeSH Brain_Ischemia_mortality_MeSH S_physiopathology_MeSH Brain_Ischemia_physiopathology_MeSH M_Cause_of_Death_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Ischemic_Attack__Transient_MeSH S_complications_MeSH Ischemic_Attack__Transient_complications_MeSH S_mortality_MeSH Ischemic_Attack__Transient_mortality_MeSH S_physiopathology_MeSH Ischemic_Attack__Transient_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Predictive_Value_of_Tests_MeSH M_Risk_Factors_MeSH 
****** 8162238
----K I
----T Ten-year mortality rate after development of acute myocardial infarction in relation to clinical history and observations during hospital stay: experience from the Goteborg metoprolol trial.
----A BACKGROUND: Previous studies on the prognosis after acute myocardial infarction (AMI) have mainly focused on the first few years. In this study, we aimed to describe the mortality rate during 10 years of follow-up after development of AMI in relation to clinical history and observations during the hospital stay. METHODS: We prospectively followed for 10 years all patients with suspected AMI, enrolled between 1976 and 1981, participating in an early intervention trial with metoprolol who fulfilled given criteria for AMI. RESULTS: A total of 809 patients developed AMI during the first 3 days in hospital, of whom 399 were randomly assigned to receive metoprolol and 410 to receive placebo. The overall 10-year mortality rate, including initial in-hospital mortality, was 51%. In a multivariate analysis considering age, sex, history of cardiovascular diseases, estimated infarct size, and the occurrence of various complications during initial hospitalization (i.e. congestive heart failure, severe ventricular arrhythmias, tachycardia, hypotension, high-degree atrioventricular block and severity of pain) the following appeared as independent predictors of death: a history of diabetes mellitus (P < 0.001), congestive heart failure during hospitalization (P < 0.001), age (P < 0.001), and a history of previous myocardial infarction (P < 0.001). CONCLUSION: Independent predictors of death during the first 10 years after AMI were a history of diabetes mellitus, congestive heart failure during hospitalization, age, and previous myocardial infarction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hospital_Mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Intervention_Studies_MeSH M_Male_MeSH M_Medical_History_Taking_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Survival_Rate_MeSH M_Sweden_MeSH M_Time_Factors_MeSH 
****** 8173687
----K E
----T Antihypertensive efficacy and tolerability of a new once-daily felodipine-metoprolol combination compared with each component alone. The Swedish/UK Study Group.
----A A double-blind, randomised, parallel-group study was performed to compare the efficacy and tolerability of a new extended-release tablet containing felodipine and metoprolol with each constituent agent as monotherapy. After a 4-week placebo period, 159 patients with mild-to-moderate essential hypertension were randomised to receive either the combination tablet of felodipine and metoprolol 10/100 mg, felodipine 10 mg or metoprolol 100 mg once daily if supine diastolic blood pressure was > or = 95 mmHg. After 12 weeks of active treatment, reductions in supine systolic/diastolic blood pressure 24 h after dosing were 20/14, 13/10 and 11/8 mmHg with felodipine-metoprolol, felodipine and metoprolol, respectively. The differences in blood pressure changes were 7/4 mmHg (p = 0.004/0.006) and 8/5 mmHg (p = 0.0002/< 0.0001) between the fixed combination and felodipine and metoprolol, respectively. Blood pressure response (defined as a diastolic blood pressure < or = 90 mmHg and/or a reduction > or = 10 mmHg) after 12 weeks of treatment was greater with the combination than with felodipine or metoprolol alone: 85% vs 72% (p = 0.06) and 54% (p = 0.001), respectively. Treatments were well tolerated and adverse events were as expected from previous studies with each agent and did not differ in frequency between groups. In conclusion, the extended-release tablet formulation of felodipine-metoprolol 10/100 mg produces a clinically relevant and significantly greater blood pressure reduction 24 h after dosing than either agent as monotherapy without decreasing tolerability.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH 
****** 8173688
----K E
----T Comparison of a felodipine-metoprolol combination tablet vs each component alone as antihypertensive therapy. The German Multicentre Study Group.
----A This was a 12-week double-blind, parallel-group study of 186 patients with supine diastolic blood pressure between 95 and 115 mmHg randomised to receive either 5 mg of felodipine or 50 mg of metoprolol, or a combination tablet containing the two drugs at the same dosages, given once daily. All drugs were extended-release formulations and blood pressure was measured 24 h after drug administration. After 12 weeks of treatment, the mean systolic/diastolic blood pressure reduction was significantly greater with the felodipine-metoprolol combination (28/18 mmHg) compared with felodipine (18/12 mmHg) or metoprolol (19/12 mmHg) alone. Antihypertensive response rate, defined as the percent of patients achieving a supine diastolic blood pressure < or = 90 mmHg and/or a reduction of > or = 10 mmHg with treatment, was significantly greater with the fixed combination (98%) than with either felodipine (79%) or metoprolol (82%) as monotherapy. The mean reduction in heart rate was significantly less with the combination (2 beats/min) than with metoprolol alone (4 beats/min), and heart rate was virtually unchanged in the felodipine group. The increased antihypertensive efficacy of the combination was associated with good tolerability that was similar to that of the monotherapies. Adverse events were mainly those related to arteriolar dilatation with felodipine and the combination, and dizziness and fatigue with metoprolol. Two patients taking the combination were withdrawn due to adverse events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH 
****** 8173689
----K E
----T Improved antihypertensive efficacy of the felodipine-metoprolol extended-release tablet compared with each drug alone.
----A In this double-blind, randomised, three-way crossover (latin square design), multicentre study, the aim was to compare the efficacy and tolerability of the fixed combination of felodipine and metoprolol with the individual components as monotherapy. A total of 58 patients with supine diastolic blood pressure of 100-115 mmHg were treated with (1) a fixed combination of felodipine plus metoprolol 5/50-10/100 mg (FM), (2) felodipine 5-10 mg (F) or (3) metoprolol 50-100 mg (M), for 12 weeks each. All treatments were extended-release formulations administered once daily and blood pressure was measured 24 h after dosing. Dose titration was performed after 6 weeks if diastolic blood pressure was > 90 mmHg. After 12 weeks of active treatment, the mean supine blood pressures were 153/89, 159/93 and 163/94 mmHg with FM, F and M, respectively. The mean differences in systolic/diastolic blood pressure were -5.6/-3.1 mmHg (p = 0.007/p = 0.002), -10.2/-4.4 mmHg (p < 0.0001/p < 0.0001) and -4.6/-1.4 mmHg (p = 0.03/p = 0.15) for FM vs F, FM vs M, and F vs M, respectively. Blood pressure control (supine diastolic blood pressure < or = 90 mmHg) after 12 weeks was achieved in a significantly greater proportion of patients during treatment with FM than with F or M; 71%, 45% and 40% were controlled with the respective treatments. With FM, 45% of the patients were taking the higher dose after 12 weeks of treatment. The corresponding figures for F and M were 60% and 67%, respectively. Thirteen of the 58 patients (22%) were controlled only with FM.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 8173698
----K E
----T Antihypertensive therapy and circadian blood pressure profiles: a retrospective analysis utilising cumulative sums.
----A The results of previous studies on the effects of antihypertensive agents on circadian blood pressure patterns are inconclusive, possibly due to the lack of a simple, objective, universally accepted method of quantifying circadian blood pressure profiles. In order to investigate for differences in the effects of antihypertensive drugs on circadian changes we utilised a recently described modified cumulative sums technique to quantify circadian alteration magnitude (CAM). CAM is simply calculated as the difference between crest and trough blood pressures, the mean blood pressures of the 6-h periods of highest and lowest sustained pressures respectively. The records from all 24-h ambulatory blood pressure monitoring performed over a 7 year period on subjects either on no medication (1208), or on treatment with a single first-line antihypertensive agent (578), were examined retrospectively. A sample (n = 40) stratified for trough diastolic blood pressure, age and sex was randomly selected from each of the following 5 groups: subjects on no medication, and subjects being treated with bendrofluazide, atenolol, class 2 calcium-channel blockers or captopril alone. Untreated subjects, those on bendrofluazide and those on a class 2 calcium channel blocker had similar circadian patterns. Subjects on atenolol therapy (25.9 +/- 1.7/18.3 +/- 1.3, systolic CAM +/- SE/diastolic CAM +/- SE) had attenuated circadian changes (p < 0.05) when compared to the untreated group (29.8 +/- 1.8/23.6 +/- 1.1), while those on captopril (34.9 +/- 2.4/25.7 +/- 1.8) exhibited markedly increased systolic and diastolic circadian blood pressure swings, which differed from those of the atenolol treated group (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8175218
----K E
----T Does captopril treatment before thrombolysis in acute myocardial infarction attenuate reperfusion damage? Short-term and long-term effects.
----A Several experimental studies carried out on animals and on isolated heart preparations show that captopril can reduce post-ischemic reperfusion injury. Our study was aimed at investigating the effects of captopril before thrombolysis in acute myocardial infarction (AMI) and included 259 patients, hospitalized within 4 h of the onset of symptoms. Patients were randomly subdivided into two groups: the first group (131 patients, Group A, pretreatment) received 6.25 mg captopril orally about 15 min before i.v. administration of urokinase (2 million), the second group (128 patients, Group B, late-treatment), received captopril about 3 days after thrombolytic treatment. Captopril doses were later increased in both groups according to blood pressure. All patients were subdivided according to the localization of infarction. Anterior AMI was shown by 166 patients (84 from Group A and 82 from Group B); 93 patients showed inferior AMI (47 from Group A and 46 from Group B). Ventricular hyperkinetic arrhythmias (VHAs) due to reperfusion were evaluated during the first 2 h. VHAs occurred in 11.9% of patients with anterior AMI in Group A vs. 37.8% in Group B (P < 0.001). CK peak normalization time in the group with anterior AMI was achieved after 58 +/- 2 h in Group A vs. 71 +/- 2 h in Group B (P < 0.001). CK peak was 1719 +/- 152 in Group A vs. 2184 +/- 164 U/l in Group B, (P < 0.039). Late arrhythmias, higher than Lown's Class 2 were found to occur in 15.4% of patients with anterior AMI of Group A vs. 31.7% in Group B (P < 0.022), at predischarge Holter test.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Myocardial_Revascularization_MeSH M_Reperfusion_Injury_MeSH S_complications_MeSH Reperfusion_Injury_complications_MeSH S_prevention_&_control_MeSH Reperfusion_Injury_prevention_&_control_MeSH P_Thrombolytic_Therapy_MeSH M_Time_Factors_MeSH 
****** 8176095
----K E
----T Effect of beta-blockade on heart rate variability in patients with coronary artery disease.
----A OBJECTIVES. This study assessed the effects of beta-blockade on heart rate variability in patients with coronary artery disease and determined whether the effects of metoprolol in a controlled-release formulation and atenolol differ with regard to electrocardiographic measures of cardiac autonomic control. BACKGROUND. Low heart rate variability is common in coronary artery disease and is associated with increased mortality. Beta-adrenergic blocking drugs may increase heart rate variability in healthy subjects, but there is limited knowledge of whether they are able to modify heart rate variability in patients with uncomplicated coronary artery disease. METHODS. In a randomly allocated, double-blind crossover study with three 2-week treatment periods, 200 mg of controlled-release metoprolol once a day, 100 mg of atenolol once a day or placebo once a day were administered in 18 male patients with stable coronary artery disease. The 24-h heart rate variability was measured in both the time and frequency domains. RESULTS. Beta-blockade induced a significant increase in heart rate variability, but no significant differences were found between atenolol and metoprolol. The average 24-h high frequency power increased by 64% after atenolol and by 62% after metoprolol. The root-mean-square successive difference of normal RR intervals increased by 70% after atenolol and by 62% after metoprolol, and the standard deviations of RR intervals increased by 20% and 16%, respectively. Beta-blockade had no significant effects on the amplitude of the circadian rhythm of heart rate variability, although both metoprolol and atenolol blunted the abrupt decrease of high frequency power after arousal. CONCLUSIONS. Beta-blockade by metoprolol and atenolol enhance the heart rate variability in patients with coronary artery disease. This may contribute to the protective effects of beta-blockade in ischemic heart disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_blood_MeSH Atenolol_blood_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography__Ambulatory_statistics_&_numerical_data_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Least-Squares_Analysis_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_blood_MeSH Metoprolol_blood_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Signal_Processing__Computer-Assisted_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8176099
----K E
----T Improved exercise hemodynamic status in dilated cardiomyopathy after beta-adrenergic blockade treatment.
----A OBJECTIVES. This study was performed to investigate exercise hemodynamic status in a double-blind, placebo-controlled trial and was a substudy in the Metoprolol in Dilated Cardiomyopathy Trial. BACKGROUND. Previous open studies have shown beneficial effects on exercise hemodynamic status after beta-adrenergic blocking agent therapy in patients with congestive heart failure. METHODS. The study included 41 patients with idiopathic dilated cardiomyopathy with ejection fraction < 0.40 (metoprolol, 20 patients; placebo, 21 patients) whose hemodynamic status was investigated at rest and during supine submaximal exercise, at baseline and after 6 and 12 months of treatment. Myocardial metabolism was evaluated in a subset of 19 patients. RESULTS. Metoprolol-treated patients responded favorably, as expressed by improved exercise cardiac index ([mean +/- SD] placebo 4.8 +/- 1.6 to 4.7 +/- 1.8 liters/min per m2, metoprolol 4.3 +/- 1.1 to 5.4 +/- 1.9 liters/min per m2, p = 0.0001) and stroke work index (placebo 44 +/- 20 to 41 +/- 27 g.m/m2, metoprolol 35 +/- 16 to 58 +/- 28 g.m/m2, p < 0.0001). Exercise systolic arterial pressure increased (placebo 161 +/- 25 to 151 +/- 23 mm Hg, metoprolol 155 +/- 29 to 165 +/- 37 mm Hg, p = 0.0003) as well as exercise oxygen consumption index (placebo 463 +/- 194 to 474 +/- 232 ml/min per m2, metoprolol 406 +/- 272 to 507 +/- 298 ml/min per m2, p = 0.045). There was a significant increase in exercise duration in the metoprolol group (63 +/- 38 s) compared with the placebo group (-24 +/- 42 s) (p = 0.01). Net myocardial lactate extraction increased in the metoprolol group, suggesting less myocardial ischemia (placebo 17 +/- 22 to 9.5 +/- 6.4 mmol/min, metoprolol -32 +/- 100 to 42 +/- 45 mmol/min, p = 0.03). Peripheral levels of norepinephrine tended to decrease at rest and during exercise, whereas myocardial net spillover was unchanged. CONCLUSIONS. Metoprolol improved hemodynamic status in patients with dilated cardiomyopathy at rest and had a more pronounced effect during exercise. These positive effects were achieved along with improved or stable myocardial metabolic data.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Analysis_of_Variance_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Cardiomyopathy__Congestive_epidemiology_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Europe_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_North_America_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8179847
----K E
----T Renal effects of immersion in essential hypertension. Carvedilol Study Group.
----A Plasma concentrations of atrial natriuretic factor (ANF) have been reported to be unchanged or increased in patients with essential hypertension. Head out of water immersion (HOI) in a thermoneutral bath induces diuresis and natriuresis, an increase in plasma ANF, and reductions in plasma renin activity and aldosterone concentrations. HOI was used in this study to stimulate the secretion of ANF, and compare its release in patients with essential hypertension (EH) (n = 14) and normotensive subjects (n = 13). Renal function changes induced by HOI were also monitored. HOI that lasted 2 h was compared with a control-seated period in each subject. Blood pressure was significantly reduced (P < .05) in normotensive controls from 112 +/- 3/74 +/- 2 to 100 +/- 3/61 +/- 2 mm Hg, and in patients with EH from 137 +/- 4/93 +/- 3 to 123 +/- 3/78 +/- 2 mm Hg. Plasma levels of ANF increased significantly (P < .05) in both groups from 5.9 +/- 1.3 to 16.3 +/- 3 pmol/L in normotensive controls and from 6.0 +/- 0.9 to 13.2 +/- 2.5 pmol/L in patients with EH. Plasma cyclic guanosine monophosphate concentrations increased more (P < .05) in the patients with EH (3.9 +/- 0.4 to 6.1 +/- 0.5 nmol/L) than in controls (3.4 +/- 0.3 to 4.8 +/- 0.4 nmol/L), whereas plasma renin activity levels decreased in controls (2.29 +/- 0.58 to 1.63 +/- 0.55 ng/mL/h) and to a greater degree in patients with EH (1.62 +/- 0.52 to 0.77 +/- 0.19 ng/mL/h, P < .05) by HOI.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Cell_Count_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Cyclic_GMP_MeSH S_blood_MeSH Cyclic_GMP_blood_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Hormones_MeSH S_blood_MeSH Hormones_blood_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_urine_MeSH Hypertension_urine_MeSH P_Immersion_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Kidney_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Natriuresis_MeSH S_physiology_MeSH Natriuresis_physiology_MeSH M_Renal_Circulation_MeSH S_physiology_MeSH Renal_Circulation_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7910028
----K E
----T Comparison of a new vasodilating beta-blocker, carvedilol, with atenolol in the treatment of mild to moderate essential hypertension.
----A Carvedilol is a new cardiovascular compound with the combined pharmacologic properties of nonselective beta-blockade and vasodilation. The aim of this study was to compare the safety and antihypertensive efficacy of 25 to 50 mg carvedilol once daily with 50 to 100 mg atenolol once daily in patients with mild to moderate essential hypertension. This was a multicenter study conducted in Europe. After a single-blind placebo run-in phase, 325 eligible patients with stable hypertension were randomized to receive 25 mg carvedilol once daily (161 patients) or 50 mg atenolol (164 patients) in a double-blind 8-week treatment phase. After 4 weeks, the dosage was doubled if there was inadequate response. The primary index of efficacy (response) was the reduction of mean sitting diastolic blood pressure to 90 mg Hg or less (normalized) or by at least 10 mm Hg from baseline. At each of three to six run-in phase visits and after 2, 4, and 8 weeks of treatment, sitting blood pressure and heart rate at trough were measured in triplicate, and body weight, adverse experiences, compliance, and use of concomitant medications were assessed. Laboratory tests, including fasting serum lipids, and electrocardiograms were also monitored during the trial. After 8 weeks of treatment, response rates in the carvedilol and atenolol treatment groups were 75% and 82%, respectively. Compared to baseline, the mean sitting blood pressure was significantly (P < .05) reduced by carvedilol from 165/104 mm Hg to 147/89 mm Hg. With atenolol, mean sitting blood pressure was significantly (P < .05) reduced from 167/104 mm Hg to 150/90 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Function_Tests_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Liver_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8181028
----K E
----T Role of vasodilator therapy in congestive heart failure. Effects on mortality.
----A Congestive heart failure is associated with a considerable reduction in survival with only about 50% of patients alive within 5 years of its diagnosis. Recent trials have demonstrated that vasodilator therapy can improve survival in this condition. Agents that have been shown to be effective in well-designed double-blind clinical trials include the combination of hydralazine-isosorbide dinitrate (in V-HeFT) and the angiotensin converting enzyme inhibitors (in SOLVD, SAVE, and CONSENSUS).
----P Journal_Article Review Review__Tutorial 
----M M_Clinical_Trials_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Vasoconstriction_MeSH S_drug_effects_MeSH Vasoconstriction_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 7910155
----K E
----T Determination of the anti-ischemic activity of nebivolol in comparison with atenolol.
----A The anti-ischemic effect of 5 mg nebivolol o.i.d., a newly developed beta 1-selective adrenoceptor blocking drug with vasodilating properties, was compared with that of atenolol (100 mg o.i.d.) following a treatment period of 6 days. The study was performed in 24 patients with documented coronary artery disease and stable angina pectoris according to a double-blind randomized study, designed using conventional symptom-limited exercise testing. Exercise testing 3 h after the first dose showed a more marked ST-segment reduction by atenolol than by nebivolol (59% vs. 18%). ST-segment depression measured 24 h after administration of the penultimate dose was statistically significantly reduced by nebivolol (from 0.19 +/- 0.07 to 0.13 +/- 0.07 mV; P = 0.0059) but not by atenolol (from 0.17 +/- 0.06 to 0.14 +/- 0.10 mV; P = 0.0703). Approximately 3 h after the last dose, the reduction was comparable (45% and 38% by nebivolol and atenolol, respectively). Exercise duration, exercise time necessary to produce ST-segment depression by 0.1 mV and exercise time to the onset of angina were also prolonged following administration of both drugs. Thus, at steady-state single daily doses of 100 mg atenolol and 5 mg nebivolol were about equieffective when measured at time of maximal effect (i.e. 3 h after drug administration). However, duration of action with respect to the ST-segment depression seems to be slightly longer for nebivolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_prevention_&_control_MeSH Angina_Pectoris_prevention_&_control_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_blood_MeSH Atenolol_blood_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_blood_MeSH Benzopyrans_blood_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_blood_MeSH Ethanolamines_blood_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_blood_MeSH Vasodilator_Agents_blood_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8182401
----K I
----T Acupuncture versus metoprolol in migraine prophylaxis: a randomized trial of trigger point inactivation.
----A OBJECTIVES. To compare the effects of dry needling of myofascial trigger points in the neck region to metoprolol in migraine prophylaxis. DESIGN. Randomized, group comparative study. patients, investigator and statistician were blinded as to treatment, the therapist was blinded as to results. SETTING. Outpatient pain clinic in the northern Copenhagen area. Patients were referred by general practitioners or respondents to newspaper advertisements. SUBJECTS. Included were patients with a history of migraine with or without aura for at least 2 years. Excluded were persons with contraindications against treatment with beta blockers, chronic pain syndromes, pregnancy or previous experience with acupuncture or beta-blocking agents. A total of 85 patients were included; 77 completed the study. INTERVENTIONS. After a 4-week run-in period, patients were allocated to a 17-week regimen either with acupuncture and placebo tablets or to placebo stimulation and metoprolol 100 mg daily. RESULTS. Both groups exhibited significant reduction in attack frequency (P < 0.01). No difference was found between the groups regarding frequency (P > 0.20) or duration (P > 0.10) of attacks, whereas we found a significant difference in global rating of attacks in favour of metoprolol (P < 0.05). CONCLUSIONS. Trigger point inactivation by dry needling is a valuable supplement to the list of migraine prophylactic tools, being equipotent to metoprolol in the influence on frequency and duration (but not severity) of attacks, and superior in terms of negative side-effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M P_Acupuncture_Therapy_MeSH S_adverse_effects_MeSH Acupuncture_Therapy_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 8186348
----K E
----T Effect of propranolol on prevention of first variceal bleed and survival in patients with chronic liver disease.
----A BACKGROUND: Propranolol has been shown to be effective in both primary and secondary treatment of variceal haemorrhage; most primary prevention trials have only included patients with large oesophageal varices. AIM OF THE STUDY: The aim of this study was to look at the effect of propranolol in the primary prevention of variceal bleeding and its long-term effects on mortality in unselected patients with chronic liver disease. METHODOLOGY: Three hundred and nineteen patients were included in a double-blind parallel group study in three centres to receive propranolol 160 mg long-acting (LA) or placebo. Patients were followed up for a minimum of one year. RESULTS: There were eleven episodes of variceal bleeding and 38 deaths with no statistically significant difference in bleeding rates between the two treatment groups. Child's group and history of ascites were the most important prognostic factors determining the likelihood of early death and variceal bleeding respectively. CONCLUSIONS: In this study we failed to demonstrate a significant effect of propranolol on first variceal bleeding or in prolonging survival in unselected patients with chronic liver disease. Our results, however, might have been influenced by the low event rate observed in these unselected group of patients and suggest that careful selection of patients who are most likely to benefit from propranolol is important.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Diseases_MeSH S_complications_MeSH Liver_Diseases_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 8192695
----K 1
----T [Vasoselective, substance-specific actions of isradipine on the great arteries of hypertensives in comparison to metoprolol]
----A The effects of isradipine (Lomir, CAS 75695-93-1) and metoprolol (CAS 37350-58-6) on geometry and arterial compliance of the arteria brachialis of 14 patients each with essential hypertension were compared acutely and after three months of therapy by means of pulsed Doppler sonography and the determination of pulse wave velocity. A calculation model was used that allowed to determine the drug-specific effects on arterial diameter and compliance under isobaric conditions. Isradipine increased measured and isobaric diameter during short-term (p < 0.05) and long-term administration (p < 0.05) whereas metoprolol did not change it. Isradipine increased measured and isobaric compliance during short-term (p < 0.05) and long-term administration (p < 0.05). Metoprolol reduced measured compliance acutely (p < 0.01) and isobaric compliance acutely (p < 0.05) and long-term (p < 0.05). Drug-specific effects on compliance were different during short-term and long-term administration (p < 0.01); the diameter was influenced differently only during short-term administration (p < 0.05). These opposite drug effects on the A. brachialis are probably due to a vasoselective relaxation of smooth muscle in large arteries by isradipine and-in the case of metoprolol-arterial constriction. The increase of arterial compliance by isradipine reduces very effectively the load on the heart and could form the basis for the improvement in the prognosis of the hypertensive patient.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Arteries_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH S_ultrasonography_MeSH Arteries_ultrasonography_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Isradipine_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 8199723
----K E
----T Felodipine, metoprolol and their combination compared with placebo in isolated systolic hypertension in the elderly.
----A This study compared with placebo the efficacy and tolerability of optimised doses of felodipine 5-20 mg daily, metoprolol 50-200 mg daily and their combination in subjects 60 years or over with isolated systolic hypertension. The study employed a randomised double-blind crossover design with allocation of treatment order within subjects by Latin squares. For each subject, after a single-blind run-in placebo phase, there were four randomised treatment phases each of six weeks duration, with a dose titration step at three weeks if necessary. Twenty-eight subjects entered the randomised phases of the study and twenty-one completed all four phases--13 male, 8 female (ages: median 71, range 59-85 years). At the end of both the felodipine and metoprolol phases systolic and diastolic pressure were reduced at 2 hours postdose compared with the placebo phase (p < 0.001), the blood pressure reduction with felodipine (-40/-20 mmHg) being greater than that with metoprolol (-15/-9 mmHg) (p < 0.01). Immediately predose (12 hours postdose) there was a persisting reduction of supine systolic blood pressure (-17 mmHg) with felodipine (p < 0.001), but there was no significant effect of metoprolol. At both measurement times the two drugs when in combination had an additive effect on blood pressure. There was a 20% increase in reported symptoms during each of the active treatment phases. Four subjects withdrew during the randomised phases because of probable drug-related adverse events and six subjects required dosage reductions during the felodipine or combination phases.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH P_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH 
****** 8202100
----K E
----T Sotalol.
----A Sotalol is a novel antiarrhythmic agent combining beta-adrenergic-antagonist actions with the ability to increase cardiac repolarization and refractoriness. The drug's electrophysiologic and clinical profile is different from that of conventional beta-receptor antagonists. As compared with other antiarrhythmic agents, sotalol prevents recurrences of arrhythmia in a higher proportion of patients, particularly among those presenting with ventricular tachycardia and aborted sudden cardiac death. The net hemodynamic effect of sotalol is the result of a balance between the depressant effects due to beta-receptor blockade and an action that tends to increase contractility. Although initially marketed in the United States for treatment of life-threatening ventricular arrhythmias, sotalol also has demonstrated efficacy in many patients with supraventricular arrhythmias. As with all drugs that prolong the QT interval, the syndrome of torsade de pointes is a serious potential adverse effect.
----P Journal_Article Review Review__Tutorial 
----M M_Action_Potentials_MeSH S_drug_effects_MeSH Action_Potentials_drug_effects_MeSH M_Animals_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Electrophysiology_MeSH M_Human_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Sotalol_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH S_pharmacokinetics_MeSH Sotalol_pharmacokinetics_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Supraventricular_MeSH S_drug_therapy_MeSH Tachycardia__Supraventricular_drug_therapy_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH 
****** 8203987
----K E
----T Effects of calcium antagonists on renal hemodynamics and progression of nondiabetic chronic renal disease.
----A In recent years, substantial investigative attention has focused on therapeutic regimens that could retard the progression of chronic renal insufficiency. Emphasis has been placed on the effects of antihypertensive treatment on renal hemodynamics and preservation of renal function. It has been suggested that some classes of antihypertensive agents may confer a greater renoprotective effect, especially agents that lower glomerular capillary pressure. Conversely, by virtue of their ability to preferentially dilate the afferent arteriole calcium antagonists theoretically could favor an increase in glomerular capillary pressure thereby accelerating the decline of renal function. In this review we survey the literature critically and conclude that in patients with essential hypertension and in patients with chronic renal insufficiency, calcium antagonists effectively reduce systemic blood pressure while maintaining glomerular filtration rate and effective renal plasma flow. Preliminary results from a few long-term studies suggest that calcium antagonists may even attenuate the decline in renal function of patients with chronic renal failure. The majority of studies in humans, however, have been nonrandomized, of too short duration, or confounded by investigative difficulties precluding definite conclusions whether calcium antagonists have renoprotective effects. Although the possibility that calcium antagonists may retard progression of renal disease remains to be ascertained, the available evidence indicates that calcium antagonists may be used in patients with renal functional impairment without further exacerbating renal function.
----P Journal_Article Review Review__Academic 
----M M_Animals_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH P_Renal_Circulation_MeSH 
****** 8205301
----K E
----T Effect of isradipine on cyclosporin A-related hypertension.
----A There is evidence that calcium antagonists may have a beneficial effect on cyclosporin A (CyA)-induced hypertension after organ transplantation. In a double-blind controlled trial, 50 consecutive non-diabetic first kidney-transplant recipients were randomized to receive either isradipine, a dihydropyridine calcium antagonist, or placebo. There were no significant differences in age, weight, gender, warm and cold ischaemic periods, and original renal disease between treatment groups. Treatment was started intravenously 2 h before the transplantation procedure and was subsequently continued orally for 3 months. The immunosuppressive treatment included oral CyA from day 5 after a short course of anti-T-lymphocyte immunoglobulins. Hypertension was treated with oral labetolol in combination with guanfacine if necessary. Antihypertensive medication was prescribed significantly more often (16 vs 7 patients; p < 0.05) in the placebo group. Standing systolic blood pressure was significantly lower in the isradipine group. The standing diastolic and both systolic and diastolic sitting blood pressures were similar in both groups. After 3 months, patients' mean serum creatinine was significantly lower with isradipine than with placebo (142.0 +/- 11.9 vs 164.0 +/- 10.8 mumol/l; p < 0.05). With isradipine, a significantly higher dose of CyA was needed to achieve adequate plasma levels (8.0 +/- 0.5 vs 6.2 +/- 0.5 mg/kg/day; p < 0.01). It can be concluded that isradipine is an effective antihypertensive agent after kidney transplantation and may have an influence on CyA metabolism. Furthermore, isradipine appears to ameliorate CyA-induced nephropathy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cyclosporine_MeSH S_adverse_effects_MeSH Cyclosporine_adverse_effects_MeSH S_blood_MeSH Cyclosporine_blood_MeSH S_therapeutic_use_MeSH Cyclosporine_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_chemically_induced_MeSH Hypertension_chemically_induced_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Isradipine_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Kidney_Transplantation_MeSH M_Postoperative_Care_MeSH M_Prospective_Studies_MeSH 
****** 1345218
----K E
----T Haemodynamic findings and response rates to beta-blocker--and diuretic monotherapy in mild and moderate hypertension. A one year randomized, double blind study in 100 men.
----A In a randomized double blind study 100 men (mean age 46 (22-64) years) with mild to moderate hypertension were followed every 3rd month for one year. Fifty were randomized to atenolol 50 mg and 50 to hydrochlorothiazide 25 mg+amiloride 5 mg (co-amiloride) once daily. The doses were doubled at 3 or 6 months if diastolic blood pressure (DBP) remained > or = 95 mmHg. If DBP was > or = 95 mmHg even at 6 or 9 months, patients were classified as non-responders, and nifedipine 20 mg b.i.d. was added. After one year 31/50 randomized to atenolol and 17/50 randomized to co-amiloride had responded to monotherapy (p < 0.05). Neither clinical findings nor haemodynamic measurements by Doppler at baseline could distinguish between co-amiloride responders and non-responders. Conversely, non-responders to atenolol as compared with atenolol responders had higher body weight (p = 0.02), higher systolic BP (p = 0.03), higher DBP (p = 0.009), stroke volume (p = 0.04), and cardiac output (p = 0.0002) combined with lower total systemic vascular resistance (p = 0.02). This suggests that some were apparent non-responders due to too low dosing of atenolol rather than true non-responders. Measurements of haemodynamics may be of importance in the assessment of optimal antihypertensive therapy according to baseline and follow-up haemodynamic aberrations.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Amiloride_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Drug_Combinations_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 7911530
----K E
----T Acute influence of beta-adrenergic antagonists on left ventricular diastolic function: contrasting results after administration of celiprolol and metoprolol.
----A Various beta-adrenergic receptor antagonists have different effects on myocardial function. A clinical study was performed in 30 patients with symptomatic coronary artery disease and systemic hypertension to compare the effects of single intravenous doses of 0.15 mg/kg celiprolol (n = 16) (third generation beta-blocking agent) and metoprolol (n = 14) (second generation) on left ventricular diastolic function. Parameters derived from pressure, volume, flow, time intervals and their combination were used to characterise diastolic function. After celiprolol administration, parameters of diastolic myocardial function improve (dp/dtip-; relaxation time constant T1, peak filling rate PFR; first-third filling rate FF1/3 or diastolic wall stress-time integral Sigdiasc) or remain unchanged. In contrast, after metoprolol administration parameters of diastolic function seem to be deteriorated (dp/dtip-, T1; Sigdiasc). This indicates an improvement in myocardial relaxation and filling under the influence of celiprolol but not under metoprolol. The left shift of the pressure-volume loops after celiprolol (n = 13), in contrast to metoprolol, supports this interpretation. Celiprolol did not show any deterioration of diastolic function in patients with coronary heart disease and arterial hypertension under these acute conditions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiology_MeSH Heart_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Regional_Blood_Flow_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 8210018
----K E
----T Sodium nitroprusside induced hypotension: haemodynamic response and dose requirements during propofol or halothane anaesthesia.
----A This study was designed to investigate the influence of anaesthesia induced and maintained with propofol on the haemodynamic effects and the dose requirements of SNP during the course of induced hypotension. Twenty-four adult ASA physical status I patients undergoing middle ear surgery were randomly assigned to receive anaesthesia with either morphine, thiopentone, d-tubocurarine, halothane 0.6% end-tidal and N2O 70% in oxygen (group I n = 12), or morphine, propofol, d-tubocurarine, propofol infusion 108 micrograms.kg-1.min-1 and N2O in oxygen (group 2 n = 12). Mean arterial blood pressure (MAP) was reduced to 60-65 mmHg in all patients using a continuous infusion of sodium nitroprusside (SNP) 0.01%. Propofol produced a significant (17%) reduction in the MAP before institution of SNP infusion. This was related to a 24% reduction in the systemic vascular resistance index (SVRI). In the halothane group SVRI was significantly reduced during SNP infusion. Halothane anaesthesia was associated with significant reflex tachycardia in response to SNP induced hypotension. Eight patients in the halothane group (66%) required propranolol 0.5-3 mg to control tachycardia. Propofol anaesthesia attenuated significantly the reflex tachycardia in response to SNP induced hypotension. Two patients in the propofol group (16%) required 0.5 mg propranolol to control reflex tachycardia. The mean SNP dose requirements were 7.25 +/- 1.6 and 2.1 +/- 1.4 micrograms. kg-1.min-1 in the halothane and propofol groups, respectively (P < 0.0001). None of the patients in the two groups developed rebound hypertension following SNP withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH P_Anesthesia__Inhalation_MeSH P_Anesthesia__Intravenous_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Female_MeSH P_Halothane_MeSH S_administration_&_dosage_MeSH Halothane_administration_&_dosage_MeSH S_pharmacology_MeSH Halothane_pharmacology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Hypotension__Controlled_MeSH M_Male_MeSH M_Nitroprusside_MeSH S_administration_&_dosage_MeSH Nitroprusside_administration_&_dosage_MeSH S_pharmacology_MeSH Nitroprusside_pharmacology_MeSH M_Propofol_MeSH S_administration_&_dosage_MeSH Propofol_administration_&_dosage_MeSH S_pharmacology_MeSH Propofol_pharmacology_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Tachycardia_MeSH S_physiopathology_MeSH Tachycardia_physiopathology_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 8004839
----K E
----T Double-blind comparison of amlodipine and hydrochlorothiazide in patients with mild to moderate hypertension.
----A In the final analysis of this study at Week 26, 26% of the patients randomized to receive amlodipine attained blood pressure control with amlodipine alone compared with 33% of the patients allocated to hydrochlorothiazide (HCTZ). Neither amlodipine nor HCTZ produced clinically significant changes in pulse rate or in the electrocardiogram. Amlodipine treatment did not appear to produce clinically significant changes in blood lipids; HCTZ, however, produced an increase in total plasma cholesterol (delta 22.9 +/- 8.6 mg/dl). The incidence of side effects and the rate of patient withdrawal in the amlodipine and HCTZ groups were comparable. As expected, HCTZ therapy caused well-recognized biochemical alterations in cholesterol and potassium levels, whereas amlodipine was metabolically neutral.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Lipoproteins__VLDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__VLDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pulse_MeSH S_drug_effects_MeSH Pulse_drug_effects_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 8004841
----K E
----T Bisoprolol, a once-a-day beta-blocking agent for patients with mild to moderate hypertension.
----A The 24-h blood pressure control of bisoprolol, a new beta-selective, beta-blocking agent, was studied in 240 mild to moderate hypertensive patients in this 4-week, randomized, double-blind, placebo-controlled trial. A once-daily dosing schedule was evaluated by comparing bisoprolol's antihypertensive effectivness and safety at 24 h postdose and 3 h postdose, the latter time intended to correspond to peak effectiveness. Results from this trial demonstrated the antihypertensive effectiveness of once-daily bisprolol at doses ranging from 5-20 mg. Mean reductions from baseline diastolic blood pressure, measured 24 h postdose, were 6.3, 8.8, and 10.1 mmHg for patients receiving bisoprolol 5, 10, and 20 mg, respectively, compared with 1.6 mmHg for placebo-treated patients (p < 0.01); mean reductions from baseline systolic blood pressure for the bisoprolol groups were 8.6, 8.6, and 10.9 mmHg, respectively, versus 3.3 mmHg for placebo (p < or = 0.01); and mean reductions from baseline heart rate for the bisoprolol groups were 5.1, 7.1, and 10.2 beats/min, respectively, compared with a 0.9 beats/min increase in heart rate for the placebo group (p < 0.01). The response rates for bisoprolol-treated patients ranged from 47 to 70% compared with 18% for patients on placebo (p < 0.01). Antihypertensive effects were dose-related and sustained over the 24-h dosing interval. Near maximal antihypertensive effects were achieved within 1 week of initiation of therapy with bisoprolol and were sustained over the course of the trial.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_blood_MeSH Bisoprolol_blood_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Patient_Dropouts_MeSH M_Placebos_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 8005121
----K E
----T Antihypertensive efficacy and tolerability of different drug regimens in isolated systolic hypertension in the elderly.
----A The pharmacological treatment, mainly based on diuretics, of isolated systolic hypertension (ISH) has recently been shown to reduce the risk of stroke and coronary heart disease in the elderly. The purpose of this study was to compare the antihypertensive effect and tolerability of different drug regimens in elderly subjects with ISH (systolic blood pressure--SBP-- > or = 160 mmHg and diastolic blood pressure--DBP-- < 90 mmHg). A multicentre, randomized, controlled open trial was planned in the general practice setting. Four widely used treatment schedules were tested: hydrochlorothiazide 25 mg plus amiloride 2.5 mg (H+Am), nifedipine slow release 20 mg (N), atenolol 50 mg (At) and atenolol 25 mg plus chlorthalidone 6.25 mg (At+C). After a baseline evaluation, 308 patients (76.3% female, mean age 75.3 +/- 7.1 years) were randomized and followed up for 6 months. After 3 months the drug dosage was doubled if the systolic blood pressure goal (SBP < 160 mmHg and SBP reduction of at least 20 mmHg) had not been reached. Ninety-four subjects (30.5%) presented contraindications to beta-blockers. At the 3rd- and 6th-month visits all treatment groups, except At, showed a significant reduction in SBP compared to the control group; DBP showed no significant reduction in any group at any time. At the end of the follow-up the percentage of hypertensives who had reached the BP goal was 14.6% in the control group, 52.9% in H+Am, 54.8% in N, 28.6% in At and 52.2% in At+C.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amiloride_MeSH S_adverse_effects_MeSH Amiloride_adverse_effects_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Drug_Combinations_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Patient_Satisfaction_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 8006249
----K E
----T The Asymptomatic Cardiac Ischemia Pilot (ACIP) study: design of a randomized clinical trial, baseline data and implications for a long-term outcome trial.
----A OBJECTIVES. The primary objectives of the Asymptomatic Cardiac Ischemia Pilot were 1) to compare the 12-week efficacy of three treatment strategies to suppress cardiac ischemia, and 2) to assess the feasibility of a prognosis trial in patients with asymptomatic cardiac ischemia. BACKGROUND. Cardiac ischemia has been associated with increased morbidity and mortality. However, most cardiac ischemia is asymptomatic, and although therapeutic strategies ranging from no medication to revascularization are being used to treat ischemia, no prospective study evaluating different treatment strategies has been reported. METHODS. Patients with angiographically documented coronary artery disease and ischemia on exercise and ambulatory electrocardiogram (ECG) in 11 clinical units were randomized to receive angina-guided medical therapy, angina-guided plus ambulatory ECG ischemia-guided medical therapy or revascularization (coronary angioplasty or bypass surgery). Patients were also randomized to receive either diltiazem plus isosorbide dinitrate or atenolol plus nifedipine when possible. After anti-ischemic medication adjustment to control angina, blinded medication was adjusted in the medical therapy groups to eliminate ischemia in the ischemia-guided group. The primary outcome was the absence of ischemia at 12 weeks. Follow-up was scheduled for 1 year. RESULTS. A total of 1,959 patients were screened by ambulatory ECG monitoring; 982 (49%) had asymptomatic ischemia, and 618 (65%) were enrolled in the study. Most patients were men, were > 60 years old and had two or more ischemic episodes, early positive exercise tests and multivessel disease. CONCLUSIONS. Design and baseline data for a pilot study of ischemia treatment strategies are described.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Myocardial_Revascularization_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Pilot_Projects_MeSH M_Research_Design_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH 
****** 8006252
----K E
----T Effects of treatment strategies to suppress ischemia in patients with coronary artery disease: 12-week results of the Asymptomatic Cardiac Ischemia Pilot (ACIP) study.
----A OBJECTIVES. The Asymptomatic Cardiac Ischemia Pilot (ACIP) study was initiated to determine the feasibility of a large trial in evaluating the effects of treatment of ischemia on outcome (mortality and myocardial infarction). The study was designed to examine the effects of medical treatment to control angina compared with treatment strategies guided by ambulatory electrocardiographic (ECG) ischemia or coronary anatomy. BACKGROUND. Treatments to suppress ischemia (asymptomatic and symptomatic) have not been evaluated in a large prospective, randomized trial. Before undertaking such a trial, issues about recruitment and treatment strategies must be addressed. METHODS. The 618 enrolled patients had coronary artery disease suitable for revascularization, ischemia on stress test and asymptomatic ischemia on ambulatory ECG. Patients were assigned randomly to one of three treatment strategies: 1) angina-guided medical strategy with titration of anti-ischemic medication to relieve angina (angina-guided strategy); 2) angina-guided plus ambulatory ECG ischemia-guided medical strategy with titration of anti-ischemic medication to eliminate both angina and ambulatory ECG ischemia (ischemia-guided strategy); and 3) revascularization by angioplasty or bypass surgery (revascularization strategy). RESULTS. Ambulatory ECG ischemia was no longer present at the week 12 visit in 39% of patients assigned to the angina-guided strategy, 41% of patients assigned to the ischemia-guided strategy and 55% of patients assigned to the revascularization strategy. All strategies reduced the median number of episodes and total duration of ST segment depression during follow-up ambulatory ECG monitoring. Revascularization was the most effective strategy. Treadmill test results were concordant with those of ambulatory ECG monitoring. For most patients in the two medical strategies, angina was controlled with low to moderate doses of anti-ischemic medication, and the majority of patients (65%) in the revascularization strategy did not require medication for angina. CONCLUSIONS. This pilot study demonstrated that cardiac ischemia can be suppressed in 40% to 55% of patients with either low or moderate doses of medication or revascularization and that a large trial is feasible.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Myocardial_Revascularization_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Pilot_Projects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH 
****** 8006923
----K E
----T Effects of selective alfa 1 and beta 1-adrenoreceptor blockade on lipoprotein and carbohydrate metabolism in hypertensive subjects, with special emphasis on insulin sensitivity.
----A The central role of insulin resistance in patients with essential hypertension was the impetus for the present study, in which carbohydrate and lipid metabolism were examined before and after three months treatment with doxazosin (n = 14) and atenolol (n = 15). After completion of a randomised parallel group trial, the study was extended in a subgroup of the patients who continued treatment with doxazosin for a further nine months (n = 18). Insulin sensitivity was measured with the euglycemic hyperinsulinaemic clamp. Blood glucose and plasma insulin were analysed in the fasting state and during an intravenous glucose tolerance test (IVGTT). Lipoprotein fractions were analysed in serum. After three months, SBP and DBP in the standing position decreased to the same extent after the two drugs whereas the decrease in supine SBP did not reach statistical significance in the doxazosin group. Doxazosin, in contrast to atenolol, decreased serum triglycerides (-17%, P < 0.04) by lowering the VLDL and LDL fractions. Serum cholesterol fell after doxazosin (-7%, P < 0.02) but not after atenolol. The effects of doxazosin on serum lipids remained the same during the long-term follow-up. At three months neither drug had significantly affected variables reflecting insulin sensitivity although atenolol tended to decrease the insulin sensitivity index (-17%, P = 0.08). After 12 months the doxazosin group showed a significant increase in the insulin sensitivity index and a significant decrease in both basal plasma insulin and in the late insulin response at IVGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Carbohydrates_MeSH S_metabolism_MeSH Carbohydrates_metabolism_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Insulin_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Lipoproteins_MeSH S_metabolism_MeSH Lipoproteins_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Adrenergic__alpha-1_MeSH S_drug_effects_MeSH Receptors__Adrenergic__alpha-1_drug_effects_MeSH M_Receptors__Adrenergic__beta-2_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta-2_drug_effects_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 1345260
----K E
----T Ambulatory blood pressure monitoring. A tool for more comprehensive assessment.
----A AIMS. To investigate the usefulness of more comprehensive blood pressure measurements, made during daily life, in the diagnosis and treatment of hypertension. METHODS. A blood pressure screening was carried out in middle-aged men and women in Kavlinge, a municipality in southern Sweden. Subjects were classified according to Swedish standard criteria. Ambulatory blood pressure (amb-BP) was recorded in a random sample of normotensives and borderline hypertensives as well as in all the untreated hypertensives identified at screening and willing to participate. A subgroup of borderline hypertensives also carried out self-measurements of blood pressure (self-BP) both at work and at home. The blood pressure lowering efficacy of atenolol 50 mg o.d. and enalapril 20 mg o.d. was compared in hypertensives at rest, during 24 hours, and during dynamic and isometric exercise. The efficacy of enalapril and lisinopril (two ACE inhibitors with different durations of action) were also compared, with special focus on the early morning hours. RESULTS. Men and women classified as normotensives clearly differed from those with hypertension, also when blood pressure was recorded with ambulatory technique. The number of correctly classified subjects did not differ between self-BP and office-BP; combining the two added little. Atenolol reduced blood pressure better during dynamic exercise than did enalapril, while there was no significant difference in effect between enalapril and lisinopril, not even 18-24 hours post-dose. CONCLUSION. More comprehensive blood pressure measurements should be considered in the evaluation of hypertension treatment. Office BP, however, seems a reasonably good tool for diagnosing hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH P_Blood_Pressure_Monitors_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Monitoring__Physiologic_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8012879
----K E
----T Canadian Consensus Conference on Coronary Thrombolysis--1994 update.
----A 
----P Consensus_Development_Conference Journal_Article Review 
----M M_Canada_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Cost-Benefit_Analysis_MeSH M_Fibrinolytic_Agents_MeSH S_administration_&_dosage_MeSH Fibrinolytic_Agents_administration_&_dosage_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thrombolytic_Therapy_MeSH S_economics_MeSH Thrombolytic_Therapy_economics_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH 
****** 8013509
----K E
----T Atropine increases the accuracy of dobutamine stress echocardiography in patients taking beta-blockers.
----A Dobutamine-atropine stress echocardiography is used for the non-invasive diagnosis of coronary artery disease, but stress test results may be influenced by beta-blockers. The aim of this study was to assess if the addition of atropine can compensate for the presence of beta-blockers in dobutamine stress echocardiography. Twenty-six patients referred for evaluation of chest pain were studied twice, on and off metoprolol 100 mg b.i.d. (in random order sequence) with a wash-out period of at least 48 h. Dobutamine stress echocardiography was performed using up to 40 micrograms.kg-1.min-1, followed, if necessary, by the addition of atropine to achieve 85% of the age-predicted maximal heart rate, unless symptoms or markers of ischaemia appeared. Atropine was given to patients on beta-blockers more often [(22/26) vs (6/26)] than to those off beta-blockers (P < 0.001). Heart rate at every stage of the test was lower on beta-blockers. Chest pain occurred in patients on beta-blockers significantly less than in those off beta-blockers (8% vs 46%), and the addition of atropine made no significant difference (31% vs 46%). During dobutamine stress, new wall motion abnormalities occurred in three patients on beta-blockers (12%); this number increased to 15 after the addition of atropine (57%). New or worsened wall motion abnormalities occurred in 12 patients (46%) off beta-blockers with dobutamine alone and in 14 patients after adding atropine (53%).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_ultrasonography_MeSH Angina_Pectoris_ultrasonography_MeSH M_Atropine_MeSH S_pharmacology_MeSH Atropine_pharmacology_MeSH M_Dobutamine_MeSH S_antagonists_&_inhibitors_MeSH Dobutamine_antagonists_&_inhibitors_MeSH S_pharmacology_MeSH Dobutamine_pharmacology_MeSH M_Drug_Synergism_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH S_methods_MeSH Echocardiography_methods_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH S_ultrasonography_MeSH Myocardial_Ischemia_ultrasonography_MeSH M_Prospective_Studies_MeSH 
****** 8016665
----K E
----T Management of ascites and renal failure in cirrhosis.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Ascites_MeSH S_etiology_MeSH Ascites_etiology_MeSH S_therapy_MeSH Ascites_therapy_MeSH M_Bed_Rest_MeSH M_Diet__Sodium-Restricted_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Kidney_Failure_MeSH S_etiology_MeSH Kidney_Failure_etiology_MeSH S_therapy_MeSH Kidney_Failure_therapy_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Liver_Transplantation_MeSH M_Peritoneovenous_Shunt_MeSH S_adverse_effects_MeSH Peritoneovenous_Shunt_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8018001
----K E
----T A multifactorial trial design to assess combination therapy in hypertension. Treatment with bisoprolol and hydrochlorothiazide.
----A BACKGROUND: The safety and effectiveness of different dosages and combinations of antihypertensive agents can be efficiently studied using a multifactorial trial design. In consultation with the Cardio-Renal Division of the Food and Drug Administration, we conducted a randomized, double-blind, placebo-controlled, 3 x 4 factorial trial of bisoprolol, a beta 1-selective adrenergic blocking agent, and hydrochlorothiazide. METHODS: A total of 512 patients with mild to moderate essential hypertension were randomized to once-daily treatment with bisoprolol (0, 2.5, 10, or 40 mg), hydrochlorothiazide (0, 6.25, or 25 mg), and all possible combinations. Diastolic and systolic blood pressures were monitored during this 12-week trial. RESULTS: The effects of bisoprolol and hydrochlorothiazide were additive with respect to reductions in diastolic and systolic blood pressures over the dosage ranges studied. The addition of hydrochlorothiazide (or bisoprolol) to therapy with bisoprolol (or hydrochlorothiazide) produced an incremental reduction in blood pressure. Dosages of hydrochlorothiazide as low as 6.25 mg/d contributed a significant antihypertensive effect. A hydrochlorothiazide dosage of 6.25 mg/d produced significantly less hypokalemia and less of an increase in uric acid levels than a dosage of 25 mg/d. The low-dose combination of bisoprolol, 2.5 mg/d, and hydrochlorothiazide, 6.25 mg/d, reduced diastolic blood pressure to lower than 90 mm Hg in 61% of patients and demonstrated a safety profile that compared favorably with that of placebo. CONCLUSIONS: The utility of factorial design trials to characterize dose-response relationships and to test the potential interactions between various antihypertensive agents has been demonstrated. The combination of low dosages of bisoprolol and hydrochlorothiazide may be a rational alternative to conventional stepped-care therapy for the initial treatment of patients with mild to moderate hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 8018004
----K E
----T Use of a standardized heparin nomogram to achieve therapeutic anticoagulation after thrombolytic therapy in myocardial infarction. TIMI 4 investigators. Thrombolysis in Myocardial Infarction.
----A BACKGROUND: The recently completed Thrombolysis in Myocardial Infarction (TIMI) 4 Study compared three thrombolytic treatment regimens for acute myocardial infarction. The treatment arms included front-loaded recombinant tissue plasminogen activator (rtPA), anistreplase (APSAC), or both, in conjunction with an intravenous bolus of 5000 U of heparin, followed by 1000 U/h. To facilitate anticoagulation, a heparin nomogram was developed to maintain the therapeutic activated partial thromboplastin time at 1 1/2 to 2 times the control value. METHODS: A poll revealed that nine centers made use of the recommended heparin nomogram and six did not, adjusting the heparin dosage according to local practice. Anticoagulation parameters, major hemorrhagic events, and the frequency of heparin interruption were compared between centers that used and did not use the nomogram. RESULTS: Subtherapeutic activated partial thromboplastin time values were noted in 4%, 14%, 29%, 46%, 37%, and 34% of patients 8, 12, 24, 48, 72, and 96 hours, respectively, after heparin treatment was begun. Patients with subtherapeutic values at 24 hours were younger (mean +/- SD, 55.2 +/- 10.6 vs 59.6 +/- 10.6 years, P = .02) and weighed more (86.4 +/- 13.5 vs 78.9 +/- 15.7 kg, P = .007) than patients with therapeutic values. Centers that used the nomogram had significantly fewer subtherapeutic values at 48 and 96 hours. In addition, heparin therapy was interrupted less frequently at centers that used the nomogram (38.1% vs 68.7%, P < .001). Major spontaneous hemorrhage, reinfarction, and reocclusion rates were low and were about the same in the two groups. CONCLUSIONS: The use of a heparin nomogram provided improved anticoagulation in patients treated with thrombolytic therapy for myocardial infarction. Weight- and age-adjusted heparin dosing may provide further improvement in anticoagulation with heparin therapy. Our findings support the need for frequent monitoring of the activated partial thromboplastin time and for a standardized approach to adjusting the heparin dosage.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heparin_MeSH S_administration_&_dosage_MeSH Heparin_administration_&_dosage_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Partial_Thromboplastin_Time_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH 
****** 8018020
----K I
----T Sexual sequelae of antihypertensive drugs: treatment effects on self-report and physiological measures in middle-aged male hypertensives.
----A Antihypertensive drugs are commonly associated with adverse side effects in both clinical and laboratory studies. We investigated the sexual sequelae of several major classes of antihypertensive drugs (e.g., beta blockers, central alpha agonists, diuretics) in normal males and in hypertensive patients. We compared the effects of four widely used agents (methyldopa, propranolol, atenolol, hydrochlorothiazide-triamterene) and placebo, in a selected sample of 21 sexually dysfunctional male hypertensives, 13 of whom completed all five phases of the study. Each study drug was administered for a 1-month treatment period, followed by a 2-week, single-blind washout phase, according to a randomized, Latin square crossover design. Dependent variables for the study included a broad range of hormonal, NPT, and self-report measures of sexual response. Results indicated a lack of consistent drug effects on measures of sexual response, although more frequent sexual and nonsexual side effects were observed with methyldopa and propranolol. As in our previous studies, age was negatively correlated with both hormonal and NPT measures, whereas changes in blood pressure were not significantly related to sexual function scores. Results do not support the hypothesis that sexually dysfunctional males are at greater risk for adverse sexual sequelae when treated with centrally active agents or diuretics.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Penile_Erection_MeSH S_drug_effects_MeSH Penile_Erection_drug_effects_MeSH M_Self_Disclosure_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH S_complications_MeSH Sex_Disorders_complications_MeSH S_physiopathology_MeSH Sex_Disorders_physiopathology_MeSH M_Sexual_Behavior_MeSH S_drug_effects_MeSH Sexual_Behavior_drug_effects_MeSH M_Testosterone_MeSH S_blood_MeSH Testosterone_blood_MeSH 
****** 8021578
----K E
----T Direct and indirect blood pressure in normotensive and hypertensive subjects.
----A OBJECTIVES. To compare intrabrachial blood pressure (I-BP) with simultaneously measured contralateral auscultatory (A-)BP in hypertensive and normotensive subjects. The question was whether differences between direct and indirect BP are influenced by the BP levels. SUBJECTS. Hypertensive subjects treated with either placebo (n = 10) or metoprolol (n = 8) and age-matched normotensive subjects (n = 15), selected from a defined patient population waiting for cholecystectomy or hernia repair. Measurements were performed pre-induction of anaesthesia. RESULTS. In the hypertensive subjects, cuff systolic BP (SBP) was lower than I-BP by an average of 8 mmHg (placebo-) and 7 mmHg (metoprolol-treated), whereas diastolic A-BP (A-DBP) was 3 and 7 mmHg higher, respectively. In the normotensive subjects, mean A-SBP and I-SBP agreed closely, whereas A-DBP was 11 mmHg higher. Thus, SBP differences (i.e. indirect-direct BP) were significantly less and DBP differences significantly greater in the normotensive than in the hypertensive subjects (P < 0.05). Plasma renin activity and adrenalin showed better correlations with A-MBP than with I-MBP. CONCLUSIONS. The drift of cuff systolic readings fell progressively below the intrabrachial values when BP increased, whilst diastolic cuff values approached the direct pressures. Since A-MBP did not significantly differ from I-MBP in any group, one must ask whether hypertension would be more correctly defined according to MBP criteria.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Blood_Pressure_Determination_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8021907
----K E
----T Effects of long-acting propranolol and verapamil on blood pressure, platelet function, metabolic and rheological properties in hypertension.
----A The newly developed antihypertensive drugs, the long-acting beta-blocker propranolol and the sustained release calcium antagonist verapamil, are compared in their antihypertensive, platelet function, rheological properties and metabolic effects. The trial was a double-blind, randomised, placebo-controlled cross-over study. Thirty patients with mild to moderate hypertension received propranolol (40-120 mg) or verapamil (80-200 mg) once daily in two separate ten week courses. After ten weeks treatment both drugs had significantly reduced both SBP and DBP. Beta-thromboglobulin (beta-TG) concentration, reflecting the status of platelet activation in vivo, was significantly decreased after propranolol (129.6 +/- 13.5 vs. 77.9 +/- 8.6 ng/ml) and verapamil (129.6 +/- 13.5 vs. 90.7 +/- 10.1 ng/ml) treatments while platelet aggregation induced by ADP, collagen, arachidonic acid or adrenaline and the production of thromboxane B2 (TXB2), 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and platelet cyclic 3'-5' adenosine monophosphate (C-AMP) concentration were not affected. Significant alterations in rheological parameters such as plasma and whole blood viscosity, fibrinogen level and red cell deformability were not found. Higher cholesterol and low-density lipoprotein-cholesterol (LDL-C) levels were observed after propranolol treatment but not in verapamil treatment. Side-effects were mild, tolerated and no patient had to be withdrawn from the study. In conclusion, propranolol and verapamil are generally effective antihypertensive as well as rheologically safe drugs. Compared with the metabolic effect on serum lipid, verapamil may be a better choice. Both drugs possess the tendency to inhibit platelet properties which is desirable in hypertension treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Flow_Velocity_MeSH M_Blood_Platelets_MeSH S_drug_effects_MeSH Blood_Platelets_drug_effects_MeSH S_physiology_MeSH Blood_Platelets_physiology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Erythrocyte_Deformability_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH S_physiology_MeSH Platelet_Aggregation_physiology_MeSH M_Platelet_Factor_4_MeSH S_analysis_MeSH Platelet_Factor_4_analysis_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thromboxane_B2_MeSH S_blood_MeSH Thromboxane_B2_blood_MeSH M_Time_Factors_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH M_beta-Thromboglobulin_MeSH S_analysis_MeSH beta-Thromboglobulin_analysis_MeSH 
****** 8023668
----K E
----T The effect of metoprolol upon blood pressure, cerebral blood flow and oxygen consumption in patients subjected to craniotomy for cerebral tumours.
----A Hypertension and cerebral hyperperfusion are often seen in the immediate postoperative period after craniotomy for supratentorial tumours. Metoprolol is known to attenuate the postoperative hypertensive response after hypotensive anaesthesia and this study was carried out to evaluate the effect of metoprolol on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) before extubation and cerebral arteriovenous oxygen content difference (AVDO2), mean arterial blood pressure (MABP), PaO2 and PaCO2 in a 180-min period after extubation. Twenty patients anaesthetized with thiopentone, fentanyl, nitrous oxide 67%, and halothane 0.5% were randomized to receive intravenous metoprolol or placebo at the end of the peroperative period. There were no significant differences in CBF- and CMRO2 values between the two groups. In the period between closure of the dura and 5 min after extubation, an increase in MABP was observed in the control group (P < 0.05), but not in the metoprolol group. During the same period a decrease in AVDO2 was observed in both groups (P < 0.05); during the next 10 min an increase was observed, but with no difference in AVDO2 values between the groups. A higher level of PaO2 in the metoprolol group was observed in the postoperative period. These findings suggest that peroperative treatment with metoprolol reduces postoperative MABP but does not influence the cerebral blood flow and metabolism.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anesthesia__Intravenous_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Temperature_MeSH M_Brain_MeSH S_metabolism_MeSH Brain_metabolism_MeSH M_Carbon_Dioxide_MeSH S_blood_MeSH Carbon_Dioxide_blood_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH P_Craniotomy_MeSH M_Double-Blind_Method_MeSH M_Dura_Mater_MeSH S_surgery_MeSH Dura_Mater_surgery_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Oxygen_MeSH S_blood_MeSH Oxygen_blood_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Placebos_MeSH M_Postoperative_Period_MeSH M_Supratentorial_Neoplasms_MeSH S_surgery_MeSH Supratentorial_Neoplasms_surgery_MeSH 
****** 8031548
----K I
----T Effects of antihypertensive medications on quality of life in elderly hypertensive women.
----A The impact of antihypertensive medications on the quality of life of elderly hypertensive women has rarely been systematically evaluated in large clinical trials using drugs from the new generations of pharmaceutic preparations. We carried out a multicenter, randomized double-blind clinical trial with 309 hypertensive women aged 60 to 80 years to assess effects of atenolol, enalapril, and isradipine on measures of quality of life over a 22-week period. The patients had mild to moderate hypertension. Hydrochlorothiazide was added to treatment if monotherapy was inadequate in lowering blood pressure. At the conclusion of the trial the three drug groups did not differ in degree of reduction of diastolic blood pressure or in supplementation with hydrochlorothiazide. Over the 22-week trial, linear trend analysis showed no differences between the treatment groups in change from baseline on quality of life measures of well-being, physical status, emotional status, cognitive functioning, and social role participation. Regarding each of 33 physical side effects over the 22 weeks, we found no general difference between atenolol, enalapril, and isradipine groups on measures of change in distress over symptoms except for enalapril patients who worsened in distress over cough (P = .001) and atenolol patients who worsened in distress over dry mouth (P = .014). Centering on three medications that are relatively new additions to the armamentarium for blood pressure control, the findings underline the increasing opportunities for the physician to select drugs that can control blood pressure while maintaining the quality of life of elderly hypertensive women.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isradipine_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8033506
----K E
----T Post-exercise Doppler-echocardiographic haemodynamics in idiopathic dilated cardiomyopathy after metoprolol infusion.
----A 1. The physiological effects of the acute administration of a beta-adrenoceptor antagonist in patients with idiopathic dilated cardiomyopathy were assessed by performing post-exercise Doppler-echocardiography study. Eleven patients and six control subjects were studied. According to a double-blind randomized protocol, 5 mg of metoprolol or placebo was administered before cycloergometer exercise. 2. In patients, after metoprolol, a significant decrease in heart rate and systolic blood pressure, as well as in peak aortic acceleration and cardiac output, was observed 2 min after exercise. Left ventricular end-diastolic diameter did not change from baseline values either after placebo or metoprolol. In normal subjects, as compared with placebo, a decrease in heart rate and peak aortic acceleration was observed after metoprolol, whereas systolic blood pressure did not change. A similar increase in cardiac output occurred after metoprolol, as compared with placebo, associated with an increase in left ventricular end-diastolic diameter and stroke volume. 3. Post-exercise Doppler echocardiography is a means of assessing haemodynamic changes occurring during exercise in patients with congestive heart failure. Although acute metoprolol administration does not provide beneficial haemodynamic effects, a decrease in the energy requirements of the heart and a faster recovery after exercise may participate in the long-term beneficial action of beta-adrenoceptor antagonists.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Depression__Chemical_MeSH M_Double-Blind_Method_MeSH P_Echocardiography__Doppler_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH 
****** 8033771
----K E
----T Metabolic effects of propranolol and hydroflumethiazide treatment in Kenyans with mild to moderate essential hypertension.
----A In a prospective single-blind comparative trial, sixty newly diagnosed mild to moderate hypertensives were randomly assigned to either propranolol or hydroflumethiazide monotherapy. Baseline fasting serum glucose lipid profiles, serum uric acid and potassium levels, were determined at the beginning of the trial. Repeat levels were determined at completion of twelve weeks of treatment. Propranolol treatment significantly reduced HDL-cholesterol (p < 0.02) and increased both VLDL and total serum triglycerides (p < 0.01). Hydroflumethiazide significantly increased total and LDL-chole-sterol, fasting serum glucose and uric acid levels (p < 0.01); potassium levels were significantly lowered (p < 0.01). Treatment with either propranolol or hydroflumethiazide is associated with significant metabolic side-effects which require regular monitoring and intervention as appropriate.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Drug_Monitoring_MeSH M_Female_MeSH M_Human_MeSH M_Hydroflumethiazide_MeSH S_therapeutic_use_MeSH Hydroflumethiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_classification_MeSH Hypertension_classification_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Kenya_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Single-Blind_Method_MeSH 
****** 8037411
----K E
----T Do nonsteroidal anti-inflammatory drugs affect blood pressure? A meta-analysis.
----A PURPOSE: A meta-analysis of randomized trials studying the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on blood pressure. DATA SOURCES AND STUDY SELECTION: Eight databases were searched, yielding 38 randomized, placebo-controlled trials and 12 randomized but not placebo-controlled trials (comparing two or more NSAIDs). DATA EXTRACTION: Pooled mean treatment effects were computed in each trial for blood pressure, weight, creatinine clearance, plasma renin activity, and daily urinary excretion of sodium and prostaglandins. Meta-analyses of these variables were done for all randomized, controlled trials; for all randomized, uncontrolled trials; and for several subgroups. DATA SYNTHESIS: When pooled, NSAIDs elevated supine mean blood pressure by 5.0 mm Hg (95% CI, 1.2 to 8.7 mm Hg) but had no effect on variables other than blood pressure. Nonsteroidal anti-inflammatory drugs antagonized the antihypertensive effect of beta-blockers (blood pressure elevation, 6.2 mm Hg; CI, 1.1 to 11.4 mm Hg) more than did vasodilators and diuretics. Among NSAIDs, piroxicam produced the most marked elevation in blood pressure (6.2 mm Hg; CI, 0.8 to 11.5 mm Hg), whereas sulindac and aspirin had the least hypertensive effect. CONCLUSIONS: Nonsteroidal anti-inflammatory drugs may elevate blood pressure and antagonize the blood pressure-lowering effect of antihypertensive medication to an extent that may potentially increase hypertension-related morbidity. Although certain NSAIDs and antihypertensive agents could be more likely to produce these effects, the underlying mechanisms require further study.
----P Journal_Article Meta-Analysis 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH S_pharmacology_MeSH Anti-Inflammatory_Agents__Non-Steroidal_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_antagonists_&_inhibitors_MeSH Antihypertensive_Agents_antagonists_&_inhibitors_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Selection_Bias_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8039850
----K E
----T Lipids and lipoproteins during antihypertensive drug therapy. Comparison of doxazosin and atenolol in a randomized, double-blind trial: the Alpha Beta Canada Study.
----A A randomized double-blind trial comparing the alpha-adrenergic blocker doxazosin and the beta-adrenergic blocker atenolol was completed by 131 patients with mild to moderate hypertension. Blood pressure and fasting blood lipids were determined at baseline and 4, 12, and 24 weeks of treatment. At entry, plasma lipids and lipoproteins were similar in those patients randomized to doxazosin or atenolol. After 24 weeks of treatment with atenolol, there were significant (P < .05) decreases in high-density lipoprotein cholesterol (HDL-C) and increases in triglycerides and very-low-density triglycerides (VLDL-T). In contrast, doxazosin was associated with significant (P < .05) increases in HDL-C and decreases in triglycerides and VLDL-T. There were no significant differences in HDL apolipoprotein (apo) A-I or low-density lipoprotein apoB between the drugs, but atenolol decreased the ratio of HDL-C to apoA-I, and doxazosin increased this ratio, differences that were statistically significant (P < .002). Neither apoA-I nor apoB concentration at baseline nor apoE phenotype was predictive of the lipid responses during antihypertensive treatment with either drug. Thus, there are significant favorable changes in HDL-C, total triglycerides, and VLDL-T between patients with mild to moderate hypertension and normal plasma lipids when treated with the alpha-blocker doxazosin compared with the beta-blocker atenolol. Plasma lipid or apo concentrations were not predictive of their lipid response during antihypertensive therapy with either of these agents.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Apolipoproteins_E_MeSH S_analysis_MeSH Apolipoproteins_E_analysis_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8042331
----K E
----T Treatment of portal hypertension in children.
----A The management of children with portal hypertension (PH) has substantially changed owing to the good results and broader application of both endoscopic sclerotherapy and orthotopic liver transplantation (OLT). Since the introduction of sclerotherapy for the treatment of bleeding esophageal varices, the number of surgical procedures has sharply decreased. Until the early 1980s, however, the treatment of choice of bleeding esophageal varices was based on different variations of two main types of open surgery: devacularization and transection operations and portosystemic shunts. The experience with nonshunt procedures is limited in the pediatric population. Literature reports from the last 25 years have emphasized a number of restrictions related to portosystemic shunts in small subjects. However, portosystemic shunts, selective or not, can be performed even in very young subjects with high rates of success. From 1974 to 1984 the distal splenorenal shunt (DSRS) was the procedure of choice for the treatment of children with variceal bleeding in our institution. Forty-two children underwent DSRS during this period. Since 1985, when endoscopic variceal sclerotherapy (EVS) replaced DSRS as the first therapeutic option in our service, this shunt has been performed in only 8 children in whom EVS has failed, none of them during the last 2 years. In this cohort of 50 cases of DSRS, the shunt patency has increased from 71% in the first 7 patients to 95% thereafter. There has been no perioperative mortality. From 1985 to April 1993, 107 children were submitted to EVS sessions for the treatment of esophageal varices bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Journal_Article Review Review__Tutorial 
----M M_Child_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Esophagus_MeSH S_surgery_MeSH Esophagus_surgery_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Liver_Transplantation_MeSH M_Portasystemic_Shunt__Surgical_MeSH M_Sclerotherapy_MeSH M_Splenorenal_Shunt__Surgical_MeSH 
****** 7726892
----K I
----T Drug treatment of hypertension in the elderly: a meta-analysis.
----A PURPOSE: A meta-analysis of the effect of antihypertensive drug treatment on mortality and morbidity in elderly patients. DATA SOURCES: A literature search of published articles from January 1980 to February 1992. STUDY SELECTION: Randomized controlled trials of drug treatment of hypertension with end points for elderly patients reported separately. DATA EXTRACTION: Mortality or morbidity end points or both in patients older than 59 years were pooled by determination of typical odds ratio. A meta-regression was used to study heterogeneity. RESULTS: Nine major trials with 15,559 patients older than 59 years were identified. Death rates in the control group varied between 2.7% and 77.2%; stroke and coronary mortality increased with the severity-of-illness rank (P < 0.001). Overall, treated patients had an approximately 12% reduction in all-cause mortality (odds ratio, 0.88; 95% CI, 0.80 to 0.97; 953 events compared with 1069 events, P = 0.009). There was a 36% reduction in stroke mortality (odds ratio, 0.64; CI, 0.49 to 0.82; 94 events compared with 149 events, P < 0.001) and a 25% reduction in coronary heart disease mortality (odds ratio, 0.75; CI, 0.64 to 0.88; 263 events compared with 350 events, P < 0.001). Coronary morbidity was reduced 15% (odds ratio, 0.85; CI, 0.73 to 0.99; 325 events compared with 379 events, P = 0.036), and stroke morbidity was reduced 35% (odds ratio, 0.65; CI, 0.55 to 0.76; 247 events compared with 382 events, P < 0.001). CONCLUSION: Overall, treatment of hypertension in elderly patients produces a significant benefit in total mortality and cardiovascular morbidity and mortality. However, this benefit may be reduced in the oldest age groups.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cerebrovascular_Disorders_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH S_mortality_MeSH Cerebrovascular_Disorders_mortality_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8044945
----K I
----T Effects of treatment on outcome in mildly symptomatic patients with ischemia during daily life. The Atenolol Silent Ischemia Study (ASIST)
----A BACKGROUND: Detection of asymptomatic ischemia in patients with coronary artery disease has been associated with increased risk for adverse outcome, but treatment of patients with asymptomatic ischemia remains controversial. Accordingly, the purpose of this study was to determine if treatment reduces adverse outcome in patients with daily life ischemia. METHODS AND RESULTS: A multicenter, randomized, double-blind, placebo-controlled study of asymptomatic or minimally symptomatic outpatients with daily life silent ischemia due to coronary artery disease was conducted. The primary outcome measure was event-free survival at 1 year by Kaplan-Meier analysis. Events were death, resuscitated ventricular tachycardia/fibrillation, myocardial infarction, hospitalization for unstable angina, aggravation of angina, or revascularization. The secondary outcome was ischemia during ambulatory ECG monitoring at 4 weeks. Three hundred six outpatients with mild or no angina (Canadian Cardiovascular Society class I or II), abnormal exercise tests, and ischemia on ambulatory monitoring were randomized to receive either atenolol (100 mg/d) or placebo. After 4 weeks of treatment, the number (mean +/- SD, 3.6 +/- 4.2 versus 1.7 +/- 4.6 episodes, P < .001) and average duration (30 +/- 3.3 versus 16.4 +/- 6.7 minutes, P < .001) of ischemic episodes per 48 hours of ambulatory monitoring decreased in atenolol- compared with placebo-assigned patients (4.4 +/- 4.6 to 3.1 +/- 6.0 episodes and 36.6 +/- 4.1 to 30 +/- 5.5 minutes). Event-free survival improved in atenolol-treated patients (P < .0066), who had an increased time to onset of first adverse event (120 versus 79 days) and fewer total first events compared with placebo (relative risk, 0.44; 95% confidence intervals, 0.26 to 0.75; P = .001). There was a nonsignificant trend for fewer serious events (death, resuscitation from ventricular tachycardia/fibrillation, nonfatal myocardial infarction, or hospitalization for unstable angina) in atenolol-treated patients (relative risk, 0.55; 95% confidence intervals, 0.22 to 1.33; P = .175). The most powerful univariate and multivariate correlate of event-free survival was absence of ischemia on ambulatory monitoring at 4 weeks. Side effects were mild and generally similar comparing atenolol- and placebo-treated patients, although bradycardia was more frequent with atenolol. CONCLUSIONS: Atenolol treatment reduced daily life ischemia and was associated with reduced risk for adverse outcome in asymptomatic and mildly symptomatic patients compared with placebo.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M P_Activities_of_Daily_Living_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_epidemiology_MeSH Myocardial_Ischemia_epidemiology_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 8045844
----K E
----T Systemic hypertension at 4,300 m is related to sympathoadrenal activity.
----A Residence at high altitude has been associated with elevation in systemic arterial blood pressure, but the time course has been little studied and the mechanism is unknown. Because plasma epinephrine (E) and norepinephrine (NE) also increase at altitude, we hypothesized that heightened sympathoadrenal activity may cause increased arterial pressure. We measured ambulatory blood pressure by cuff monitor in relation to 24-h urinary excretion of E and NE at sea level and during 3 wk of residence at 4,300 m (Pikes Peak, CO) in 11 healthy men. In five subjects taking placebo, arterial pressure progressively increased at 4,300 m from 82 +/- 1 (SE) mmHg at sea level to 88 +/- 3 on day 2, 91 +/- 3 on day 8, and 97 +/- 6 on day 17. In six subjects, propranolol (240 mg/day) decreased pressure from 85 +/- 4 to 77 +/- 1 mmHg at sea level but did not prevent sustained increase in pressure at 4,300 m (84 +/- 1, 81 +/- 1, and 85 +/- 3 mmHg on days 2, 8, and 17, respectively). Compared with the placebo group, blood pressure did not increase further over the initial elevation observed on day 2 in the propranolol group. There was interindividual variability in the blood pressure responses in both groups, with some subjects demonstrating a more marked increase in blood pressure. Urinary excretion of NE increased concomitantly with pressure at altitude in both groups, with a greater rise in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenal_Glands_MeSH S_physiopathology_MeSH Adrenal_Glands_physiopathology_MeSH M_Adult_MeSH P_Altitude_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Epinephrine_MeSH S_urine_MeSH Epinephrine_urine_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isoproterenol_MeSH S_pharmacology_MeSH Isoproterenol_pharmacology_MeSH M_Male_MeSH M_Norepinephrine_MeSH S_urine_MeSH Norepinephrine_urine_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Pulmonary_Gas_Exchange_MeSH S_physiology_MeSH Pulmonary_Gas_Exchange_physiology_MeSH M_Receptors__Adrenergic__alpha_MeSH S_drug_effects_MeSH Receptors__Adrenergic__alpha_drug_effects_MeSH M_Respiratory_Function_Tests_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Sympathetic_Nervous_System_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH 
****** 8046193
----K E
----T Improving treatment of late life depression in primary care: a randomized clinical trial.
----A OBJECTIVE: Facilitate primary care physicians' compliance with recommended standards of care for late life depression by reducing barriers to recognition and treatment. DESIGN: Randomized controlled clinical trial of physician-targeted interventions. SETTING: Academic primary care group practice caring for an urban, medically indigent patient population. PATIENTS/PARTICIPANTS: Patients aged 60 and older who exceeded the threshold on the Centers for Epidemiologic Studies Depression Scale (CES-D) and the Hamilton Depression Rating Scale (HAM-D) and their primary care physicians. INTERVENTION: Physicians of intervention patients were provided with patient-specific treatment recommendations during 3 special visits scheduled specifically to address the patient's symptoms of depression. In general, physicians were encouraged to establish a diagnosis of depression and educate their patient about the diagnosis, discontinue medications that can cause or exacerbate depressive symptoms, initiate antidepressants when appropriate, and consider referral to psychiatry. Guidelines for prescribing antidepressants were provided. Control physicians received no intervention, and control patients received usual care. MAIN OUTCOME MEASURES: Frequency of recording a depression diagnosis, stopping medications associated with depression, initiating antidepressant medication, and psychiatry referral; mean changes in HAM-D and Sickness Impact Profile (SIP) scores. RESULTS: One hundred three physicians and 175 patients were involved in the clinical trial. Physicians of intervention patients were more likely to diagnose depression and prescribe antidepressants (P < 0.01). There were no differences between the groups in the frequency of stopping medications associated with depression or referrals to psychiatry. Medications with the strongest cause and effect relationship to depression were infrequently used in this cohort of patients. Although both groups showed improvement in HAM-D and SIP scores, we were unable to demonstrate significant differences in HAM-D or SIP scores between the 2 groups. CONCLUSIONS: Intensive screening and feedback of patient-specific treatment recommendations increased the recognition and treatment of late life depression by primary care physicians. However, we were unable to demonstrate significant improvement in depression or disability severity among intervention patients despite the informational support provided to their physicians. Efforts to improve the functional status of these patients may require more integrated interventions and more aggressive attempts to target psychosocial stressors traditionally outside the purview of primary care.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Depressive_Disorder_MeSH S_diagnosis_MeSH Depressive_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH S_psychology_MeSH Depressive_Disorder_psychology_MeSH M_Education__Medical__Continuing_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Primary_Health_Care_MeSH M_Prognosis_MeSH M_Psychiatric_Status_Rating_Scales_MeSH M_Psychiatry_MeSH M_Referral_and_Consultation_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7914122
----K I
----T [The comparative efficacy of individually adjusted doses of proxodolol and propranolol for one-time and regular administration in stenocardia patients]
----A The comparative efficacy of single and regular doses of the new Russian alpha- and beta-adrenoblocker proxodolol (Pd) and the beta-adrenoblocker propranolol (Pr) was studied in 12 male patients with stable angina on effort. The effect of single doses was evaluated with paired bicycle ergometries (PBE); that of course therapy was assessed with crossover randomized placebo-controlled tests of the two agents. During PBE, an adequate antianginal effect of Pd given in single doses of 0.04-0.08 g was seen in 66.5% and that of Pr used in the same doses was observed in 58.4% (p > 0.05). The exercise tolerance in patients given either agent in a single dose was similar. During 1-month course treatment with Pd in a mean daily dose of 186 +/- 24 mg, anginal episodes caused an over 3-fold reduction, which is similar to the clinical effect displayed by Pr, 182 +/- 25 mg/day. A single dose of Pd of 0.04 g produced a more pronounced chronotropic and antihypertensive effect than did the same dose of Pr. No differences were found during their course therapy. Pd was found to cause no orthostatic antihypertensive phenomenon.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH S_instrumentation_MeSH Exercise_Test_instrumentation_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxadiazoles_MeSH S_administration_&_dosage_MeSH Oxadiazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Oxadiazoles_adverse_effects_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Time_Factors_MeSH 
****** 8053282
----K E
----T Carvedilol in the treatment of mild to moderate hypertension: experience with ambulatory blood pressure monitoring.
----A An open randomized study was conducted in mild to moderate hypertensive patients to evaluate, over a 3 months treatment period, the efficacy and tolerability of carvedilol 25 mg OD and to compare, in case of insufficient results with 25 mg, the efficacy and tolerance of carvedilol 50 mg and carvedilol 25 mg coadministered with diuretics. Mean office blood pressure (sitting) of the 91 patients who completed the study according to the protocol was reduced from 161/100 to 147/91 mm Hg after 4 weeks of treatment carvedilol 25 mg OD. Continuation of carvedilol 25 mg produced no further reduction in blood pressure. Increasing carvedilol to 50 mg OD or addition of diuretics further reduced blood pressure. Ambulatory blood pressure measurements showed a significant reduction in both SBP and DBP after 3 months treatment in the three groups, as well as with respect to the circadian profile of blood pressure and heart rate. Large differences between ambulatory and office blood pressure were observed: 37% of the patients diagnosed as mild to moderate hypertensives according to office blood pressure before treatment had mean daytime DBP < 90 mm Hg and 39% mean daytime SBP < 140 mm Hg. Twenty-eight percent of the patients experienced adverse events; they occurred mainly at the beginning of treatment; less than 5% of participants withdrew due to adverse events. The most frequent adverse events were fatigue, vertigo and asthenia. This study showed that carvedilol is safe and effective in the treatment of mild to moderate hypertension and that there is a high prevalence (nearly 40%) of low ambulatory blood pressure means in a population labelled as mild to moderate hypertensive.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Monitoring__Physiologic_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 8058230
----K E
----T Nicardipine versus metoprolol in the treatment of hypertension during pregnancy: a randomized comparative trial.
----A OBJECTIVE: To compare the effects of treatment with nicardipine and metoprolol in patients with hypertension during pregnancy. METHODS: One hundred pregnant patients with mild or moderate hypertension followed at the Centre Hospitalier Intercommunal de Creteil (France) were randomly allocated to treatment with either nicardipine or metoprolol. Changes in maternal blood pressure (BP), laboratory indices, umbilical Doppler velocimetry, and neonatal outcome were compared by means of Student t test, chi 2 test, and analysis of variance. RESULTS: Nicardipine decreased maternal systolic and diastolic BP more than metoprolol (P < .001). Umbilical artery resistance was lower in nicardipine-treated patients (P < .001). Plasma uric acid and creatinine concentrations were increased less markedly in the nicardipine group (P < .05 and P < .01, respectively). The incidence of cesarean delivery for fetal distress was lower in the nicardipine group (P < .01). There was a trend toward higher birth weights in the nicardipine group but no significant difference in neonatal outcome. CONCLUSION: Nicardipine is more effective than metoprolol in decreasing maternal BP; neonatal outcome is not significantly different.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Birth_Weight_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cesarean_Section_MeSH S_statistics_&_numerical_data_MeSH Cesarean_Section_statistics_&_numerical_data_MeSH M_Comparative_Study_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant__Newborn_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Nicardipine_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Pre-Eclampsia_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Pregnancy_Outcome_MeSH 
****** 8061854
----K E
----T Effects of antihypertensive medication on hypertension in patients with sleep apnoea.
----A The present study was to investigate the effect of four different antihypertensive medications [atenolol, hydrochlorothiazide (HCTZ), isradipine and spirapril] on the blood pressure and metabolic state of 18 patients with obstructive sleep apnoea. All patients received each of the drugs for a period of 8 weeks according to a randomized crossover design. Although all of the medications decreased systolic blood pressure (SBP), only spirapril decreased SBP significantly (17 +/- 15 mmHg; p < 0.001). All of the medications decreased diastolic blood pressure (DBP) significantly, but spirapril produced the greatest reduction (5-8 vs 10 mmHg, respectively). Both HCTZ and isradipine increased fasting serum total cholesterol concentration (0.3 +/- 0.5 and 0.3 +/- 0.4 mmol/l, respectively; p < 0.05). Atenolol decreased fasting serum high-density lipoprotein (HDL)-cholesterol concentration significantly (0.12 +/- 0.15 mmol/l; p < 0.01). Both HCTZ and isradipine increased fasting serum glucose concentration significantly (0.7 +/- 0.8 mmol/l and 0.6 +/- 0.7 mmol/l, respectively; p < 0.01). No significant effect on serum lipid and glucose levels was observed with spirapril. On the basis of these results, spirapril was the best medication for hypertensive patients with obstructive sleep apnoea.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sleep_Apnea_Syndromes_MeSH S_complications_MeSH Sleep_Apnea_Syndromes_complications_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8062314
----K E
----T Ambulatory blood pressure and heart rate during once-daily, randomized, crossover administration of carteolol and atenolol.
----A This study evaluated the effect of beta-adrenoceptor blocking agents (beta-blockers) with or without intrinsic sympathomimetic activity on the 24-hour blood pressure profile of 15 untreated patients with essential hypertension. After a 4-week run-in period, subjects were randomly assigned to an 8-week treatment period of once-daily carteolol (15 mg/d) or atenolol (50 mg/d). The groups were crossed over at week 8. Office blood pressure and heart rate were recorded every 2 weeks and 24-hour ambulatory blood pressure monitoring was performed immediately preceding and at the conclusion of each period. Both drugs significantly reduced (P < 0.01) office blood pressure and heart rate throughout the two treatment periods. The 24-hour ambulatory blood pressure monitoring at 0.5- and 1-hour intervals revealed that systolic blood pressure in 2 of 8 sleeping hours and diastolic blood pressure in 4 of 8 sleeping hours were significantly higher (P < 0.05) after carteolol treatment than after atenolol treatment. The average values for both daytime and nighttime blood pressures, however, were significantly lower at the end of both periods. Although atenolol lowered heart rate throughout the 24-hour period, there was a smaller reduction in heart rate with carteolol than with atenolol during daytime (-5.4 +/- 4.9 beats/min vs -12.7 +/- 6.6 beats/min, P < 0.005, respectively). Heart rate increased during nighttime (P < 0.02) and was significantly greater than with atenolol treatment (5.0 +/- 7.2 beats/min vs -5.7 +/- 8.0 beats/min, P < 0.001, respectively). These results suggest that the different effects of the two beta-blockers on heart rate and nighttime blood pressure may be attributed to the presence or absence of intrinsic sympathomimetic activity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Ambulatory_Care_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carteolol_MeSH S_administration_&_dosage_MeSH Carteolol_administration_&_dosage_MeSH S_pharmacology_MeSH Carteolol_pharmacology_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sleep_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8066478
----K E
----T Management of mild pregnancy-induced hypertension remote from term.
----A The goal in the management of patients with pregnancy-induced hypertension is delivery of infants who will thrive physically and mentally without compromising maternal health in the process. Many therapeutic approaches have been recommended; however, none except delivery are curative. In the interest of maternal health, delivery is essential regardless of gestational age when severe preeclampsia or eclampsia is diagnosed. Conversely, women with mild pregnancy-induced hypertension remote from term may be managed conservatively with efforts directed toward prolonging gestation in order to maximize perinatal outcome. The regimen used at Parkland Memorial Hospital has proven to be safe and effective. We will continue to use this method of inpatient management until well-controlled studies are designed and conducted and yield comparably safe and efficacious outcomes.
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Ambulatory_Care_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bed_Rest_MeSH M_Dehydroepiandrosterone_MeSH S_analogs_&_derivatives_MeSH Dehydroepiandrosterone_analogs_&_derivatives_MeSH S_metabolism_MeSH Dehydroepiandrosterone_metabolism_MeSH M_Dehydroepiandrosterone_Sulfate_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Metabolic_Clearance_Rate_MeSH M_Placenta_MeSH S_blood_supply_MeSH Placenta_blood_supply_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH M_Time_Factors_MeSH M_Uterus_MeSH S_blood_supply_MeSH Uterus_blood_supply_MeSH 
****** 7915221
----K E
----T Impact of clinical trials on the use of beta blockers after acute myocardial infarction and its relation to other risk indicators for death and 1-year mortality rate.
----A Based on selected patient populations, several randomized trials have shown beta blockers to decrease mortality after acute myocardial infarction (AMI). The purpose of this study was to describe the use of beta blockers in various subsets of patients admitted to Sahlgren's Hospital between February 15, 1986, and November 9, 1987, with AMI, and the relation of AMI to other risk indicators for death and to a 1-year mortality rate. Beta blockers, mainly metoprolol, were prescribed for 66% of all survivors at discharge. They were more frequently prescribed for younger patients and for those with a previous history of AMI and hypertension, but less frequently for those with a history of congestive heart failure and diabetes mellitus. Patients for whom beta blockers were not prescribed haa a 1-year mortality of 27% versus 11% for the rest (p < 0.001). Independent predictors of 1-year mortality after discharge were age (p < 0.001), history of hypertension (p < 0.001), prescription of beta blockers at discharge (p < 0.001), congestive heart failure during hospitalization (p < 0.001), and a history of AMI (p < 0.01). P values were corrected for baseline differences. Beta blockers were not prescribed at discharge for one-third of survivors after AMI. This group had a very high mortality during the first year. When simultaneously considering various risk indicators for death, prescription of beta blockers at discharge was associated with an increased rate of survival.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Clinical_Trials_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Sweden_MeSH 
****** 7915237
----K I
----T The long-term effects of metoprolol and epanolol on tissue-type plasminogen activator and plasminogen activator inhibitor 1 in patients with ischaemic heart disease.
----A This double-blind, randomized parallel group study investigated the effect of 6 months beta-adrenoceptor antagonist therapy with either metoprolol (beta 1-selective without intrinsic sympathomimetic activity [ISA]) or epanolol (beta 1-selective with ISA) on markers of endogenous fibrinolysis in 20 patients with chronic stable angina receiving concurrent treatment with nifedipine. Neither drug had an effect on tissue-type plasminogen activator or plasminogen activator inhibitor type 1 (PAI-1). A significant correlation between fasting insulin and PAI-1 has previously been described and was confirmed in this study. The group treated with metoprolol showed a significant rise in fasting insulin after 6 months with no change in PAI-1. This suggests that the previously described link between these two may not be causal.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH P_Benzeneacetamides_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Plasminogen_Activator_Inhibitor_1_MeSH S_blood_MeSH Plasminogen_Activator_Inhibitor_1_blood_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Tissue_Plasminogen_Activator_MeSH S_blood_MeSH Tissue_Plasminogen_Activator_blood_MeSH 
****** 8070610
----K E
----T Impact of lisinopril and atenolol on kidney function in hypertensive NIDDM subjects with diabetic nephropathy.
----A Diabetic nephropathy is characterized by hypertension and a relentless decline in kidney function. Angiotensin-converting enzyme inhibitors have been claimed to preserve kidney function better than an equal blood pressure (BP) reduction with conventional antihypertensive treatment (renoprotection). We compared the effect on kidney function of lisinopril (10-20 mg/day) and atenolol (50-100 mg/day) in hypertensive NIDDM patients (mean age 60 +/- 8 years) with diabetic nephropathy. Forty-three (21 lisinopril and 22 atenolol) patients were enrolled in a 1-year randomized double-blind parallel study. Eight patients dropped out, and the results for the remaining 35 patients (16 lisinopril and 19 atenolol) are presented. Diuretics were required in 10 of 16 lisinopril patients and 12 of 19 atenolol patients. The following variables were measured: 24-hour ambulatory BP (Takeda TM2420), albuminuria (enzyme-linked immunosorbent assay), fractional albumin clearance, and glomerular filtration rate (GFR) ([51Cr]EDTA technique). The average reduction in mean arterial BP during the 12 months was identical in the two groups 12 +/- 2 vs. 11 +/- 1 mmHg in the lisinopril and atenolol group, respectively. Albuminuria was on average reduced 45% in the lisinopril group vs. 12% in the atenolol group (P < 0.01), and fractional albumin clearance was on average reduced 49% in the lisinopril group vs. 1% in the atenolol group (P < 0.05). GFR declined identically in the two groups 11.7 +/- 2.3 vs. 11.6 +/- 2.3 ml.min-1.year-1 in the lisinopril and atenolol groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Albuminuria_MeSH M_Apolipoproteins_MeSH S_analysis_MeSH Apolipoproteins_analysis_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Nephropathies_MeSH S_physiopathology_MeSH Diabetic_Nephropathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH P_Lipoprotein(a)_MeSH M_Lisinopril_MeSH S_adverse_effects_MeSH Lisinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Serum_Albumin_MeSH S_metabolism_MeSH Serum_Albumin_metabolism_MeSH M_Sodium_MeSH S_blood_MeSH Sodium_blood_MeSH M_Time_Factors_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 8074049
----K I
----T Decrease in mortality by propranolol in patients with heart disease and complex ventricular arrhythmias is more an anti-ischemic than an antiarrhythmic effect.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Single-Blind_Method_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH 
****** 8074426
----K 1
----T [Comparative study of bisoprolol and celiprolol in to moderate hypertension using casual as well as ambulatory blood pressure measurements]
----A A randomised, parallel, double-blind trial was undertaken in 80 patients to compare the efficacy of bisoprolol with that of celiprolol, using causal (BPc) as well as ambulatory (AMBP) blood pressure measurement. After a two week wash-out and two week placebo run-in, patients in whom diastolic blood pressure (DBP) was between 95 and 114 mmHg were given either bisoprolol (10 mg/day) or celiprolol (200 mg/day) for 12 weeks. When efficacy was insufficient (DBP > 95 mmHg), the dose could be doubled after 4 weeks and a diuretic added after 8 weeks. BPc was measured at each visit and an AMBP obtained the day before the start of active treatment and at its end. Six patients dropped out of the trial because of adverse events. Clinical safety/acceptability of both drugs was good. Demographic data, and blood pressure and heart rate figures in both groups were comparable at the end of the placebo period. Mean fall in BPc in the bisoprolol group was 32.5/20.3 mmHg and 23/17.4 mmHg in the celiprolol group, with a significant difference between the two groups concerning systolic pressure (SBP). Ambulatory measurement showed evidence during the periods 24 hours (H), day and night, of a greater fall with bisoprolol (10.7/8.9 mmHg; 13.9/10.8 mmHg; 7.3/7.2 mmHg) than in the celiprolol group (4.9/21.6; 7.3/3.8; 2.9/2 mmHg), the difference being significant for diastolic blood pressure (DBP: p < 0.01; p < 0.05; p < 0.05. Thus bisoprolol was more effective than celiprolol in mild to moderate hypertension, but the difference was significant for SBP by casual measurement and for DBP by ambulatory measurement.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Ambulatory_Care_MeSH M_Blood_Pressure_Determination_MeSH S_instrumentation_MeSH Blood_Pressure_Determination_instrumentation_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH P_Blood_Pressure_Monitors_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 7915625
----K E
----T Beneficial effects of beta-adrenergic blockade in coronary artery surgery: clinical research.
----A In an attempt to resolve the controversy concerning use of beta-adrenoceptor blockade in patients undergoing coronary artery revascularization, 40 consecutive patients with ischaemic heart disease receiving chronic beta-adrenergic blocking therapy (study group) were entered into a randomized trial and were compared with 40 patients receiving no beta-blocking therapy (control group). The postoperative requirement for positive inotropic agents between the two groups was compared. The clinical and operative characteristics of the two groups were similar. After surgery, 2% of patients in the study group required positive inotropic agents compared with 18% of those in the control group (P < 0.05). It is concluded that this difference resulted from an increase in density of beta 1-adrenergic receptors induced by beta-adrenergic blockade, and an increase in the level of catecholamines in the early postoperative period.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_administration_&_dosage_MeSH Acebutolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Acebutolol_adverse_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_surgery_MeSH Hypertension_surgery_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH P_Premedication_MeSH 
****** 8077067
----K E
----T Ten-year mortality rate among patients in whom acute myocardial infarction was not confirmed in relation to clinical history and observations during hospital stay: experiences from the Goteborg Metoprolol Trial.
----A BACKGROUND: The majority of patients hospitalized due to suspected acute myocardial infarction (AMI) will eventually not develop infarction. Information about the long-term prognosis in this patient population is limited. AIM: To describe the mortality during 10 years of follow-up in patients hospitalized due to an initially strong suspicion of AMI, but in whom the diagnosis of AMI could not be confirmed. PATIENTS: All patients participating in an early intervention trial with metoprolol in suspected AMI, but in whom the diagnosis was not confirmed. Patients were included during 1976-1981. RESULTS: In all 1395 patients were included in the study, of whom 586 did not fulfil the criteria for confirmed AMI. The overall mortality during 10 years of follow-up in this population was 26%. In a multivariate analysis considering age, sex, history of cardiovascular diseases, initial heart rate and various complications during the hospital stay, including congestive heart failure, severe ventricular arrhythmias, tachycardia, hypotension, high degree AV-block and severe chest pain, the following appeared as independent predictors of death: previous infarction (P < 0.001), age (P < 0.001), history of diabetes mellitus (P < 0.001) history of smoking (P < 0.05), history of hypertension (P < 0.05), male sex (P < 0.05), and the initial heart rate (P < 0.05). CONCLUSION: Among patients in whom AMI was not confirmed the major risk indicators for death during 10 years of follow-up were: a history of cardiovascular diseases and smoking, age, male sex and high heart rate on admission to hospital.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH 
****** 7916004
----K E
----T Osmotic release oral drug delivery system of metoprolol in hypertensive asthmatic patients. Pharmacodynamic effects on beta 2-adrenergic receptors.
----A This study investigated the effects of an osmotic release oral drug delivery system of metoprolol on the changes induced by cumulative doses of inhaled salbutamol on bronchomotor tone, skeletal muscle, and the circulatory system after single (day 1) and multiple (day 7) dosing in 18 hypertensive asthmatic patients (forced expiratory volume in 1 second > 50% predicted; diastolic blood pressure > 90 mm Hg). The patients were given 14/190 mg metoprolol, 100 mg atenolol, and placebo once daily for a 7-day period each in a randomized, double-blind, crossover design. At the estimated time of peak plasma concentrations, cumulative doses of salbutamol (12.5, 37.5, 112.5, 412.5, 812.5, and 1612.5 micrograms) were applied every 20 minutes. Specific airway conductance, finger tremor amplitude, heart rate, and blood pressure were registered at baseline and at each dose increment. The slopes of the salbutamol dose-response curves of specific airway conductance did not differ on day 1 (P > .05). On day 7, atenolol caused a shift of the dose-response curves of specific airway conductance to the right (P < .05), whereas metoprolol was indistinguishable from placebo (P > .05). The median cumulative salbutamol concentrations causing a 50% increase in specific airway conductance were 416 and 384 micrograms (days 1 and 7, respectively) for placebo, 594 and 444 micrograms for metoprolol, and 562 and 1419 micrograms for atenolol. The median cumulative salbutamol concentrations causing a 35% increase in tremor were 732 and 706 micrograms for placebo, 812 and 1213 micrograms for metoprolol, and 797 and 1323 micrograms for atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Inhalation_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Albuterol_MeSH S_administration_&_dosage_MeSH Albuterol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Albuterol_therapeutic_use_MeSH M_Asthma_MeSH S_complications_MeSH Asthma_complications_MeSH S_drug_therapy_MeSH Asthma_drug_therapy_MeSH S_physiopathology_MeSH Asthma_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Delivery_Systems_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Mouth_MeSH S_metabolism_MeSH Mouth_metabolism_MeSH M_Osmosis_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH S_metabolism_MeSH Receptors__Adrenergic__beta_metabolism_MeSH 
****** 8087974
----K E
----T Guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association.
----A 
----P Guideline Journal_Article Practice_Guideline 
----M M_Acute_Disease_MeSH M_Brain_Ischemia_MeSH S_diagnosis_MeSH Brain_Ischemia_diagnosis_MeSH S_therapy_MeSH Brain_Ischemia_therapy_MeSH M_Cerebrovascular_Disorders_MeSH S_therapy_MeSH Cerebrovascular_Disorders_therapy_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Hemodilution_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_diagnostic_use_MeSH Platelet_Aggregation_Inhibitors_diagnostic_use_MeSH M_Thrombolytic_Therapy_MeSH 
****** 7917158
----K E
----T Comparative effects of quinapril, atenolol, and verapamil on blood pressure and forearm hemodynamics during handgrip exercise.
----A We compared the effects of angiotensin-converting enzyme inhibition with quinapril to those of selective beta-blockade with atenolol and calcium channel blockade with verapamil in 10 hypertensive subjects in a randomized double-blind placebo-controlled crossover study. All antihypertensive agents reduced baseline mean arterial pressure equally and did not modify forearm vascular resistance compared to placebo. In response to sustained handgrip exercise, both quinapril and verapamil, but not atenolol, attenuated the pressor response. However, verapamil was associated with an exaggerated increase in forearm vascular resistance during handgrip, whereas quinapril did not alter this response compared to placebo. It is concluded that quinapril and verapamil reduce the pressor response during isometric exercise by quantitatively different effects on the vasoconstrictor response in, as well as outside of, skeletal muscles.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isoquinolines_MeSH S_pharmacology_MeSH Isoquinolines_pharmacology_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH P_Tetrahydroisoquinolines_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Verapamil_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH 
****** 7917794
----K I
----T A comparison of the antianginal efficacy of nifedipine alone and the fixed combination of atenolol and nifedipine.
----A The antianginal efficacy of a fixed combination of atenolol (50 mg) and nifedipine (20 mg) was compared with nifedipine (20 mg) alone; 102 patients experiencing three or more anginal attacks on their current monotherapy received each treatment twice daily for 3 weeks in a randomised, double-blind crossover trial. Both treatments reduced the weekly number of angina attacks compared with existing therapy; treatment with the fixed combination resulted in significantly fewer angina attacks per week than treatment with nifedipine alone. Also, when the fixed combination treatment followed the period of nifedipine therapy a further decrease in weekly angina attack rate was apparent. Comparison of individual patient response to each treatment showed that twice as many patients reported lower attack rates while on the fixed combination: 6 patients were withdrawn while receiving fixed combination compared with 10 patients on nifedipine alone. However, the incidence of commonly reported complaints was similar with both treatments.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_epidemiology_MeSH Angina_Pectoris_epidemiology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 7923309
----K E
----T Effect of combination therapy with atenolol and the angiotensin-converting enzyme inhibitor benazepril.
----A The purpose of this study was to determine whether patients whose blood pressure failed to normalize while receiving monotherapy with atenolol would experience further blood pressure lowering by adding the angiotensin-converting enzyme (ACE) inhibitor benazepril hydrochloride to their treatment regimen. Seventy-four of the original 127 patients treated with atenolol met the criteria for entry into the 4-week, double-blind phase of the study, in which either benazepril 10 mg twice daily (increased after 1 week, if necessary, to 20 mg twice daily) or placebo was added to atenolol. At end point, 46% of the benazepril group had achieved an excellent or good response (ie, diastolic blood pressure [DBP] < 90 mm Hg or a decrease of > or = 10 mm Hg below the baseline) compared with 14% of the placebo group (P < 0.01). The mean fall in DBP at end point was -5.6 mm Hg in the benazepril group and -3.7 mm Hg in the placebo group. Because six patients in the benazepril group experienced an increase of blood pressure that offset the fall observed in the responders, the difference in DBP response between the benazepril group and the placebo group was not statistically significant. We conclude that adding benazepril to the regimen of patients whose blood pressure is inadequately controlled while receiving atenolol monotherapy can produce an additional decrease in blood pressure in almost half the patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzazepines_MeSH S_therapeutic_use_MeSH Benzazepines_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7923660
----K I
----T A randomized trial of beta-blockade in heart failure. The Cardiac Insufficiency Bisoprolol Study (CIBIS). CIBIS Investigators and Committees.
----A BACKGROUND: Functional benefit in heart failure due to idiopathic dilated cardiomyopathy has been observed after beta-blockade, but improvement in survival has not been established in a large-scale randomized trial. This was the main objective of the Cardiac Insufficiency Bisoprolol Study (CIBIS). METHODS AND RESULTS: Six hundred forty-one patients with chronic heart failure of various etiologies and a left ventricular ejection fraction of < 40% entered this placebo-controlled, randomized, double-blind study. Patients were in New York Heart Association functional class III (95%) or IV (5%) at inclusion. All received background diuretic and vasodilator therapy (an angiotensin-converting enzyme inhibitor in 90% of cases). A total of 320 patients was randomized to bisoprolol and 321 to placebo. Mean follow-up was 1.9 years. Bisoprolol was well tolerated without between group difference in premature treatment withdrawals (82 on placebo, 75 on bisoprolol; NS). The observed difference in mortality between groups did not reach statistical significance: 67 patients died on placebo, 53 on bisoprolol (P = .22; relative risk, 0.80; 95% confidence interval, 0.56 to 1.15). No significant difference was observed in sudden death rate (17 on placebo, 15 on bisoprolol) or death related to documented ventricular tachycardia or fibrillation (7 on placebo, 4 on bisoprolol). Bisoprolol significantly improved the functional status of the patients; fewer patients in the bisoprolol group required hospitalization for cardiac decompensation (90 on placebo versus 61 on bisoprolol, P < .01), and more patients improved by at least one New York Heart Association functional class (48 on placebo versus 68 on bisoprolol, P = .04) by the end of follow-up period. CONCLUSIONS: These results confirm previous trials evidence that a progressively increasing dose of beta-blocker in severe heart failure confers functional benefit. Subgroup analysis suggested that benefit from beta-blockade therapy was greater for those with nonischemic cardiomyopathy. However, improvement in survival while on beta-blockade remains to be demonstrated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_etiology_MeSH Cardiac_Output__Low_etiology_MeSH S_mortality_MeSH Cardiac_Output__Low_mortality_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH M_Survival_Analysis_MeSH 
****** 7926346
----K E
----T Captopril and atenolol are equally effective in retarding progression of diabetic nephropathy. Results of a 2-year prospective, randomized study.
----A The progression of diabetic nephropathy can be positively influenced by maintaining a low blood pressure level. This has been shown in studies with conventional antihypertensive treatment as well as with ACE inhibitors. Whether the latter group of drugs is more effective remains to be proven and was the aim of our study. In a prospective randomized study we compared the effects of ACE inhibition and beta-blockade on retarding progression of renal function in IDDM patients with an early stage of overt diabetic nephropathy. Twenty-nine patients were studied for 2 years, 15 were randomized for treatment with captopril and 14 for atenolol. Every 6 weeks blood pressure and urinary albumin and total protein excretion were measured. GFR was measured every 6 months as 51Cr-EDTA clearance. Baseline values for blood pressure, renal function and albuminuria were identical in the two groups. The effect of both drugs on blood pressure was not significantly different. In the captopril-treated patients MAP before and after 2 years was 110 +/- 3 (SEM) and 100 +/- 2 mm Hg, respectively and in the atenolol-treated patients 105 +/- 2 vs 101 +/- 2 mm Hg. Both drugs reduced albuminuria and total proteinuria to the same extent. With captopril albuminuria decreased from 1549 (989-2399) to 851 (537-1380) mg/24 h and proteinuria from 2.5 (1.6-3.8) to 1.2 (0.8-1.8) g/24 h. With atenolol albuminuria decreased from 933 (603-1445) to 676 (437-1047) mg/24 h and proteinuria from 1.5 (1.0-2.4) to 0.9 (0.6-1.5) g/24 h.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Albuminuria_MeSH S_urine_MeSH Albuminuria_urine_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_I_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_I_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_I_physiopathology_MeSH S_urine_MeSH Diabetes_Mellitus__Type_I_urine_MeSH M_Diabetic_Nephropathies_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Nephropathies_physiopathology_MeSH S_urine_MeSH Diabetic_Nephropathies_urine_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_urine_MeSH Proteinuria_urine_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 7929868
----K I
----T Effects of 100 mg of controlled-release metoprolol and 100 mg of atenolol on blood pressure, central nervous system-related symptoms, and general well being.
----A Central nervous system (CNS)-related symptoms and quality of life during treatment with controlled-release (CR) metoprolol and a standard formulation of atenolol were compared in a double-blind crossover study in 60 patients with mild to moderate hypertension. After a 4-week placebo run-in period, each beta 1-adrenoceptor blocker was administered at a dosage of 100 mg once daily for 6 weeks. Quality of life was assessed regularly during the active treatment phases by use of two standardized self-administered questionnaires, the minor symptom evaluation (MSE) profile, and the psychologic general well-being (PGWB) index. Both questionnaires have previously been shown to be effective in detecting CNS symptoms and changes in well being produced by beta-blockers. Blood pressure and heart rate were monitored to assess the antihypertensive efficacy of the two drugs. Metoprolol CR and atenolol produced equivalent, clinically effective reductions in systolic and diastolic blood pressures measured 24 hours after administration. The drugs were found to exert similar effects on general well being, as assessed by the PGWB index, and there were no significant differences between the two treatments with regard to the three dimensions of the MSE profile, contentment, vitality, and sleep. Thus, at equivalent antihypertensive dosages, metoprolol CR and atenolol are clinically comparable with regard to the degree of CNS-related symptoms produced and effects on general well being. Because these agents differ markedly in lipophilicity, other factors, such as beta 1-selectivity/nonselectivity, may be more important determinants of whether these subjective symptoms occur during therapy with beta-blockers.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Central_Nervous_System_MeSH S_drug_effects_MeSH Central_Nervous_System_drug_effects_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7930255
----K E
----T Effect of metoprolol on myocardial function and energetics in patients with nonischemic dilated cardiomyopathy: a randomized, double-blind, placebo-controlled study.
----A OBJECTIVES. This study examined the effects of metoprolol on left ventricular performance, efficiency, neurohormonal activation and myocardial respiratory quotient in patients with dilated cardiomyopathy. BACKGROUND. The mechanism by which beta-adrenergic blockade improves ejection fraction in patients with dilated cardiomyopathy remains an enigma. Thus, we undertook an extensive hemodynamic evaluation of this mechanism. In addition, because animal models have shown that catecholamine exposure may increase relative fatty acid utilization, we hypothesized that antagonism of sympathetic stimulation may result in increased carbohydrate utilization. METHODS. This was a randomized, double-blind, prospective trial in which 24 men with nonischemic dilated cardiomyopathy underwent cardiac catheterization before and after 3 months of therapy with metoprolol (n = 15) or placebo (n = 9) in addition to standard therapy. Pressure-volume relations were examined using a micromanometer catheter and digital ventriculography. RESULTS. At baseline, the placebo-treated patients had somewhat more advanced left ventricular dysfunction. Ejection fraction and left ventricular performance improved only in the metoprolol-treated patients. Stroke and minute work increased without an increase in myocardial oxygen consumption, suggesting increased myocardial efficiency. Further increases in ejection fraction were seen between 3 and 6 months in the metoprolol group. The placebo group had a significant increase in ejection fraction only after crossover to metoprolol. A significant relation between the change in coronary sinus norepinephrine and myocardial respiratory quotient was seen, suggesting a possible effect of adrenergic deactivation on substrate utilization. CONCLUSIONS. These data demonstrate that in patients with cardiomyopathy, metoprolol treatment improves myocardial performance and energetics, and favorably alters substrate utilization. Beta-adrenergic blocking agents, such as metoprolol, are hemodynamically and energetically beneficial in the treatment of myocardial failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Cardiomyopathy__Congestive_radionuclide_imaging_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Energy_Metabolism_MeSH S_drug_effects_MeSH Energy_Metabolism_drug_effects_MeSH M_Follow-Up_Studies_MeSH M_Heart_Catheterization_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Norepinephrine_MeSH S_metabolism_MeSH Norepinephrine_metabolism_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7942414
----K I
----T The management of atrial fibrillation: current perspectives.
----A The management of atrial fibrillation is evolving in response to recently published data. Low-risk patients with new-onset atrial fibrillation may not need to be hospitalized. Beta blockers may be the most effective drugs for controlling the heart rate. When a patient does not respond to drug therapy, it is still appropriate to search for the cause of the arrhythmia and to use direct-current cardioversion. Clear evidence now exists that patients with chronic atrial fibrillation should be given anticoagulant drugs to reduce the risk of stroke. Antiarrhythmic drugs should be used cautiously, because they may cause life-threatening arrhythmias.
----P Journal_Article Review Review__Tutorial 
----M M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Decision_Trees_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7944835
----K I
----T Impact of the treatment of isolated systolic hypertension on behavioral variables. Results from the systolic hypertension in the elderly program.
----A BACKGROUND: Little information has been published on the impact of antihypertensive medications on quality of life in older persons. Particular concern has existed that lowering systolic blood pressure in older persons might have adverse consequences on cognition, mood, or leisure activities. METHODS: A multicenter double-blind randomized controlled trial was conducted over an average of 5 years' followup involving 16 academic clinical trial clinics. Participants consisted of 4736 persons (1.06%) selected from 447,921 screenees aged 60 years and older. Systolic blood pressure at baseline ranged from 160 to 219 mm Hg, while diastolic blood pressure was less than 90 mm Hg. Participants were randomized to active antihypertensive drug therapy or matching placebo. Active treatment consisted of 12.5 to 25 mg of chlorthalidone for step 1, while step 2 consisted of 25 to 50 mg of atenolol. If atenolol was contraindicated, 0.05 to 0.10 mg of reserpine could be used for the second-step drug. The impact of drug treatment on measures of cognitive, emotional, and physical function and leisure activities was assessed. RESULTS: Our analyses demonstrate that active treatment of isolated systolic hypertension in the Systolic Hypertension in the Elderly Program cohort had no measured negative effects and, for some measures, a slight positive effect on cognitive, physical, and leisure function. The positive findings in favor of the treatment group were small. There was no effect on measures related to emotional state. Measures of cognitive and emotional function were stable in both groups for the duration of the study. Both treatment groups showed a modest trend toward deterioration of some measures of physical and leisure function over the study period. CONCLUSIONS: The overall study cohort exhibited decline over time in activities of daily living, particularly the more strenuous ones, and some decline in certain leisure activities. However, mood, cognitive function, basic self-care, and moderate leisure activity were remarkably stable for both the active and the placebo groups throughout the entire study. Results of this study support the inference that medical treatment of isolated systolic hypertension does not cause deterioration in measures of cognition, emotional state, physical function, or leisure activities.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Activities_of_Daily_Living_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Cerebrovascular_Disorders_MeSH S_epidemiology_MeSH Cerebrovascular_Disorders_epidemiology_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH M_Chlorthalidone_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH M_Cognition_Disorders_MeSH S_chemically_induced_MeSH Cognition_Disorders_chemically_induced_MeSH S_epidemiology_MeSH Cognition_Disorders_epidemiology_MeSH M_Depressive_Disorder_MeSH S_chemically_induced_MeSH Depressive_Disorder_chemically_induced_MeSH S_epidemiology_MeSH Depressive_Disorder_epidemiology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH P_Leisure_Activities_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Reserpine_MeSH S_adverse_effects_MeSH Reserpine_adverse_effects_MeSH M_Self_Care_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH 
****** 7950564
----K E
----T Postural hypotension in elderly patients given carvedilol.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypotension__Orthostatic_MeSH S_chemically_induced_MeSH Hypotension__Orthostatic_chemically_induced_MeSH M_Male_MeSH M_Posture_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7950612
----K E
----T Randomised controlled trial of enalapril and beta blockers in non-diabetic chronic renal failure.
----A OBJECTIVE--To compare the ability of angiotensin converting enzyme inhibitors and beta blockers to slow the development of end stage renal failure in non-diabetic patients with chronic renal failure. DESIGN--Open randomised multicentre trial with three year follow up. SETTING--Outpatient departments of six French hospitals. PATIENTS--100 hypertensive patients with chronic renal failure (initial serum creatinine 200-400 mumol/l. 52 randomised to enalapril and 48 to beta blockers (conventional treatment). INTERVENTIONS--Enalapril or beta blocker was combined with frusemide and, if necessary, a calcium blocker or centrally acting drug in patients whose diastolic pressure remained above 90 mm Hg. RESULTS--17 patients receiving conventional treatment and 10 receiving enalapril developed end stage renal failure. The cumulative renal survival rate was significantly better in the enalapril group than in the conventional group (P < 0.05). The slope of the reciprocal serum creatinine concentration was steeper in the conventionally treated patients (-6.89 x 10(-5)l/mumol/month) than in the enalapril group (-4.17 x 10(-5)l/mumol/month; P < 0.05). No difference in blood pressure was found between groups. CONCLUSION--In hypertensive patients with chronic renal failure enalapril slows progression towards end stage renal failure compared with beta blockers. This effect was probably not mediated through controlling blood pressure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_adverse_effects_MeSH Acebutolol_adverse_effects_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Body_Weight_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Kidney_Failure__Chronic_MeSH S_drug_therapy_MeSH Kidney_Failure__Chronic_drug_therapy_MeSH S_mortality_MeSH Kidney_Failure__Chronic_mortality_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7957538
----K E
----T Metabolic effects of long-term angiotensin-converting enzyme inhibition with fosinopril in patients with essential hypertension: relationship to angiotensin-converting enzyme inhibition.
----A Fifty patients with mild to moderate essential hypertension were randomized to receive either 20 mg fosinopril daily for 16 weeks or placebo for 4 weeks followed by 12 weeks of 50 mg atenolol daily. Prior to these 16 weeks there was a placebo wash-out period of 2-6 weeks. Blood pressure measurements, euglycaemic, hyperinsulinaemic glucose clamps, and intravenous glucose tolerance tests (IVGTT) were performed at baseline and after 4 and 16 weeks. Blood lipid status was evaluated at baseline and 16 weeks. The insulin sensitivity index (M/I) increased by 12% during the prolonged placebo period, and subsequently decreased by 12% during treatment with atenolol in that group. A post-hoc analysis of covariance indicated that the increase in insulin sensitivity during the initial 4 weeks may have been due to carry-over effects from previous antihypertensive treatment. Fosinopril increased glucose disappearance during IVGTT at 4 and 16 weeks (k values 1.46 and 1.33 vs 1.10 at baseline) but had no effect on insulin sensitivity. The change in insulin sensitivity and serum triglycerides during treatment with fosinopril was related to angiotensin-converting enzyme inhibition in serum. In conclusion, carry-over effects from previous antihypertensive medication were indicated in this study, probably because of an insufficient wash-out period in many patients. Therefore, 4 weeks of placebo wash-out in all patients is advisable in this kind of investigation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Fosinopril_MeSH S_adverse_effects_MeSH Fosinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Glucose_Tolerance_Test_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH M_Insulin_Resistance_MeSH S_physiology_MeSH Insulin_Resistance_physiology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7963104
----K E
----T Comparison of front-loaded recombinant tissue-type plasminogen activator, anistreplase and combination thrombolytic therapy for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 4 trial.
----A OBJECTIVES. The aim of our study was to determine a superior thrombolytic regimen from three: anistreplase (APSAC), front-loaded recombinant tissue-type plasminogen activator (rt-PA) or combination thrombolytic therapy. BACKGROUND. Although thrombolytic therapy has been shown to reduce mortality and morbidity after acute myocardial infarction, it has not been clear whether more aggressive thrombolytic-antithrombotic regimens could improve the outcome achieved with standard regimens. METHODS. To address this issue, 382 patients with acute myocardial infarction were randomized to receive in a double-blind fashion (along with intravenous heparin and aspirin) APSAC, front-loaded rt-PA or a combination of both agents. The primary end point "unsatisfactory outcome" was a composite clinical end point assessed through hospital discharge. RESULTS. Patency of the infarct-related artery (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow) at 60 min after the start of thrombolysis was significantly higher in rt-PA-treated patients (77.8% vs. 59.5% for APSAC-treated patients and 59.3% for combination-treated patients [rt-PA vs. APSAC, p = 0.02; rt-PA vs. combination, p = 0.03]). At 90 min, the incidence of both infarct-related artery patency and TIMI grade 3 flow was significantly higher in rt-PA-treated patients (60.2% had TIMI grade 3 flow vs. 42.9% and 44.8% of APSAC- and combination-treated patients, respectively [rt-PA vs. APSAC, p < 0.01; rt-PA vs. combination, p = 0.02]). The incidence of unsatisfactory outcome was 41.3% for rt-PA compared with 49% for APSAC and 53.6% for the combination (rt-PA vs. APSAC, p = 0.19; rt-PA vs. combination, p = 0.06). The mortality rate at 6 weeks was lowest in the rt-PA-treated patients (2.2% vs. 8.8% for APSAC and 7.2% for combination thrombolytic therapy [rt-PA vs. APSAC, p = 0.02; rt-PA vs. combination, p = 0.06]). CONCLUSIONS. Front-loaded rt-PA achieved significantly higher rates of early reperfusion and was associated with trends toward better overall clinical benefit and survival than those achieved with a standard thrombolytic agent or combination thrombolytic therapy. These findings support the concept that more rapid reperfusion of the infarct-related artery is associated with improved clinical outcome.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Anistreplase_MeSH S_adverse_effects_MeSH Anistreplase_adverse_effects_MeSH S_therapeutic_use_MeSH Anistreplase_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Vascular_Patency_MeSH 
****** 7963199
----K E
----T Age, race, and gender variation in the utilization of coronary artery bypass surgery and angioplasty in SHEP. SHEP Cooperative Research Group. Systolic Hypertension in the Elderly Program.
----A OBJECTIVE: To assess variability in the use of coronary artery bypass grafting (CABG) and percutaneous transluminal angioplasty (PTCA) in the Systolic Hypertension in the Elderly Program (SHEP) cohort with incident coronary heart disease (CHD) by age, sex, and race. DESIGN: Retrospective analysis of a multicenter prospective cohort study. SETTING: Community-based ambulatory population in academic centers. PATIENTS: Among 4736 subjects initially enrolled in SHEP, there were 432 incident cases of CHD, excluding those patients who experienced rapid or sudden cardiac death. MAIN OUTCOME MEASURE: Incident cases of CHD who underwent CABG or PTCA. RESULTS: Of those participants > or = 60 and < 75 years of age, 7.3% underwent PTCA, compared with 3.9% of those > or = 75 years (P = 0.14). 15.4% of those < 75 underwent CABG surgery, compared with 7.8% of those 75 and older (P = 0.018). When both of these endpoints, CABG and PTCA, were combined, 22.4% of those < 75 underwent a procedure, while only 11.7% of the older cohort did (P = 0.005). Twenty-six percent of men underwent either CABG or PTCA, while only 9.1% of women did (P < 0.001). Of those < 75 years of age, 31.1% of men and 12.3% of women underwent CABG or PTCA (P < 0.001). In the 75 and older age category, 19.5% of men underwent these interventions, compared with 5.9% of women (P = 0.005). Active treatment group was significantly associated with decreased use of procedures in participants < 75 year old with CHD. Race, activity limitations, number of comorbid conditions, education level, marital status, employment status, and social support were not significantly associated with CABG or PTCA use. When the variables studied were entered into a logistic regression model, increased age and female sex remained independently associated with decreased CABG and PTCA use. CONCLUSION: In the SHEP trial older patients and women, regardless of comorbid conditions, socioeconomic status, and social support, underwent less intensive cardiovascular interventions than did younger patients and men when they developed CHD.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_utilization_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_utilization_MeSH M_Comorbidity_MeSH M_Continental_Population_Groups_MeSH M_Coronary_Artery_Bypass_MeSH S_utilization_MeSH Coronary_Artery_Bypass_utilization_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Incidence_MeSH M_Logistic_Models_MeSH M_Male_MeSH P_Patient_Selection_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Prospective_Studies_MeSH M_Retrospective_Studies_MeSH M_Sex_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH 
****** 7963426
----K E
----T Prevention of rebleeding from oesophageal varices: two-year follow up of a prospective controlled trial of propranolol in addition to sclerotherapy.
----A A prospective randomised trial comparing propranolol and sclerotherapy to sclerotherapy alone was conducted over a 2-year follow up in a district hospital setting of unselected patients. Rebleeding and survival were analysed. Thirty-nine patients were randomised to propranolol plus sclerotherapy and 34 to sclerotherapy alone. The two groups were clinically comparable. There was no significant difference in the cumulative percent of patients free of rebleeding; 54% of the sclerotherapy group rebled compared to 52% of the group treated with propranolol plus sclerotherapy (Hazard ratio 1.09 (0.54-2.22) and p = 0.81, NS). Two-year actuarial survival was also not significantly different, with 77% of the propanolol plus sclerotherapy group surviving, compared to 74% of sclerotherapy alone (Hazard ratio 1.08 (0.35-2.22) and p = 0.79, NS). The mean time to eradication of varices was not significantly different between the two groups (propranolol plus sclerotherapy 222 days, sclerotherapy alone 243 days), nor did the rate of variceal recurrence differ (72.7 vs 72 days). This study did not show long-term improvement in rebleeding or survival using propranolol in addition to a regular sclerotherapy programme.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Liver_Cirrhosis__Alcoholic_MeSH S_complications_MeSH Liver_Cirrhosis__Alcoholic_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH M_Survival_Analysis_MeSH M_Survival_Rate_MeSH 
****** 7526065
----K E
----T Felodipine versus placebo in stable effort-induced angina pectoris in patients inadequately controlled with metoprolol--a dose-finding study.
----A We compared the antianginal and antiischemic effect and tolerability of four different doses of felodipine extended-release (ER) tablets with placebo in patients with stable effort-induced angina pectoris treated with beta-blocker [metoprolol controlled release (CR) 100 mg once daily, o.d.]. Seventy-five patients were enrolled in the study. At the end of a 2-week single-blind period, all patients performed two exercise tests. If total exercise time did not vary by > 15% between the two tests and both tests were limited by anginal discomfort and concomitant ST depression of at least 1 mm, the patients were randomized to double-blind treatment (66 patients). Each patient received three of the following treatments: felodipine 2.5, 5, 10, or 20 mg, or placebo. The treatments were given o.d. in a cross-over, balanced incomplete block design with three of 3-week treatment periods. Exercise tests were performed 12 and 24 h after dose intake at the end of each treatment period. Fifty-nine patients completed the study. Twelve hours after dose administration, 10 and 20 mg felodipine increased time to onset of anginal pain by 60 and 63 s on the average, respectively, as compared with placebo (p = 0.001). Time to 1-mm ST depression was prolonged by 29 s after 10 mg (p = 0.14) and by 30 s after 20 mg (p = 0.13) felodipine. Time to end of exercise was increased by 28 s (p = 0.07) and 15 s (p > 0.20), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Delayed-Action_Preparations_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 7973215
----K E
----T Interim analysis: the alpha spending function approach.
----A Interim analysis of accumulating data in a clinical trial is now an established practice for ethical and scientific reasons. Repeatedly testing interim data can inflate false positive error rates if not handled appropriately. Group sequential methods are a commonly used frequentist approach to control this error rate. Motivated by experience of clinical trials, the alpha spending function is one way to implement group sequential boundaries that control the type I error rate while allowing flexibility in how many interim analyses are to be conducted and at what times. In this paper, we review the alpha spending function approach, and detail its applicability to a variety of commonly used statistical procedures, including survival and longitudinal methods.
----P Journal_Article 
----M M_Bias_(Epidemiology)_MeSH M_Clinical_Trials_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH P_Data_Interpretation__Statistical_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Longitudinal_Studies_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Survival_Analysis_MeSH 
****** 7975357
----K 1
----T [The importance of studying the renin-angiotensin-aldosterone system in essential arterial hypertension in clinical practice. Activity of the renin-angiotensin-aldosterone system during treatment of hypertension with ACE-inhibitors and beta blockers]
----A The authors assessed in 20 subjects with mild or medium severe arterial hypertension basal and stimulated values of plasma renin activity (PRA) and aldosterone before onset of treatment and after 6-week therapy with enalapril (ENAP KRKA) or metoprolol (Vasocardin Slovakofarma). PRA and aldosterone secretion was stimulated by a vertical position and by administration of 40 mg furosemide by the i.v. This test proved suitable for assessment of secondary arterial hypertension in different forms of primary hyperaldosteronism and for expressing suspicion of renovascular hypertension and hypertension with affection of the renal arteries resp. Based on PRA levels, arterial hypertension can be divided into normorenin, high-renin and low-renin hypertension. This classification is, however, of no value for selection of treatment and the prognosis of hypertension. Each level of PRA can be associated with three different aldosterone levels. PRA and aldosterone did not correlate with urinary K, Na excretion nor with blood pressure. During treatment with ACE inhibitor PRA rose while basal as well as stimulated aldosterone levels declined. After administration of betablockers basal as well as stimulated PRA and aldosterone levels declined.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Cross-Over_Studies_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH P_Renin-Angiotensin_System_MeSH 
****** 7976233
----K I
----T Tolfenamic acid versus propranolol in the prophylactic treatment of migraine.
----A The prophylactic effect of tolfenamic acid and propranolol was studied in a randomized double-blind cross-over trial of 76 patients with migraine with or without aura. After a 4-week run-in period patients were randomly allocated to treatment with either tolfenamic acid 100 mg three times daily or propranolol 40 mg three times daily for 12 weeks. After a placebo wash-out period of 4 weeks the patients got the alternative drug for 12 weeks; 56 patients completed the study. Both drugs significantly reduced migraine attacks as judged from the reduction in the efficacy parameters (migraine hours, migraine days, and migraine intensity) in the treatment periods compared with the run-in period. No statistical significant difference in any efficacy parameter was found between the two drugs (level 2 alpha = 0.05, alpha = 0.10). The adverse effects showed no statistical difference in frequency between the 2 treatments. Twenty patients discontinued the study: 12 patients on propranolol and 8 patients on tolfenamic acid. Side effects were the cause of premature discontinuation of study medicine in 9 patients during propranolol treatment (dizziness, fatigue, and fall in blood pressure) and in 5 patients during tolfenamic acid treatment (gastrointestinal symptoms).
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anthranilic_Acids_MeSH S_adverse_effects_MeSH Anthranilic_Acids_adverse_effects_MeSH S_therapeutic_use_MeSH Anthranilic_Acids_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Severity_of_Illness_Index_MeSH 
****** 7977065
----K E
----T Efficacy of metoprolol and diltiazem in treating silent myocardial ischemia.
----A Recent studies strongly support the prognostic importance of transient silent ischemia. Because patients with silent ischemia are at higher risk of a cardiac event, they are likely to benefit not only from control of symptoms, but also from treatment directed at prevention of ischemia. The efficacy of controlled-release metoprolol 200 mg once daily and diltiazem 60 mg 4 times daily was assessed in a randomized, double-blind, crossover study in 32 patients with proven coronary artery disease, predominantly asymptomatic myocardial ischemia, positive bicycle exercise test results, and > or = 5 minutes of asymptomatic ST-segment depression on a 24-hour screening ambulatory electrocardiogram (ECG). At the beginning and at the end of both 3-week treatment periods, an exercise test was performed and a 72-hour ambulatory ECG was recorded. Both active treatment periods were preceded by a 2-week placebo phase. Both treatments effectively reduced and postponed exercise-induced ST depression and reduced the total ischemic integral on the ambulatory ECG. Only metoprolol significantly reduced the mean number of ischemic episodes (54%, p = 0.0003, vs 31% for diltiazem, p = NS) and the mean duration of ischemia (51%, p = 0.012, vs 27% for diltiazem, p = NS) compared with baseline values. Metoprolol strongly blunted the morning and afternoon peak in the circadian distribution of ischemia, whereas diltiazem did not change the circadian distribution of ischemia at all.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_classification_MeSH Angina_Pectoris_classification_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 7977090
----K I
----T Comparison between felodipine and isosorbide mononitrate as adjunct to beta blockade in patients > 65 years of age with angina pectoris.
----A Coronary artery disease is an increasingly common medical problem in the elderly, and relatively few studies investigating drug therapy focus on this population. To assess the efficacy and safety of the calcium channel blocker, felodipine, and isosorbide mononitrate (ISMN), as adjunct to optimal beta-blocker therapy in elderly patients, a placebo-controlled, double-blind study was conducted in 46 patients, aged between 65 and 80 years, with documented stress-induced angina pectoris and myocardial ischemia. With use of a latin-square design, with 3 periods of 4 weeks each, exercise testing was performed after each period. Felodipine, 5 mg once daily, significantly improved both time to ischemic threshold and pain threshold (p = 0.02 and p = 0.003, respectively, vs placebo), and tended to increase total exercise time (p = 0.06 vs placebo). In contrast, ISMN, 20 mg twice daily, did not significantly affect these parameters. Comparison of the 2 active treatment arms showed that, overall, felodipine was more effective than ISMN, with a statistically significant difference for time to ischemic threshold (p = 0.02). With regard to safety, felodipine was also better tolerated than ISMN, which led to more patients discontinuing study medication with ISMN (p < 0.05 between ISMN and felodipine). It is concluded that in elderly patients who are treated with optimal beta blockade, felodipine, but not ISMN, leads to an additional significant reduction in ischemic parameters during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 7979639
----K I
----T Propranolol reduces mortality in patients with portal hypertension secondary to schistosomiasis.
----A Although beta-adrenoceptor antagonists improve morbidity and mortality in patients with portal hypertension associated with cirrhosis, this has not been demonstrated in non-cirrhotic patients. In the present, double-blind, 24-month, prospective study of patients with endoscopically-proven varices and ultrasonographically-confirmed hepatic fibrosis, the effects of propranolol 160 mg LA and placebo on the incidence of rebleeding and mortality were compared in 82 patients with portal hypertension secondary to schistosomiasis. The results, analysed on intention-to-treat basis, indicated a reduction in rebleeding (median time to rebleeding 589 days for propanol v. 252 days for placebo; P < 0.02) and increased survival in the propranolol-treated patients (three deaths v. seven deaths on placebo; P < 0.02). Fifteen patients withdrew from the propranolol group and 18 from the placebo group. A positive prognostic indicator was a large portal vein diameter whereas a small liver size indicated a negative outcome.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH S_mortality_MeSH Hypertension__Portal_mortality_MeSH M_Liver_MeSH S_pathology_MeSH Liver_pathology_MeSH M_Male_MeSH M_Portal_Vein_MeSH S_pathology_MeSH Portal_Vein_pathology_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Schistosomiasis_MeSH S_complications_MeSH Schistosomiasis_complications_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 7982651
----K 5
----T Propranolol plus isosorbide-5-mononitrate for portal hypertension in cirrhosis: long-term hemodynamic and renal effects.
----A The effect on kidney function, vasoactive systems and ascites outcome of long-term treatment with propranolol plus isosorbide-5-mononitrate, a combined therapy proven more effective than propranolol alone in decreasing portal pressure in the cirrhotic patient, is unknown. Thirty cirrhotic patients who survived acute variceal bleeding and were treated with propranolol plus isosorbide-5-mononitrate were studied. Portal and systemic hemodynamics (n = 15), inulin clearance, free water clearance, plasma renin activity, aldosterone concentration and prostaglandin E2 excretion (n = 20) were measured before and after 3 mo of treatment. In addition, data on ascites outcome in the entire series after a mean follow-up of 9.6 mo were compared with those of 30 patients undergoing elective sclerotherapy and with those of 30 patients treated with propranolol alone matched for age, sex, presence of ascites, Child-Pugh class and mean follow-up length included in other randomized controlled trials. Combined therapy significantly decreased the hepatic venous pressure gradient and azygos blood flow. In addition, no changes in inulin clearance, free water clearance, plasma renin activity, aldosterone concentration and prostaglandin E2 excretion occurred, despite a mild decrease in mean arterial pressure. Moreover, no differences among the three groups of patients studied in ascites outcome were found. These results suggest that long-term treatment with propranolol plus isosorbide-5-mononitrate does not impair kidney function, vasoactive systems or ascites outcome in cirrhotic patients.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Analysis_of_Variance_MeSH M_Body_Water_MeSH S_metabolism_MeSH Body_Water_metabolism_MeSH M_Chi-Square_Distribution_MeSH M_Dinoprostone_MeSH S_urine_MeSH Dinoprostone_urine_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Inulin_MeSH S_metabolism_MeSH Inulin_metabolism_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_Pressure_MeSH S_drug_effects_MeSH Portal_Pressure_drug_effects_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 7527328
----K E
----T Lacidipine. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the treatment of hypertension.
----A Lacidipine is an orally administered calcium channel blocker of the dihydropyridine class, which shows selectivity for vascular smooth muscle over cardiac tissue and has a long duration of action. In studies using ambulatory blood pressure monitoring, lacidipine 2 to 8mg administered once daily in the morning reduced blood pressure over 24 hours, with the reductions being greater during the day than at night in some studies. 77 to 87% of patients with mild to moderate hypertension had their blood pressure controlled by treatment with lacidipine 2 to 8 mg/day for 1 to 4 months in dose-finding studies. When administered once daily, lacidipine 4 to 6 mg was equivalent in antihypertensive efficacy to hydrochlorothiazide 25 to 50 mg/day, atenolol 50 to 100 mg/day, and the prototype calcium channel blocker nifedipine 20 to 40 mg twice daily (sustained-release formulation). The adverse effects of lacidipine are those common to other dihydropyridine calcium channel blockers, and include headache, flushing, ankle oedema, dizziness and palpitations. The long term effects of lacidipine on cardiovascular morbidity and mortality, and possible additional clinical benefits in terms of its antiatherosclerotic effects, are under investigation; the outcome of these studies will be important in defining the future role of this agent in the treatment of hypertension. Thus, available evidence suggests lacidipine provides a further alternative to the dihydropyridine calcium channel blockers currently available for the treatment of essential hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Academic 
----M M_Adult_MeSH M_Aging_MeSH S_metabolism_MeSH Aging_metabolism_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Dihydropyridines_MeSH S_pharmacokinetics_MeSH Dihydropyridines_pharmacokinetics_MeSH S_pharmacology_MeSH Dihydropyridines_pharmacology_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Disease_Models__Animal_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Tissue_Distribution_MeSH 
****** 7988629
----K E
----T Conventional and controlled release diltiazem. Bioavailability in healthy volunteers and anti-anginal effects in combination with metoprolol in stable angina pectoris.
----A Diltiazem CR tablets 120 mg b.i.d. for 1 week were compared with plain tablets 60 mg q.i.d. in 13 healthy male volunteers in a study of pharmacokinetic variables. Their antianginal efficacy was also compared in 23 patients with stable angina pectoris who were already on metoprolol. Both studies were of randomised, cross over design, and the clinical study was double blind. The pharmacokinetic variables of the two formulations were very similar except for the longer tmax of 4.4 h for diltiazem CR in comparison to 2.9 h for the plain tablets. The mean relative bioavailability of diltiazem CR in comparison with plain tablets was 1.14. The clinical study showed that after four weeks on diltiazem CR 120 mg b.i.d. or diltiazem plain tablets 60 mg q.i.d. in addition to metoprolol, there were significant decreases in weekly anginal attacks from 11 to 5 attacks/week, the number of nitroglycerin tablets consumed from 6 to 3 tablets/week, and an increase in the maximum workload from 116 to 126 and 123 W for diltiazem CR and plain diltiazem tablets, respectively, as compared to placebo. Five of the patients were angina free during diltiazem treatment. No difference in anti-anginal efficacy between the two preparations was seen. It was concluded that CR 120 mg b.i.d. appears bioequivalent to plain diltiazem tablets 60 mg q.i.d.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Biological_Availability_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Delayed-Action_Preparations_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Diltiazem_pharmacokinetics_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 7990246
----K I
----T Hypertension in the elderly. Implications and generalizability of randomized trials.
----A OBJECTIVE--To estimate morbidity and mortality benefits of drug therapy for hypertensive elderly subjects, compare these benefits with effects in younger subjects, and provide a framework for generalizing results derived from trials to actual patients. DATA SOURCES--A literature search using MEDLINE from 1966 to 1993, references from reviews and trial articles, and experts. STUDY SELECTION--Randomized trials lasting at least 1 year that evaluated effects of drug treatment on morbidity and mortality outcomes in hypertensive persons. DATA EXTRACTION--Four independent reviewers appraised protocol characteristics and quality of selected trials. DATA SYNTHESIS--There were 13 trials involving 16,564 elderly persons (age 60 years and older). The prevalence of cardiovascular risk factors, cardiovascular disease, and competing comorbid diseases was lower among trial participants than the general population of hypertensive elderly persons. When the six large high-quality trials were combined, trial results showed 43 subjects (95% confidence interval [CI], 31 to 69) and 61 subjects (95% CI, 39 to 141) needed to be treated for 5 years to prevent one cerebrovascular event and one coronary heart disease event, respectively. Including the other seven trials did not change the results significantly. Only 18 subjects (95% CI, 14 to 25) needed to be treated to prevent one cardiovascular event (cerebrovascular or cardiac). Twelve trials in primarily younger and middle-aged adults involved approximately 33,000 persons. For all outcomes except cardiac mortality, two to four times as many of the younger subjects as the older subjects needed to be treated for 5 years to prevent morbid and mortal events. No significant effect on cardiac mortality was seen among younger subjects, while 78 older subjects (95% CI, 50 to 180) needed to be treated to prevent a fatal cardiac event. CONCLUSIONS--Randomized trials demonstrate that treating healthy older persons with hypertension is highly efficacious. Five-year morbidity and mortality benefits derived from trials are greater for older than younger subjects. Extrapolating benefits from trials to individual patients is difficult, but should take into account multiple issues including the patient's risk factors, preexisting cardiovascular disease, and competing comorbid illnesses.
----P Journal_Article Review Review_Literature 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Middle_Aged_MeSH M_Models__Statistical_MeSH M_Morbidity_MeSH P_Randomized_Controlled_Trials_MeSH M_Survival_Analysis_MeSH 
****** 7994448
----K E
----T Hemodynamic and humoral effects of low-dose aspirin in treated and untreated essential hypertensive patients.
----A Aspirin at low doses is used as an inhibitor of platelet aggregation and is frequently administered to essential hypertensive patients with arterial thrombotic complications. However, it is unknown whether aspirin can modify blood pressure values either in treated or untreated hypertensive patients, as described for other non steroidal anti-inflammatory drugs. Thus 30 patients. 10 with mild uncomplicated and untreated essential hypertension, 10 with essential hypertension under chronic treatment with captopril, 50 mg bid, and 10 with essential hypertension under chronic treatment with atenolol, 100 mg oid, received aspirin, 100 mg oid, and the corresponding placebo for one month, according to a double blind randomized cross-over design. At the end of each treatment, blood pressure, heart rate, generated serum thromboxane B2 and urinary excretion of thromboxane B2 and 6 keto prostaglandin F1 alpha and plasma renin activity were measured. Both in treated and untreated essential hypertensive patients, aspirin administration did not affect blood pressure, heart rate and urinary 6 keto prostaglandin F1 alpha, while it significantly reduced serum and urinary excretion of thromboxane B2 and plasma renin activity. In conclusion, while the present data confirm that low doses of aspirin selectively inhibit thromboxane B2 synthesis, they indicate that aspirin at 100 mg oid can be administered to treated and untreated essential hypertensive patients without any harmful effect on blood pressure values.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Aspirin_MeSH S_pharmacology_MeSH Aspirin_pharmacology_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Thromboxane_B2_MeSH S_metabolism_MeSH Thromboxane_B2_metabolism_MeSH 
****** 7528129
----K E
----T Choosing the right beta-blocker. A guide to selection.
----A beta-Blockers have been in clinical use for 30 years, and have an accepted role in (among others) the treatment of high blood pressure, the secondary prevention of myocardial infarction and the treatment of arrhythmias. Their place in the treatment of heart failure is currently under investigation. The drugs available in the 1970s and early 1980s were subjected to intense investigation. A new generation of beta-blockers, including some such as carvedilol and bucindolol, with vasodilating properties, is now appearing. As yet these later agents have not been the subject of large clinical trials. Clinical practice involves the treatment of individual patients with defined dosages of particular drugs. It is, therefore, not acceptable to base practice on theories derived from the clinical pharmacology of a particular drug, on the results of small trials or on a meta-analysis of results from a number of trials that were individually inadequate. Clinical practice must follow the results of large-scale trials in defined populations. The major trials in hypertension, myocardial infarction, arrhythmias and heart failure provide the best evidence for the use of individual beta-blockers in each of these clinical situations. In patients with high blood pressure, beta-blockers do not seem to have any particular advantage over other hypotensive agents. In myocardial infarction, relatively late use of a beta-blocker undoubtedly reduces fatality, though the value of early treatment is less clear. beta-Blockers are not powerful antiarrhythmics, but they do appear to prevent sudden death. Their possible role in heart failure is perhaps the most interesting current field of beta-blocker research. There are very few comparative studies of beta-blockers, and it is difficult to make precise recommendations. None of the new generation of beta-blockers has yet been used in a trial that is large enough trial for any of them to be accepted for routine use in preference to older drugs. The use of individual beta-blockers, as with any drug, should follow the results of clinical trials. Propranolol and atenolol have been studied most intensely in hypertension. For secondary prevention of myocardial infarction, the evidence is best for timolol. Sotalol is probably the best antiarrhythmic among the beta-blockers. Whether any individual beta-blocker is best for heart failure remains to be seen.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Receptors__Adrenergic_MeSH S_drug_effects_MeSH Receptors__Adrenergic_drug_effects_MeSH 
****** 7814158
----K I
----T Effects of the administration of captopril, metoprolol and of the captopril-metoprolol combination as adjuvant therapy during thrombolysis in acute myocardial infarction.
----A The aim of the study was to verify, during thrombolysis in patients with anterior acute myocardial infarction, the safety and effects of beta-blockers or ACE-inhibitors and their combination in the short and long term. One-hundred sixty-six patients hospitalized within 4 h from the onset of the symptoms (first episode), eligible for thrombolysis, Killip class I-II, were randomized (single blind) into four groups. Group A (42 patients) received 6.25 mg captopril (orally) 15 min before thrombolysis and metoprolol (i.v.) not later than 1 h, and orally afterwards. Group B (42 patients) received 6.25 mg captopril 15 min before thrombolysis. Group C (37 patients) received metoprolol not later than 1 h. Group D (45 patients) received thrombolysis only. Later (day 3), groups C and D also received captopril. We checked ventricular arrhythmias (first 2h) from thrombolysis, creatine kinase peak, creatine kinase peak normalization time, late ventricular arrhythmias at Holter test pre-discharge (Lown's class > 2). At follow-up (mean 30.5 +/- 2 months), mortality was evaluated for reinfarction and ventricular failure. Age and sex were similar. Results: Early ventricular arrhythmias: Group A, five cases; Group B, five cases; Group C, 15 cases; Group D, 16 cases. Creatine kinase peak: Group A, 1875 +/- 220 U/l; Group B, 1566 +/- 168 U/l; Group C, 2274 +/- 212 U/l; Group D 2103 +/- 232 U/l. Creatine kinase peak normalization time: Group A, 57.7 +/- 3 h; Group B, 58.1 +/- 3 h; Group C, 72.7 +/- 3 h; Group D, 69.5 +/- 2 h (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH M_Comparative_Study_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH S_drug_effects_MeSH Creatine_Kinase_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Stroke_Volume_MeSH M_Survival_Rate_MeSH M_Tachycardia__Ventricular_MeSH S_epidemiology_MeSH Tachycardia__Ventricular_epidemiology_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Thrombolytic_Therapy_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH M_Time_Factors_MeSH 
****** 7824411
----K E
----T The management of pregnancy in hypertensive patients.
----A 
----P Journal_Article Review Review__Academic 
----M M_Abnormalities_MeSH S_etiology_MeSH Abnormalities_etiology_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_therapy_MeSH Hypertension__Renal_therapy_MeSH M_Maternal_Age_MeSH M_Pre-Eclampsia_MeSH S_prevention_&_control_MeSH Pre-Eclampsia_prevention_&_control_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH M_Pregnancy_in_Diabetics_MeSH M_Prenatal_Care_MeSH M_Proteinuria_MeSH S_diagnosis_MeSH Proteinuria_diagnosis_MeSH 
****** 7826557
----K E
----T Lack of effectiveness of a low-sodium/high-potassium diet in reducing antihypertensive medication requirements in overweight persons with mild hypertension. TAIM Research Group. Trial of Antihypertensive Interventions and Management.
----A The Trial of Antihypertensive Interventions and Management (TAIM) was a multicenter randomized drug (double-blind, placebo-controlled)-diet trial. One objective of TAIM was to assess the long-term ability of a low-sodium/high-potassium (Na+ decreases/K+ increases) diet to maintain blood pressure control in persons at 110% to 160% ideal weight with diastolic blood pressure from 90 to 100 mm Hg who were on no drugs or on low-dose monotherapy. Participants, 56% men and 33% black, were randomized to usual diet (n = 296) or to Na+ decreases/K+ increases diet (n = 291) and within each diet group to placebo, 25 mg/day chlorthalidone, or 50 mg/day atenolol. Treatment failure was defined as lack of blood pressure control requiring additional drugs according to specified criteria. At baseline, the mean value for age was 48 years; blood pressure, 143/93 mm Hg; weight, 88 kg; and 24-h urinary sodium and potassium excretion rates, 133 and 57 mmol/day, respectively. At 3 years, the net difference in 24-h urinary sodium/potassium excretion rates between the Na+ decreases/K+ increases and the usual diet groups was -30 and +11 mmol/L/day. The relative risk of treatment failure for Na+ decreases/K+ increases compared to usual diet by proportional hazards regression was 0.95 (P = .71). This study provides no support for the sole use of a low-sodium/high-potassium diet as a practical therapeutic strategy in maintaining blood pressure control in the moderately obese.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH P_Diet__Sodium-Restricted_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diet_therapy_MeSH Hypertension_diet_therapy_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Potassium_MeSH S_urine_MeSH Potassium_urine_MeSH P_Potassium__Dietary_MeSH M_Proportional_Hazards_Models_MeSH M_Sodium_MeSH S_urine_MeSH Sodium_urine_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 7830324
----K E
----T Effect of two different therapeutic approaches on total and cardiovascular mortality in a Cardiovascular Study in the Elderly (CASTEL).
----A Although limited numbers of elderly subjects have occasionally been included in population-based studies, only a few studies have been conducted specifically on elderly hypertensives, and practically none at a population level. We studied 655 hypertensive subjects from a cohort of 2,254 elderly subjects. The intervention consisted of the creation of a Hypertension Outpatients' Clinic under our auspices but with complete co-operation from general practitioners, randomizing the identified hypertensive patients into pre-established therapeutic drug regimens, and early follow-up recording of mortality for 7 years. The drugs used were clonidine (n = 61), nifedipine (n = 146) and the fixed combination of atenolol+chlorthalidone (n = 144); 304 subjects underwent "free therapy" by their personal physicians without any special intervention. There were 1,404 normotensive subjects. Overall 7-year follow-up mortality was 34.9% in the hypertensive subjects receiving "free therapy", 22.5% in those receiving "special care", and 24.2% in the normotensives. Cardiovascular mortality was respectively 23.7%, 12.2%, and 12.0%. Overall and cardiovascular annual cumulative mortality were significantly lower in the << special therapy >> than in the << free therapy >> group. The fixed combination of atenolol and chlorthalidone reduced mortality below that of the normotensives, independent of other cardiovascular risk factors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH M_Clonidine_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Diseases_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Male_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Survival_Analysis_MeSH 
****** 7835362
----K E
----T Effect of beta-blockade on baroreflex sensitivity and cardiovascular autonomic function tests in patients with coronary artery disease.
----A We wished to assess the effects of beta-blockade on baroreflex sensitivity and standard tests of integrity of autonomic nervous function in patients with coronary artery disease, and to determine whether the effects of lipophilic (metoprolol) and hydrophilic (atenolol) beta-blockers differ. Beta-blocking drugs increase spontaneous heart rate variability in healthy subjects and in patients with coronary heart disease, but little is known about their effects on baroreflex sensitivity and heart-rate based tests of autonomic integrity. In a randomly allocated double-blind crossover study with three 2-week treatment periods, metoprolol CR 200 mg once a day, or atenolol 100 mg once a day, or placebo once a day, were administered to 18 male patients with stable coronary artery disease. Baroreflex sensitivity was determined from the natural baroreflex challenge of Valsalva strain. Heart rate reactions to standard stimuli were measured. No significant differences were found between the effects of atenolol and metoprolol. Beta-blockade did not significantly affect the baroreflex sensitivity, but it diminished the Valsalva ratio significantly (P < 0.001). The difference between maximum and minimum heart rate during hyperventilation was also significantly lower during beta-blockade. The heart rate response to standing up and the ratio of maximum to minimum heart rate during deep breathing were not influenced by beta-blockade. Discontinuation of beta-blockade seems to be unnecessary for reliable determination of baroreflex sensitivity in patients with coronary artery disease, when the natural pressure challenge of Valsalva strain is sued. Both hydrophilic and lipophilic bet-blockers interfere with certain diagnostic tests of autonomic nervous function.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_blood_MeSH Atenolol_blood_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Heart_Function_Tests_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_blood_MeSH Metoprolol_blood_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Valsalva_Maneuver_MeSH S_drug_effects_MeSH Valsalva_Maneuver_drug_effects_MeSH 
****** 7835373
----K I
----T Cardiorespiratory and symptomatic variables during maximal and submaximal exercise in men with stable effort angina: a comparison of atenolol and celiprolol.
----A Celiprolol is a novel beta 1 selective adrenoreceptor blocker with partial beta 2 agonism and direct vasodilator activity. These ancillary properties may reduce symptomatic breathlessness and fatigue and modify respiration during exercise. To test this hypothesis 20 men with stable effort angina were enrolled in a double-blind crossover study to investigate the effects of atenolol 100 mg once daily (A) and celiprolol 400 mg once daily (C) on cardiorespiratory and symptomatic variables during maximal and submaximal exercise. Total exercise time on a modified Bruce protocol was similar on both treatments: C12.5 min, A 13.1 min. During steady state submaximal exercise at 60-75% (mean 68%) of maximum work capacity, minute ventilation (C33.81 min-1, A 33.51 min-1), oxygen uptake (C14.6 ml.kg-1.min-1, A15.1 ml.kg-1.min-1), respiratory exchange ratio (C 0.89, A 0.87), ratio of VE/VCO2 (C 33.6, A 33.4), ratio of VE/VO2 (C 2.34, A 2.72), Borg perceived exertion score (C 11.2, A 10.9) and visual analogue scores for breathlessness (C 29.5, A 25.9) and muscle fatigue (C 28.9, A 26.0) were all similar on both treatments. At maximal exercise capacity on the modified Bruce protocol, minute ventilation (C 58.31 min-1, A 60.41 min-1), oxygen uptake (C 21.3 ml.kg-1.min-1, A 21.7 ml.kg-1.min-1), respiratory exchange ratio (C 1.02, A.1.05), ratio VE/VCO2 (C 34.8, A 35.9), and ratio VE/VO2 (C 2.80, A 2.83) were also similar on both drugs. Over a 10 day period anginal attacks (C 10.1 +/- 10.4, A 5.4 +/- 5.9) and sublingual GTN use (C 5.9 +/- 10.3, A 4.4 +/- 9.8) were both more frequent on celiprolol).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Respiration_MeSH S_drug_effects_MeSH Respiration_drug_effects_MeSH M_Treatment_Outcome_MeSH 
****** 7840730
----K 1
----T [Fasting and postprandial lipids and lipoproteins during the chronic administration of antihypertensive drugs]
----A To evaluate the effect of various antihypertensive drugs on fasting and postprandial lipids and lipoproteins, we studied 39 normolipidemic hypertensive patients, 28 men and 11 women aged 52.3 +/- 9.0 and 58.5 +/- 7 years, respectively. After four weeks of placebo administration, lipids and lipoproteins were measured in the fasting state and every three hours for a period of nine hours after intake of a standardized fat mixed load (65 g/m2). Following this test, the patients were randomly assigned to one of four treatment groups: group I metoprolol (n = 10), 100 mg/day; group II nicardipine (n = 9), 90 mg/day; group III captopril (n = 11), 75 mg/day. At the end of week four of treatment the fasting and postprandial lipid measurements were repeated. Blood pressure mean values were significantly (p < 0.05) reduced in the four treatment groups. We found no statistically significant lipids or lipoproteins changes neither in the fasting nor in the postprandial state, but a trend toward lower concentrations in the postprandial lipemia after treatment was observed in three groups (metoprolol, nicardipine and captopril), whereas no change was observed in the chlorthalidone group. These data confirm that fasting lipids and lipoproteins in normolipidemic hypertensive patients are not unfavorably changed by low doses of the drugs studied. In addition, we inform that postprandial lipemia is not affected by these four drugs in the doses used.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dietary_Fats_MeSH S_administration_&_dosage_MeSH Dietary_Fats_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_English_Abstract_MeSH M_Fasting_MeSH S_blood_MeSH Fasting_blood_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 7843470
----K E
----T One year comparative trial of metformin and glipizide in type 2 diabetes mellitus.
----A Forty-eight diabetic subjects with diet-failed Type 2 mellitus, aged 40-69 years, were randomised to metformin (24 patients) or glipizide (24 patients) therapy, and followed prospectively for 12 months. Most subjects were obese. Metformin gave better fasting plasma glucose control compared to glipizide at 24 (p < 0.01), 36 (p < 0.05) and 52 weeks (p < 0.05) with a lower HbA1 concentration at 52 weeks (p < 0.05). Metformin treated patients lost weight whereas glipizide treated subjects gained weight. The weight change between the treatment groups reached significance at 4 weeks (p < 0.05) and was highly significant (p < 0.001) at 8, 12, 24, 36 and 52 weeks. There were no significant changes in either fasting plasma lipid or blood lactate levels in either the metformin or glipizide treated groups. Both drugs caused a similar reduction in albumin excretion rates. In conclusion, metformin gave better glycaemic control than glipizide, with weight loss rather than weight gain in obese Type 2 patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Female_MeSH M_Glipizide_MeSH S_therapeutic_use_MeSH Glipizide_therapeutic_use_MeSH M_Human_MeSH M_Lactates_MeSH S_blood_MeSH Lactates_blood_MeSH M_Lactic_Acid_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metformin_MeSH S_therapeutic_use_MeSH Metformin_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 7851072
----K E
----T Hypertension in Diabetes Study. III. Prospective study of therapy of hypertension in type 2 diabetic patients: efficacy of ACE inhibition and beta-blockade.
----A The Hypertension in Diabetes Study (HDS) is an ongoing, multicentre, prospective randomized intervention trial of therapy of hypertension (> or = 160 and/or > or = 90 mmHg) in Type 2 diabetic patients. It compares tight blood pressure control (aim: < 150/85 mmHg) versus less tight control (aim: < 180/105 mmHg) and, within the tight control group, an ACE inhibitor, captopril, versus a beta blocker, atenolol. We report the efficacy, side-effects of treatment, biochemical responses and incidence of hypoglycaemia in 755 patients (mean age 57 years, blood pressure 150/94 mmHg) followed for 2 years. At 2 years, blood pressure was 143/84 in the tight control and 156/90 mmHg in the less tight control group (p < 0.0001). Blood pressure reduction, adherence to therapy, incidence of side-effects and of hypoglycaemia were similar on captopril and on atenolol. Patients on atenolol had a greater increase in body weight (+2.3 vs +0.7 kg, p < 0.01) and a non-significant trend to a greater increase in triglyceride than patients on captopril. A large blood pressure difference between the tight control and less tight control groups was obtained, with captopril and atenolol having similar hypotensive effects. The study has the potential to determine whether strict blood pressure control reduces the incidence of diabetic complications and whether ACE inhibitor or beta-blocker therapy is clinically advantageous.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 7852749
----K E
----T Within-patient correlation between the antihypertensive effects of atenolol, lisinopril and nifedipine.
----A OBJECTIVE: To investigate whether there are definable subgroups of patients with essential hypertension who respond specifically to particular antihypertensive drugs. DESIGN: Randomized cross-over comparison of the antihypertensive effect of 50 mg atenolol per day, 10 mg lisinopril per day and 20 mg nifedipine retard twice a day. Ambulatory blood pressure monitoring was used to assess the blood pressure level both for recruitment and at the end of each treatment period. The treatment periods lasted 4 weeks and were preceded by 4 weeks of placebo. PATIENTS: Seventy-two untreated hypertensive patients with a mean age of 52 (SD 8.4) years were recruited from six general practices and from the hospital outpatient clinic. Sixty-eight patients completed the trial. MAIN OUTCOME MEASURES: To assess the within-patient correlations among the blood pressure responses to each drug and explore the possible role of simple characteristics, such as the initial blood pressure, plasma renin concentration and age, in identifying the responders to a particular drug. RESULTS: Systolic/diastolic blood pressure fell significantly with each agent (P < 0.001): atenolol reduced it by 16.3 +/- 13.3/9.9 +/- 8.8, lisinopril by 14.8 +/- 15.0/9.4 +/- 9.1 and nifedipine by 11.6 +/- 12.3/6.7 +/- 8.3 mmHg. There was a low degree of correlation between the changes in blood pressure with the three drugs in individual patients. With each drug there was a small percentage (8.9-14.7%) of non-responders. The initial level of systolic blood pressure was weakly correlated with the antihypertensive effect of nifedipine (r = 0.47, P < 0.001) and plasma renin concentration was related to the effect of atenolol (r = 0.32, P < 0.01). Age did not predict the blood pressure response to any agent. CONCLUSIONS: The low level of the correlation between the blood pressure changes with the three drugs suggests that different mechanisms may be involved in the aetiology of essential hypertension. Plasma renin concentration and the initial level of systolic blood pressure contribute only weakly to the identification of responders to the three drugs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7856622
----K E
----T Venlafaxine: a heterocyclic antidepressant.
----A The pharmacology, pharmacokinetics, and clinical efficacy of venlafaxine hydrochloride, a new antidepressant, are described. Venlafaxine inhibits the reuptake of serotonin, norepinephrine, and, to a lesser extent, dopamine. In animal models, it does not significantly inhibit muscarinic, histaminic, or adrenergic receptor activity and does not inhibit monoamine oxidase. Venlafaxine is rapidly absorbed and metabolized in the liver to its active metabolite, O-desmethylvenlafaxine (ODV). Time to peak concentration is one to two hours for the parent compound and four to five hours for ODV. The pharmacokinetics of venlafaxine might be dose-dependent, although pharmacokinetic studies have had conflicting results. The major route of elimination is renal; thus, patients with renal dysfunction may require lower doses. In double-blind, placebo-controlled trials of venlafaxine for maintenance therapy, venlafaxine has shown effective antidepressant activity in severely ill patients with major depression. Antidepressant effectiveness may be apparent within two weeks; this finding needs to be replicated. The dosage is 75-375 mg/day administered in two or three divided doses. The strength of the antidepressant response may be correlated with increasing dosage. Nausea is the most commonly reported adverse drug reaction (ADR). Others include somnolence, dizziness, dry mouth, and sweating. All ADRs have commonly occurred at the beginning of therapy and decreased with time. Overall, venlafaxine is well tolerated. Venlafaxine is as effective as other available antidepressants. It may cause fewer anticholinergic, antihistaminic, and antiadrenergic ADRs and may have a quicker onset of therapeutic action than existing antidepressants.
----P Journal_Article Review Review__Tutorial 
----M P_Antidepressive_Agents__Second-Generation_MeSH S_pharmacokinetics_MeSH Antidepressive_Agents__Second-Generation_pharmacokinetics_MeSH S_pharmacology_MeSH Antidepressive_Agents__Second-Generation_pharmacology_MeSH M_Clinical_Trials__Phase_II_MeSH M_Clinical_Trials__Phase_III_MeSH M_Comparative_Study_MeSH P_Cyclohexanols_MeSH S_pharmacokinetics_MeSH Cyclohexanols_pharmacokinetics_MeSH S_pharmacology_MeSH Cyclohexanols_pharmacology_MeSH M_Depression_MeSH S_drug_therapy_MeSH Depression_drug_therapy_MeSH M_Drug_Interactions_MeSH M_Human_MeSH P_Serotonin_Uptake_Inhibitors_MeSH S_pharmacokinetics_MeSH Serotonin_Uptake_Inhibitors_pharmacokinetics_MeSH S_pharmacology_MeSH Serotonin_Uptake_Inhibitors_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7857585
----K I
----T Influence of chronic beta-adrenoreceptor blocker treatment on melatonin secretion and sleep quality in patients with essential hypertension.
----A The nocturnal production of melatonin synthesis has been associated with circadian mechanisms of the organization of sleep. It is well known that the synthesis of melatonin is under the control of pineal beta 1-adrenoreceptors. In this study the effect of ten weeks treatment with the beta-adrenoreceptor (beta-AR) blockers propranolol and ridazolol on melatonin synthesis and on sleep quality was examined in 42 patients suffering from essential hypertension. Before and after 6 and 10 weeks of beta-AR-blocker administration urinary sulfatoxymelatonin excretion rates were measured and sleep factors were evaluated by using a standardized sleep inventory consisting of self-rating sleepiness scales. After 6 and 10 weeks of treatment, a significant about 50 percent reduction of sulfatoxymelatonin was measured. No relationship between these reductions and changes in sleep factors was found. The results indicate that a reduced nightly amplitude of melatonin has minor significance for the organization of physiological sleep. Furthermore, it is suggested that pineal mechanisms beside the beta 1-adrenergic receptor transduction system serve to maintain the melatonin signal to a considerable extent during a chronic beta 1-AR blockade.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Comparative_Study_MeSH M_Depression__Chemical_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Melatonin_MeSH S_analogs_&_derivatives_MeSH Melatonin_analogs_&_derivatives_MeSH S_secretion_MeSH Melatonin_secretion_MeSH S_urine_MeSH Melatonin_urine_MeSH M_Middle_Aged_MeSH M_Pineal_Gland_MeSH S_drug_effects_MeSH Pineal_Gland_drug_effects_MeSH S_physiology_MeSH Pineal_Gland_physiology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Pyridazines_MeSH S_pharmacology_MeSH Pyridazines_pharmacology_MeSH S_therapeutic_use_MeSH Pyridazines_therapeutic_use_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH S_physiology_MeSH Receptors__Adrenergic__beta_physiology_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta-1_drug_effects_MeSH S_physiology_MeSH Receptors__Adrenergic__beta-1_physiology_MeSH M_Secretory_Rate_MeSH S_drug_effects_MeSH Secretory_Rate_drug_effects_MeSH M_Sleep_MeSH S_drug_effects_MeSH Sleep_drug_effects_MeSH S_physiology_MeSH Sleep_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7867240
----K E
----T Effects of atenolol and diltiazem-SR on exercise and pressure load in hypertensive patients.
----A The effects of monotherapy with atenolol or diltiazem-SR on blood pressure, 24-h blood pressure (BP) load, and exercise capacity were tested in patients with mild to moderate (stages I and II) essential hypertension. After 3-week single-blind placebo therapy, patients with sitting diastolic blood pressure (SDBP) of 94-114 mmHg were randomized to atenolol 50 mg/day (62 patients) or diltiazem-SR 90 mg b.i.d. (60 patients) in a double-blind parallel study. Depending on SDBP response, the dose was increased to 100 mg/day for atenolol and 180 mg b.i.d. for diltiazem-SR. Twenty-four-hour ambulatory blood pressure measurements and exercise tolerance test by the Bruce protocol were done at the end of placebo and active treatment. Compared with placebo, both atenolol and diltiazem-SR significantly decreased heart rate (HR), sitting systolic blood pressure (SSBP), SDBP, ambulatory BP, BP load for waking and sleeping hours, area under the BP curve, rate-pressure product (p < 0.001), and exercise time (NS). Atenolol exerted a greater effect on ambulatory BP, HR, rate-pressure product, waking diastolic BP load, and area under the 24-h BP curve. The drugs were well tolerated and caused no serious side effects necessitating discontinuation of treatment. These findings indicate that (1) monotherapy for hypertension with atenolol or diltiazem-SR is effective and well tolerated, (2) it decreases the 24-h BP load, (3) it does not interfere with exercise capacity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7876657
----K E
----T Correlation between clinical course and quantitative analysis of the ischemia related artery in patients with unstable angina pectoris, refractory to medical treatment. Results of two randomized trials. The European Cooperative Study Group.
----A Patients with unstable angina, refractory to intensive medical therapy, are at high risk for developing thrombotic complications, such as recurrent ischemia, myocardial infarction and coronary occlusion during coronary angioplasty. As both platelet aggregation and/or thrombus formation play an important role in this ongoing ischemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) or thrombolytic therapy (alteplase) might be able to modify the clinical course and underlying coronary lesion morphology. To evaluate whether alteplase or c7E3 could influence the incidence of complications, we randomized 36 and 60 patients, respectively to alteplase or placebo, or c7E3 or placebo. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite maximal tolerated medical therapy. Patients were randomized in both studies after initial angiography had demonstrated a culprit lesion amenable for angioplasty. After study drug infusion quantitative angiography was repeated and angioplasty performed. Recurrent ischemia during study drug infusion occurred in 5, 6, 9 and 16 patients from the alteplase, placebo, c7E3 and placebo group, respectively. Major events defined as death, myocardial infarction or urgent intervention occurred in 7, 3, 1 and 7 patients, respectively. Two patients died: one in the alteplase group and one in the placebo group from the c7E3 study. The first patient due to retroperitoneal hemorrhage, the second as a result of recurrent infarction. Qualitative angiography showed resolution of clots in the c7E3 group only, while the same group of patients showed in 20% an improvement in TIMI flow grade, without deterioration in any patient from this group.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_complications_MeSH Angina__Unstable_complications_MeSH S_radiography_MeSH Angina__Unstable_radiography_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH M_Antibodies__Monoclonal_MeSH S_therapeutic_use_MeSH Antibodies__Monoclonal_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Immunoglobulins__Fab_MeSH S_therapeutic_use_MeSH Immunoglobulins__Fab_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Membrane_Glycoproteins_MeSH S_antagonists_&_inhibitors_MeSH Platelet_Membrane_Glycoproteins_antagonists_&_inhibitors_MeSH M_Recurrence_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Treatment_Failure_MeSH 
****** 7887106
----K E
----T Thoracic epidural analgesia in aortocoronary bypass surgery. I: Haemodynamic effects.
----A Tachycardia and hypertension may cause myocardial ischaemia in patients with coronary heart disease going through major surgery. Thoracic epidural analgesia (TEA) has been reported to be beneficial in this situation. The haemodynamic effects of TEA in aortocoronary bypass surgery were investigated in 30 male patients < 65 years old and with ejection fraction > 0.5. They were randomized into 3 groups: the high dose fentanyl (HF) group receiving high-dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group receiving the same fentanyl dose+TEA with 10 ml bupivacaine 5 mg.ml-1 followed by 4 ml every hour, and the low dose fentanyl (LF) + TEA group receiving low-dose fentanyl (15 micrograms.kg-1) anaesthesia+TEA. Haemodynamic parameters, the use of vasoactive and inotropic drugs and fluid balance were followed during the operation and for 20 h postoperatively. Before bypass the only significant difference between groups was a higher mean pulmonary arterial pressure in the HF+TEA group and a lower systemic vascular resistance (SVR) in the LF+TEA group, both compared to the HF group. 89% of epidural group patients needed small doses of ephedrine whereas more HF group patients were given nitroglycerine. During bypass SVR and mean arterial pressure (MAP) were significantly higher and pump flow lower in the HF group compared to the LF+TEA group. More ketanserin to HF group patients and methoxamine to epidural group patients were given. After bypass heart rate increased in all groups. Lower MAP 0.5 h after bypass and higher filling pressures in the early post bypass period in the epidural groups, most pronounced in the HF+TEA group, were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M P_Analgesia__Epidural_MeSH M_Anesthesia__Intravenous_MeSH M_Bupivacaine_MeSH S_administration_&_dosage_MeSH Bupivacaine_administration_&_dosage_MeSH S_pharmacology_MeSH Bupivacaine_pharmacology_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Extracorporeal_Circulation_MeSH M_Fentanyl_MeSH S_administration_&_dosage_MeSH Fentanyl_administration_&_dosage_MeSH S_pharmacology_MeSH Fentanyl_pharmacology_MeSH P_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 7889236
----K E
----T Flecainide.
----A Flecainide is a Class IC antiarrhythmic agent whose primary electrophysiologic effect is a slowing of conduction in a wide range of cardiac tissues. It is well absorbed and effective in suppressing isolated premature ventricular contractions (PVCs) or nonsustained ventricular arrhythmia but has only a modest efficacy when electrophysiologic testing is used as an endpoint. Its adverse effect on mortality in the CAST trial suggested a propensity to proarrhythmia--a phenomenon to which the Class IC agents appear particularly prone. Despite the applicability of the CAST study only to patients with a prior myocardial infarction, there has been a shift away from flecainide in ventricular arrhythmia, but the low noncardiac side effect profile of the agent allows for its continued use in a wide variety of supraventricular arrhythmias.
----P Journal_Article Review Review__Tutorial 
----M M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH P_Flecainide_MeSH S_adverse_effects_MeSH Flecainide_adverse_effects_MeSH S_pharmacology_MeSH Flecainide_pharmacology_MeSH S_therapeutic_use_MeSH Flecainide_therapeutic_use_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH 
****** 7898065
----K E
----T Effects of carvedilol on the metabolic, hemodynamic, and electrocardiographic responses to increased plasma epinephrine in normal subjects.
----A To study the effects of the new vasodilating beta-blocking agent carvedilol on a variety of metabolic, hemodynamic, and ECG parameters of importance for the clinical outcome of acute myocardial infarction (AMI), we infused epinephrine (EPI) in healthy male volunteers on two separate occasions to serum concentrations of the same level reached in AMI. Before the EPI infusions, the volunteers were pretreated for 2 weeks with either carvedilol or placebo in randomized order. EPI caused significant decreases in serum levels: S-potassium (0.62 mM), S-magnesium (0.07 mM), S-calcium (0.12 mM), and S-phosphate (0.26 mM). After pretreatment with carvedilol, the decreases in S-calcium and S-phosphate were partly prevented and those in S-potassium and S-magnesium were completely inhibited. Short-term treatment with carvedilol significantly decreased S-insulin and serum C-peptide and significantly attenuated the EPI-induced increase in B-glucose observed after placebo. The EPI infusion significantly increased serum concentrations of free fatty acids and glycerol. These increases were significantly attenuated by carvedilol, whereas carvedilol had no significant affects of a variety of other lipid variables. EPI infusion caused a significant (p < 0.01) increase in systolic blood pressure (SBP) from 124.8 +/- 8.1 to 135.8 +/- 12.5 mm Hg and an increase in heart rate (HR) from 71.0 +/- 11.5 to 77.2 +/- 12.2, resulting in a significant increase in rate-pressure product (RPP). This estimate of cardiac work was significantly (p < 0.05) reduced by pretreatment with carvedilol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH M_Drug_Interactions_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Electrolytes_MeSH S_blood_MeSH Electrolytes_blood_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH S_pharmacology_MeSH Epinephrine_pharmacology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7719523
----K I
----T Adrenoreceptors, endothelial function, and lipid profile: effects of atenolol, doxazosin, and carvedilol.
----A BACKGROUND: The use of effective blood-pressure-lowering drugs has not achieved the expected reduction in the incidence of ischaemic heart disease in hypertensive patients. This study examined the cardiovascular effects of adrenergic blockade (alpha or beta, or both) and its effect on the fibrinolytic response of the endothelium to anoxia and lipoprotein metabolism in 78 hypertensive patients with ischaemic heart disease. METHODS: All patients had stable angina on positive exercise testing and silent ischaemia on 24 h Holter monitoring at baseline and 6 months after effective blood-pressure-lowering treatment with the selective beta-blocker atenolol, the alpha 1-inhibitor doxazosin, or the dual-action drug carvedilol. RESULTS: Atenolol increased the effort time (P < 0.05), total ischaemia (P < 0.05), and the number of ischaemic episodes (P < 0.05). It reduced the lipoprotein ratio (P < 0.05) but did not modify the fibrinolytic activity of the endothelium. Doxazosin increased the fibrinolytic index (ratio of plasminogen activator to its main inhibitor) before (P < 0.05) and after anoxia (P < 0.0001) and the lipoprotein ratio (P < 0.001), without an anti-ischaemic effect. Carvedilol increased the effort time (P < 0.05), reducing total ischaemia (P < 0.05), the number of ischaemic episodes (P < 0.01), and increasing the post-anoxia fibrinolytic index (P < 0.05) without modifying the lipid profile. CONCLUSIONS: At antihypertensive equipotent doses, the inhibition of alpha 1-receptors improves the endothelial fibrinolytic activity and the lipid profile. beta-Blockade has an anti-ischaemic action, but reduces the lipoprotein ratio (ApoA/ApoB) and does not improve endothelial fibrinolytic activity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Ergometry_MeSH S_drug_effects_MeSH Ergometry_drug_effects_MeSH M_Female_MeSH M_Fibrinolysis_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_blood_MeSH Myocardial_Ischemia_blood_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Tissue_Plasminogen_Activator_MeSH S_drug_effects_MeSH Tissue_Plasminogen_Activator_drug_effects_MeSH S_metabolism_MeSH Tissue_Plasminogen_Activator_metabolism_MeSH M_Treatment_Outcome_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 7738212
----K E
----T Sequential monotherapy of hypertension.
----A In most cases, the antihypertensive therapy for an individual patient is selected through a process of trial and error. This study determined if, by treating each hypertensive patient sequentially, with six antihypertensive drugs, one from each of the major classes, one could decide on the best possible drug for control of hypertension. In a randomized open-label crossover study, 19 patients (16 male and 3 female), 28-70 years of age with a sitting diastolic blood pressure of 95-110 mm Hg were given atenolol, captopril, clonidine, indapamide, prazosin, and verapamil in a sequential manner. Each drug was started at the minimum recommended or lower dose and titrated upwards every 2 weeks, if well tolerated, until blood pressure was controlled (diastolic BP < 90 mm Hg). If blood pressure was controlled, the drug was continued for another 2 weeks. A washout period of at least 2 weeks was allowed between drugs. Both systolic and diastolic blood pressures were reduced significantly with all of the six drugs. In 18 of the 19 patients, blood pressure was controlled with at least one of six drugs, frequently with the lowest dose. The authors conclude that if hypertension is not controlled with the lowest recommended dose of a drug, other antihypertensive drugs should be tried sequentially rather than increasing the dose or adding a second drug.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indapamide_MeSH S_pharmacology_MeSH Indapamide_pharmacology_MeSH S_therapeutic_use_MeSH Indapamide_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 1366265
----K E
----T Metabolic effects of pindolol and propranolol in a double-blind cross-over study in hypertensive patients.
----A Metabolic effects of pindolol and propranolol were investigated in a randomised study of double-blind, double-dummy design in 39 Caucasians with newly detected hypertension. Each active treatment period was 6 months long. A euglycaemic hyperinsulinaemic clamp test was done to measure insulin sensitivity, and i.v. glucose tolerance was investigated with insulin determinations. Lipoprotein concentrations were quantified and lipoprotein lipase activities were determined in muscle and adipose tissue and in plasma after heparin injection. The blood pressure was significantly reduced by both regimes. The insulin sensitivity index was decreased by 34% during propranolol treatment and by 17% during pindolol treatment. The insulin concentrations in plasma were elevated at the end of the i.v. glucose tolerance test but were not high enough to compensate for the insulin resistance, so HbA1c and glucose concentrations were increased. A significant reduction of lipoprotein lipase activity in skeletal muscle during propranolol treatment probably explains the pronounced increase in serum triglyceride concentration during propranolol treatment despite lower free fatty acids and higher lipoprotein lipase activity in adipose tissue. These changes of lipoprotein lipase activity were not correlated to the changes in insulin sensitivity. In summary, the metabolic effects were significantly less pronounced with pindolol than with propranolol, which probably can be ascribed to the agonistic effect of pindolol on beta 2 adrenoceptors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_MeSH S_metabolism_MeSH Glucose_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7743529
----K E
----T What happened to intravenous atenolol in acute myocardial infarction?
----A Randomized clinical trials are essential in objectively assessing treatment options. However, badly designed trials can generate impressive results, and good trial data may be interpreted differently by practicing clinicians. One example of the latter is the use of intravenous atenolol in acute myocardial infarction where, despite a large trial clearly demonstrating that immediate therapy is relatively safe in patients with acute myocardial infarction and reduces in-hospital mortality, its routine use remains extremely variable. The reasons for the poor uptake of atenolol in acute myocardial infarction, including anticipated clinical drawbacks, the way the trial data were published, and the marketing of beta blockers, are discussed in this paper.
----P Journal_Article 
----M M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Physician's_Practice_Patterns_MeSH P_Randomized_Controlled_Trials_MeSH 
****** 7755476
----K 1
----T [Prospective study of the effects of an angiotensin converting enzyme inhibitor and a beta blockader on the structure and function of resistant arteries in mild essential hypertension]
----A Seventeen male untreated mild essential hypertensive patients with a mean age of 41 years agreed to participate in a double-blind randomized trial to test the effects of treatment with cilazapril, an inhibitor of angiotensin I converting enzyme, in comparison to treatment with atenolol, a beta-blocker, on the structure and function of subcutaneous resistance arteries. Patients were randomized to receive either cilazapril 2.5-5 mg or atenolol 25-100 mg per day per day. Blood pressure before treatment was 147/99 and 148/99 mmHg in both groups respectively. At 1 year of treatment blood pressure was 132/86 and 131/85 mmHg in both groups of patients respectively. Treatment for one year with cilazapril resulted in a reduction in the media/lumen ratio of resistance arteries (150-400 microns lumen diameter) dissected from subcutaneous gluteal biopsies from 7.5 +/- 0.3% before treatment to 6.3 +/- 0.2% 1 year later (p < 0.05), still slightly but significantly larger (p < 0.05) than the media/lumen ratio of resistance arteries of normotensive controls (5.1 +/- 0.3%). In arteries from patients treated with atenolol there was no significant change with treatment (8.0 +/- 0.6% before and 8.1 +/- 0.5% after 1 year of treatment). Active wall tension responses to endothelin-1 were blunted in hypertensive patients and normalized in the cilazapril-treated patients, but were unchanged in those taking atenolol. Relaxation in response to acetylcholine of norepinephrine pre-contracted arteries was still significantly reduced after one year (< 0.05) in comparison to those of normotensive patients in the patients treated with atenolol, whereas they were not in those who had received cilazapril.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH M_Clinical_Protocols_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 7775548
----K E
----T Perioperative infusion of nifedipine and metoprolol provides antiischemic and antiarrhythmic protection in patients undergoing elective aortocoronary by-pass surgery.
----A A randomised study was performed on 70 patients undergoing elective coronary by-pass procedure to examine whether the combined, perioperative, 24-hour infusion of nifedipine and metoprolol reduces the incidence of perioperative myocardial ischemia and arrhythmias. The control group received nifedipine only. Repeated assessments of serum enzyme levels and 12-lead-ECG together with a 3-channel Holter monitoring over 48h were used to classify perioperative myocardial ischemia and supraventricular and ventricular arrhythmias. The two groups did not differ with respect to their demographic data, extracorporeal circulation, aortic cross-clamping time, or number of distal anastomosis. No perioperative myocardial infarction in either group was detected. However, a significantly lower incidence of transient ischemic event was observed in the NM group as compared transient ischemic events was observed in the NM group as compared to the N group. In addition, there was a tendency towards lower CK-MB-level and peak-values of CK- and CK-MB-enzymes in the NM group. With regard to perioperative dysrhythmias, there was a significantly lower incidence of sinus tachycardia and atrial flutter/fibrillation in the NM group as compared to the N group. In addition, postoperative heart rate was lower in the NM group starting from the 6th hour after opening the aortic cross-clamp. In conclusion, the combined perioperative infusion of nifedipine and metoprolol is superior in preventing perioperative myocardial ischemia and decreasing the incidence of supraventricular arrhythmias as compared to a single-drug regimen with nifedipine.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH M_Electrocardiography__Ambulatory_MeSH M_Endarterectomy_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Intraoperative_Care_MeSH M_Intraoperative_Complications_MeSH S_prevention_&_control_MeSH Intraoperative_Complications_prevention_&_control_MeSH M_Isoenzymes_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Time_Factors_MeSH 
****** 7786690
----K E
----T Long-term follow-up after acute myocardial infarction in patients randomized to treatment with intravenous magnesium or intravenous propranolol in the acute phase.
----A Ninety-five patients with acute myocardial infarction were followed up for 6 months to 3 years (mean 25.4 months) in a preliminary study to compare the effects of intravenous magnesium (49 patients) with that of intravenous propranolol (44 patients) given immediately after admission to the intensive care unit. There were four cardiac deaths in the propranolol group and no deaths in the magnesium group (P < 0.046) and 27 per cent of patients who received propranolol subsequently developed cardiac failure as opposed to 12 per cent of those who had received magnesium (P < 0.04). Intravenous magnesium given in the early stages of myocardial infarction reduces the subsequent cardiac death rate possibly by reducing infarct size.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Magnesium_Sulfate_MeSH S_administration_&_dosage_MeSH Magnesium_Sulfate_administration_&_dosage_MeSH S_therapeutic_use_MeSH Magnesium_Sulfate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH M_Treatment_Outcome_MeSH 
****** 7611920
----K E
----T [Use of carvedilol compared to nifedipine in the treatment of mild and moderate essential arterial hypertension]
----A PURPOSE--To compare the efficacy of carvedilol, a new antihypertensive drug that combines vasodilatory and beta-blocker properties, with nifedipine. METHODS--In a multicenter double-blind trial, 106 mild to moderate essential hypertensive patients were treated with either carvedilol (n = 51), or nifedipine (n = 55) as monotherapy. Following 4 weeks of wash-out/run-in period, patients from the carvedilol group received this drug once a day at a dosage of 25 mg/day for 8 consecutive weeks. In order to maintain the double-blind character of the study, a placebo was administered in the carvedilol group at identical dosage intervals as used in the nifedipine s.r. group. Nifedipine was also administered for 8 weeks at a dosage of 40 mg/day given b.i.d. RESULTS--Both treatments were equally efficient in reducing blood pressure in the seated and upright positions. Blood pressure response to treatment was obtained in 79% and 78% of patients treated with carvedilol and nifedipine, respectively. The carvedilol group did not develop reflex tachycardia which is usually seen when prescribing vasodilators. Blood biochemistry remained unchanged with both treatments. Besides similar blood pressure efficacy, side effects by patients taking carvedilol were less frequent than nifedipine group. CONCLUSION--Carvedilol is a safe, efficient, once/day choice as monotherapy for mild to moderate essential hypertensive patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Protocols_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 10535718
----K E
----T Daytime-selective antihypertensive activity of celiprolol.
----A Day-activity rhythms of heart rate and blood pressure are thought to be mediated mainly through the sympathetic nervous system and may have greater amplitudes in patients with hypertension owing to increased daytime and largely normal nighttime values. Drug-induced nighttime hypotension in patients with chronic hypertension has been associated with the precipitation of cardiac failure and a fall in cerebral flow. The authors examined the effects of a single dose and of a 4-week treatment with different classes of antihypertensive drugs on ambulatory blood pressure (ABP) in 10 patients with mild hypertension. Data were assessed by polynomial analysis (Harvard Graphics 3). A single oral dose of enalapril 10 mg, amlodipine 5 mg, carvedilol 25 mg, and celiprolol 200 mg produced a mean reduction of 24-hour ABP compared to placebo of, respectively, 24/11, 11/5, 13/6, and 12/5 mm Hg (p values between <0.02 and <0.001). With enalapril, amlodipine, and carvedilol, between-subject variability contributed significantly to the overall variability in the measurements (p values between 0.05 and 0.01 versus zero), whereas with celiprolol this was not so. Although the beta blockers reduced daytime blood pressures similarly to the ACE inhibitor or the calcium channel blocker, they did not reduce nighttime blood pressures. These results were confirmed by an 8-week crossover trial comparing enalapril 10 mg daily with celiprolol 200 mg daily in the same group of patients. The authors conclude (1) that beta blockers produce a more stable reduction of blood pressure in patients with mild hypertension less affected by pressor effects through the sympathetic nervous system; (2) that beta blockers, unlike ACE inhibitors and calcium channel blockers, do not give rise to nighttime hypotension in this category of patients; and (3) that the selective beta blocker celiprolol may even perform better in these respects than the nonselective beta blocker carvedilol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_chemically_induced_MeSH Cardiac_Output__Low_chemically_induced_MeSH M_Celiprolol_MeSH S_administration_&_dosage_MeSH Celiprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH P_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH 
****** 10539811
----K E
----T Angiotensin-converting enzyme inhibitor compliance and dosing among patients with heart failure.
----A BACKGROUND: The efficacy of angiotensin-converting enzyme (ACE) inhibitors in treating heart failure is well established, but there is concern that these agents are underutilized. Proper treatment is contingent both on appropriate medication dosing by the physician and on patient compliance with therapy. This study examined dosing and compliance with ACE inhibitors in routine clinical practice. METHODS AND RESULTS: Data were integrated medical and pharmacy claims from 869 patients with heart failure. Compliance and dosing of ACE inhibitors was examined for each patient over a 10- to 17-month period. Patients had ACE inhibitors available on 71% of the days assessed. At 180 days after their index prescription, 86% of patients continued to take an ACE inhibitor. The mean percentage of an adequate daily dose of ACE inhibitors dispensed per prescription was 79%, but only 34% of patients were dispensed >/=100% of an adequate daily dose. A number of variables were found to independently predict compliance and dosing levels in the multivariate analyses. CONCLUSIONS: Both physician-dependent and patient-dependent factors contributed significantly to ACE inhibitor underutilization. Each of these factors must be addressed to improve compliance and dosing of ACE inhibitors in routine clinical care.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Patient_Compliance_MeSH M_Physician's_Practice_Patterns_MeSH M_Prescriptions__Drug_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 10539815
----K E
----T Predictors of decreased renal function in patients with heart failure during angiotensin-converting enzyme inhibitor therapy: results from the studies of left ventricular dysfunction (SOLVD)
----A BACKGROUND: Although angiotensin-converting enzyme inhibitor therapy reduces mortality rates in patients with congestive heart failure (CHF), it may also cause decreased renal function. Little information is available to predict which patients are at highest risk for this complication. OBJECTIVE: To quantify specific clinical predictors of reduction in renal function in patients with CHF who are prescribed angiotensin-converting enzyme inhibitor therapy. METHOD: We analyzed data from the Studies of Left Ventricular Dysfunction (SOLVD), a randomized, double-blind, placebo-controlled trial of enalapril for the treatment of CHF. There were 3379 patients randomly assigned to enalapril with a median follow-up of 974 days and 3379 patients randomly assigned to placebo with a mean follow-up of 967 days. Decreased renal function was defined as a rise in serum creatinine >/=0.5 mg/dL (44 micromol/L) from baseline. We used time-to-event analysis to identify potential predictors of decrease in renal function including age, baseline ejection fraction, baseline creatinine, low systolic blood pressure (<100 mm Hg), history of hypertension, diabetes, and use of antiplatelet, diuretic, and beta-blocker therapy. RESULTS: Patients randomly assigned to enalapril had a 33% greater likelihood of decreased renal function than controls (P =.003). By multivariate analysis, in both the placebo and enalapril groups older age, diuretic therapy, and diabetes were associated with decreased renal function, whereas beta-blocker therapy and higher ejection fraction were renoprotective. Older age was associated with a greater risk of developing decreased renal function in both groups, but significantly more so in the enalapril group (enalapril: risk ratio [RR] 1.42 per 10 years, 95% confidence interval [CI] 1.32-1.52 with enalapril; placebo: RR 1.18, 95% CI 1.12-1.25). Diuretic therapy was likewise associated with a greater risk of decreased renal function in the enalapril group (RR 1.89, 95% CI 1.70-2.08) than in the placebo group (RR 1.35, 95% CI 1.09-1.66). Conversely, enalapril had a relative renoprotective effect (RR 1.33, 95% CI 1.13-1.53) compared with placebo (RR 1.96, 95% CI 1.57-2.44) in patients with diabetes. A lower risk of renal impairment was seen in both groups with beta-blocker therapy (RR 0.70, 95% CI 0.57-0.85) and higher baseline ejection fraction (RR 0.93 per 5% increment, 95% CI 0.91-0. 96). CONCLUSIONS: Enalapril use caused a 33% increase in the risk of decreased renal function in patients with CHF. Diuretic use and advanced age increased this risk. Diabetes was associated with an increased risk of renal impairment in all patients with CHF, but this risk was reduced in the enalapril group compared with the placebo group. beta-Blocker therapy and higher ejection fraction were renoprotective in all patients regardless of therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_blood_MeSH Kidney_Failure__Chronic_blood_MeSH S_chemically_induced_MeSH Kidney_Failure__Chronic_chemically_induced_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Kidney_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 10546124
----K 1
----T Prospective clinical evaluation and follow-up of a cohort of consecutive VT/VF patients, using a staged-care protocol, including coronary arteriography, programmed electrical stimulation and cardiac surgery.
----A The prospective evaluation and follow-up of 39 consecutive subjects with VT/VF, 6 of whom, with cardiac arrest (CA), are reported. Patients were enrolled in a specific staged-care approach protocol, which included coronary arteriography (CAR) and ventriculography (VC), in order to exclude the need of cardiac surgery, including coronary artery bypass graft (CABG), with and without left ventricular aneurysmectomy (LVA). The protocol included inducibility of VT/VF, which was verified by programmed electrical stimulation (PES) in control conditions and after antiarrhythmic therapy (ADT), to assess persistent inducibility and mainly to verify the hemodynamic sequelae of VT. VT that showed poor hemodynamic tolerance was treated with ICD, while well-tolerated VT was treated by ADT or ablation when indicated. Furthermore, PES was obtained after surgical procedures. As a first step, the patients were assigned to receive amiodarone (AMIO) (200-400 mg/daily) in the presence of EF% < 30% or contraindication to sotalol, (Group A), or sotalol (SOT) (80-140 mg/daily) in the presence of EF > or = 31%. (Group C). Conversely, in case of recurrences, patients were assigned to receive AMIO (200-300 mg/daily) plus metoprolol (MET) (20-100 mg/daily), (Group B) or, in case of intolerance to beta-blockers, to AMIO plus mexiletine (MEX) (200 mg/daily) (Group D). The four groups were similar for the type of VA, with recurrent ventricular tachycardia (RVT) being the most frequent one. The most frequent underlying cardiac disease of VA in this study was post-AMI CAD, with a rate of over 60% in all four groups. Single- and two-vessel lesions were found at CAR in various patients in all four groups, in 5/13 (38%) in Group A, in 8/14 (57%) in Group B, in 5/7 (71%) in Group C, and in 3/5 (60%) in Group D. Cardiac surgery was performed in a similar and limited number of patients in all four groups, in 4/13 (30%) in Group A, in 4/14 (35%) in Group B, in 2/7 (28%) in Group C, and in 2/5 (40%) in Group D. In 8/39 (20.5%) of the patients who underwent CABG, there was no operative or late mortality; 4/39 (10.2%) received CABG and LVA, and two died. For the amiodarone plus metoprolol and sotalol patients only, PES showed a lower residual inducibility, in comparison to the amiodarone and amiodarone + mexiletine groups. In the entire group, 7 out of 26 (27%) were still inducibile at PES while in 19/26 (64%) of the patients, an apparently effective treatment could be found, documenting the relative usefulness of PES. Recurrence rate was the highest in the amiodarone + mexiletine group and in patients with previous CA. Our data show the potential utility and limitations of ADT, even using the most effective antiarrhythmic drugs and association of drugs, mainly because of the high recurrence rate of VT observed in the present study, even in non-inducible patients [14/39 (36%)]. In conclusion, in a prospective and staged-care approach protocol of management of VT/VF patients, only a few patients with VT/VF benefited from cardiac surgery. PES could still play a role in the evaluation of the most effective ADT. Amiodarone + metoprolol seems to be the most effective ADT in these patients. Nevertheless, a high recurrence rate was observed in this patient population, even with an aggressive protocol, in the short follow-up period of 12 +/- 8 months, confirming recent data on the superiority of ICD to ADT, in patients with frequent recurrences or hemodynamically poorly-tolerated VT. In these patients, ICD therapy should definitively be preferred to ADT.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH P_Cardiac_Surgical_Procedures_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH P_Coronary_Angiography_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Defibrillators__Implantable_MeSH M_Electric_Stimulation_MeSH M_Follow-Up_Studies_MeSH M_Heart_Aneurysm_MeSH S_surgery_MeSH Heart_Aneurysm_surgery_MeSH M_Heart_Catheterization_MeSH M_Heart-Lung_Transplantation_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Time_Factors_MeSH M_Ventricular_Fibrillation_MeSH S_diagnosis_MeSH Ventricular_Fibrillation_diagnosis_MeSH S_therapy_MeSH Ventricular_Fibrillation_therapy_MeSH 
****** 10548187
----K E
----T Prevention of secondary ischemic insults after severe head injury.
----A OBJECTIVE: The purpose of this study was to compare the effects of two acute-care management strategies on the frequency of jugular venous desaturation and refractory intracranial hypertension and on long-term neurologic outcome in patients with severe head injury. DESIGN: Randomized clinical trial. SETTING: Level I trauma hospital. PATIENTS: One hundred eighty-nine adults admitted in coma because of severe head injury. INTERVENTIONS: Patients were assigned to either cerebral blood flow (CBF)-targeted or intracranial pressure (ICP)-targeted management protocols during randomly assigned time blocks. In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and PaCO2 was kept at approximately 35 torr (4.67 kPa). In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa) was used to treat intracranial hypertension. MEASUREMENTS AND MAIN RESULTS: The CBF-targeted protocol reduced the frequency of jugular desaturation from 50.6% to 30% (p = .006). Even when the frequency of jugular desaturation was adjusted for all confounding factors that were significant, the risk of cerebral ischemia was 2.4-fold greater with the ICP-targeted protocol. Despite the reduction in secondary ischemic insults, there was no difference in neurologic outcome. Failure to alter long-term neurologic outcome was probably attributable to two major factors. A low jugular venous oxygen saturation was treated in both groups, minimizing the injury that occurred in the ICP-targeted group. The beneficial effects of the CBF-targeted protocol may have been offset by a five-fold increase in the frequency of adult respiratory distress syndrome. CONCLUSIONS: Secondary ischemic insults caused by systemic factors after severe head injury can be prevented with a targeted management protocol. However, potential adverse effects of this management strategy may offset these beneficial effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Analgesics__Opioid_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Brain_Injuries_MeSH S_complications_MeSH Brain_Injuries_complications_MeSH S_diagnosis_MeSH Brain_Injuries_diagnosis_MeSH S_drug_therapy_MeSH Brain_Injuries_drug_therapy_MeSH M_Brain_Ischemia_MeSH S_diagnosis_MeSH Brain_Ischemia_diagnosis_MeSH S_etiology_MeSH Brain_Ischemia_etiology_MeSH S_prevention_&_control_MeSH Brain_Ischemia_prevention_&_control_MeSH M_Catheterization__Central_Venous_MeSH M_Cerebrovascular_Circulation_MeSH M_Comparative_Study_MeSH M_Diuretics__Osmotic_MeSH S_therapeutic_use_MeSH Diuretics__Osmotic_therapeutic_use_MeSH M_Drainage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypnotics_and_Sedatives_MeSH S_therapeutic_use_MeSH Hypnotics_and_Sedatives_therapeutic_use_MeSH M_Intensive_Care_MeSH S_methods_MeSH Intensive_Care_methods_MeSH M_Intracranial_Hypertension_MeSH S_diagnosis_MeSH Intracranial_Hypertension_diagnosis_MeSH S_etiology_MeSH Intracranial_Hypertension_etiology_MeSH S_prevention_&_control_MeSH Intracranial_Hypertension_prevention_&_control_MeSH M_Intracranial_Pressure_MeSH M_Jugular_Veins_MeSH S_metabolism_MeSH Jugular_Veins_metabolism_MeSH M_Male_MeSH M_Oxygen_MeSH S_blood_MeSH Oxygen_blood_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Tomography__X-Ray_Computed_MeSH M_Trauma_Centers_MeSH M_Trauma_Severity_Indices_MeSH M_Treatment_Outcome_MeSH 
****** 10545432
----K E
----T Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation.
----A BACKGROUND:Atrial fibrillation (AF) can be initiated by ectopic beats originating from the atrial or great venous tissues. This study investigated the anatomic characteristics and electrophysiological properties of pulmonary veins (PVs), as well as the possible mechanisms and response to drugs of ectopic foci, and assessed the effects of radiofrequency (RF) ablation on AF initiated by ectopic beats originating from PVs. METHODS AND RESULTS:Seventy-nine patients with frequent episodes of paroxysmal AF and 10 control patients were included. Distal PVs showed the shortest effective refractory periods (ERPs), and right superior PVs showed a higher incidence of intra-PV conduction block than left superior PVs. Superior and left PVs had longer myocardial sleeves than inferior and right PVs, respectively. These electrophysiological characteristics were similar between AF and control patients. Propranolol, verapamil, and procainamide suppressed ectopic beats that originated from the PVs. Of 116 ectopic foci that initiated AF, 103 (88.8%) originated from PVs. A mean of 7+/-3 RF applications completely eliminated 110 ectopic foci (94.8%). During the 6+/-2-month follow-up period, 68 patients (86. 1%) were free of AF without any antiarrhythmic drugs. Follow-up transesophageal echocardiogram showed 42.4% of ablated PVs had focal stenosis. One patient had mild exertional dyspnea after ablation, but it resolved 3 months later; 1 patient had onset of mild exertional dyspnea 5 months after ablation. CONCLUSIONS:Electrophysiological characteristics of PVs are different from those in the atria. Ectopic beats from PVs can initiate AF, and beta-adrenergic receptor blocker, calcium channel blockers, and sodium channel blockers can suppress these ectopic beats. Careful mapping and elimination of these ectopic foci can cure paroxysmal AF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Atrial_Premature_Complexes_MeSH S_complications_MeSH Atrial_Premature_Complexes_complications_MeSH S_physiopathology_MeSH Atrial_Premature_Complexes_physiopathology_MeSH S_therapy_MeSH Atrial_Premature_Complexes_therapy_MeSH P_Catheter_Ablation_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Procainamide_MeSH S_therapeutic_use_MeSH Procainamide_therapeutic_use_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Pulmonary_Veins_MeSH S_physiopathology_MeSH Pulmonary_Veins_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10551702
----K I
----T Beta-blockade in heart failure: a comparison of carvedilol with metoprolol.
----A OBJECTIVES: This study was performed to compare the long-term clinical efficacy of treatment with metoprolol versus carvedilol in patients with chronic heart failure. BACKGROUND: Beta-adrenergic blockade is of proven value in chronic heart failure. Metoprolol, a selective beta-blocker, is widely used, but recent trials suggest carvedilol, a nonselective beta-blocker with alpha-1-receptor antagonist activity and antioxidant activities, is also effective. It is uncertain, however, if these additional properties of carvedilol provide further clinical benefit compared with metoprolol. METHODS: In this randomized double-blind control trial, 51 patients with chronic heart failure and mean left ventricular (LV) ejection fraction of 26% +/- 1.8% were randomly assigned treatment with metoprolol 50 mg twice daily or carvedilol 25 mg twice daily in addition to standard therapy after a four-week dose titration period for a total of 12 weeks. Response was assessed by a quality of life questionnaire, New York Heart Association class, exercise capacity (6-min walk test), radionucleotide ventriculography for LV ejection fraction, two-dimensional echocardiography measurement of LV dimensions and diastolic filling and 24-h electrocardiograph monitoring to assess heart rate variability. RESULTS: Both carvedilol and metoprolol produced highly significant improvement in symptoms (p < 0.001), exercise capacity (p < 0.05) and LV ejection fraction (p < 0.001), and there were no significant differences between the two drugs. Carvedilol had a significantly greater effect on sitting and standing blood pressure, LV end-diastolic dimension and normalized the mitral E wave deceleration time. CONCLUSIONS: Both metoprolol and carvedilol were equally effective in improving symptoms, quality of life, exercise capacity and LV ejection fraction, although carvedilol lowers blood pressure more than metoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10552234
----K E
----T Episodic vertigo related to migraine (90 cases): vestibular migraine?
----A A retrospective study was conducted on 90 patients with episodic vertigo that could be related to migraine as the most probable pathomechanism. Since the majority of the patients did not fulfill the criteria of the International Headache Society (IHS) for basilar migraine, the diagnosis was substantiated by disease course, medical efficacy in treating (ergotamines) and preventing (metoprolol, flunarizine) attacks, ocular motor abnormalities in the symptom-free interval, and careful exclusion of the most relevant differential diagnoses, such as transient ischemic attacks, Meniere's disease, and vestibular paroxysmia. The following clinical features were elaborated. The initial manifestation could occur at any time throughout life, with a peak in the fourth decade in men and a "plateau" between the third and fifth decades in women. The duration of rotational (78%) and/or to-and-fro vertigo (38%) could last from a few seconds to several hours or, less frequently, even days; duration of a few minutes or of several hours was most frequent. Monosymptomatic audiovestibular attacks (78%) occurred as vertigo associated with auditory symptoms in only 16%. Vertigo was not associated with headache in 32% of the patients. In the symptom-free interval 66% of the patients showed mild central ocular motor signs such as vertical (48%) and/or horizontal (22%) saccadic pursuit, gaze-evoked nystagmus (27%), moderate positional nystagmus (11%), and spontaneous nystagmus (11%). Combinations with other forms of migraine were found in 52%. Thus, migraine is a relevant differential diagnosis for episodic vertigo. According to the criteria of the IHS, only 7.8% of these patients would be diagnosed as having basilar migraine. However, to ensure that at least those presenting with monosymptomatic episodic vertigo (78% in our study) receive effective treatment, we propose the use of the more appropriate term "vestibular migraine."
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Age_of_Onset_MeSH M_Aged_MeSH M_Child_MeSH M_Electronystagmography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_classification_MeSH Migraine_classification_MeSH S_complications_MeSH Migraine_complications_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH M_Ocular_Motility_Disorders_MeSH S_chemically_induced_MeSH Ocular_Motility_Disorders_chemically_induced_MeSH S_complications_MeSH Ocular_Motility_Disorders_complications_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vertigo_MeSH S_complications_MeSH Vertigo_complications_MeSH S_diagnosis_MeSH Vertigo_diagnosis_MeSH S_epidemiology_MeSH Vertigo_epidemiology_MeSH S_etiology_MeSH Vertigo_etiology_MeSH S_physiopathology_MeSH Vertigo_physiopathology_MeSH 
****** 10552188
----K 1
----T [Effects of the K(+) channel blocker tedisamil on hemodynamics, myocardial ischemia and neurohumoral systems in patients with stable angina pectoris. A comparison with the beta blocker atenolol]
----A BACKGROUND: Clinical drawbacks of beta-blocker treatment in stable angina have motivated researchers to provide alternative heart rat lowering agents, such as tedisamil which additionally exerts anti-ischemic and antiarrhythmic effects by blockade of cellular repolarizing K(+) currents. METHODS AND RESULTS: 48 patients with stable angina pectoris were investigated (double-blind, randomized, parallel grouped) comparing the hemodynamic, anti-ischemic, metabolic and neurohumoral effects of tedisamil 100 mg b.i.d and atenolol 50 mg b.i.d. after a single dose and over 6 days of treatment. Tedisamil and atenolol produced a decrease in heart rate both at rest (day 1: -13.6 vs -15.4 bpm; p > 0.05; day 6: -14.8 vs -22.2 bpm; resp.; p > 0.05) and exercise (day 1: -9.1 vs -18.3 bpm; p = 0. 001; day 6: -12.0 vs -24.8 bpm, resp.; p = 0.001), while anginal threshold increased. Cardiac output decreased with tedisamil and atenolol at rest (day 1: -1.01 vs -1.19 l/min; p > 0.05; day 6: -0. 86 vs -1.10 l/min, resp.; p > 0.05) and exercise (day 1: -0.82 vs -1. 28 l/min; p > 0.05; day 6: -0.65 vs -2.68 l/min, resp.; p = 0.03), while stroke volume remained unchanged. Right atrial pressure changed during exercise only: It decreased with tedisamil (-1.7 mm Hg) and increased with atenolol (+3.7 mm Hg). Mean pulmonary capillary wedge pressures decreased at rest (-0.5 mm Hg) and exercise (-6.9 mm Hg) in the tedisamil group, but tended to increase with atenolol on day 6 (rest: +1.7; exercise: +3.7 mm Hg) (p = 0.03). Arterial pressure decreased under atenolol treatment only. Exercise-induced plasma norepinephrine levels were reduced by tedisamil (-93 pg/ml) but elevated by atenolol (+172 pg/ml) (p = 0. 001). As compared to atenolol, tedisamil produced a significant prolongation of QT (c) interval (+31 vs -8 ms) (p = 0.002) at initial values of 0.408 +/- 0.018 s with PQ and QRS remaining unaltered. CONCLUSIONS: In the present study, tedisamil (100 mg b.i.d. ) generated favorable hemodynamic, neurohumoral and anti-ischemic effects in patients with stable angina pectoris. The anti-ischemic efficacy of tedisamil, as measured by ST segment depression and angina threshold, is comparable to that of atenolol (50 mg b.i.d.).
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bicyclo_Compounds__Heterocyclic_MeSH S_adverse_effects_MeSH Bicyclo_Compounds__Heterocyclic_adverse_effects_MeSH S_therapeutic_use_MeSH Bicyclo_Compounds__Heterocyclic_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Cyclopropanes_MeSH S_adverse_effects_MeSH Cyclopropanes_adverse_effects_MeSH S_therapeutic_use_MeSH Cyclopropanes_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH P_Potassium_Channel_Blockers_MeSH M_Treatment_Outcome_MeSH 
****** 10555240
----K E
----T One doctor's 25-year experience of beta-blocker treatment to the same group of hypertensive women.
----A OBJECTIVE: To assess the importance of long-term doctor-patient relationship, and to assess the effect of long-term treatment with beta-blockers of hypertensive women. DESIGN: A 25-year follow-up study of hypertensive women, compared with participants in a prospective population study of women of the same age. SETTING: Gothenburg, Sweden. SUBJECTS: 57 hypertensive women and 1462 participants in the population study. RESULTS: The women's blood pressure was well-controlled over the years, and no serious side-effects occurred. There was no increased mortality in these groups of hypertensive women compared with women in the general population of the same age. CONCLUSIONS: The favourable effects over the years with respect to the management of blood pressure and survival indicate the beneficial effect of a stable doctor-patient relationship and the beneficial long-term effect of beta-blockers as a base for antihypertensive treatment.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Alprenolol_MeSH S_therapeutic_use_MeSH Alprenolol_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Body_Weight_MeSH M_Continuity_of_Patient_Care_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH P_Physician-Patient_Relations_MeSH M_Prospective_Studies_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH 
****** 10561948
----K E
----T Bioequivalence study of generic atenolol tablets in healthy Thai volunteers.
----A Two preparations of 50 mg and 100 mg atenolol tablets were evaluated for their bioequivalence in twelve healthy Thai subjects (Prenolol, Berlin Pharmaceutical Industry, as the test formulations vs Tenormin, Zeneca Limited, as the reference formulations). A single oral dose of each preparation was administered in a randomized two-way crossover design, starting from either 50 mg of Prenolol vs Tenormin, thereafter, either 100 mg of Prenolol vs Tenormin. The washout period between each treatment was one week. Atenolol plasma concentrations were determined by the HPLC technique with fluorometric detection. Pharmacokinetic parameters were analyzed by the noncompartmental pharmacokinetic method using TOPFIT. The means and parametric 90 per cent confidence intervals of the ratio [Prenolol/Tenormin] of AUC0-infinity and Cmax were 1.16 (1.05-1.27) and 1.23 (1.07-1.38) for 50 mg preparations and 1.10 (1.00-1.20) and 1.13 (0.95-1.31) for 100 mg preparations, respectively. These values were well within the acceptable bioequivalence ranges. The mean differences of Tmax [Prenolol-Tenormin] were less than 20 per cent for both 50 mg and 100 mg preparations. Hence, Prenolol and Tenormin were bioequivalent with respect to the rate and extent of absorption.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH M_Adult_MeSH M_Atenolol_MeSH S_blood_MeSH Atenolol_blood_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Thailand_MeSH M_Therapeutic_Equivalency_MeSH 
****** 10569322
----K E
----T Prognostic implications of ambulatory myocardial ischemia and arrhythmias and relations to ischemia on exercise in chronic stable angina pectoris (the Angina Prognosis Study in Stockholm [APSIS]).
----A The prognostic significance of ambulatory ischemia, alone and in relation to ischemia during exercise was assessed in 686 patients (475 men) with chronic stable angina pectoris taking part in the Angina Prognosis Study In Stockholm (APSIS), who had 24-hour ambulatory electrocardiographic registrations and exercise tests at baseline (n = 678) and after 1 month (n = 607) of double-blind treatment with metoprolol or verapamil. Ambulatory electrocardiograms were analyzed for ventricular premature complexes and ST-segment depression. During a median follow-up of 40 months, 29 patients died of cardiovascular (CV) causes, 27 had a nonfatal myocardial infarction, and 89 underwent revascularization. Patients with CV death had more episodes (median 5 vs. 1; p<0.01) and longer median duration (24 vs. 3 minutes; p<0.01) of ST-segment depression than patients without events. For those who had undergone revascularization, the duration was also longer (12 vs. 3 minutes; p<0.05). In a multivariate Cox model including sex, history of previous myocardial infarction, hypertension, and diabetes, the duration of ST-segment depression independently predicted CV death. When exercise testing was included, ambulatory ischemia carried additional prognostic information only among patients with ST-segment depression > or =2 mm during exercise. When the treatment given and treatment effects on ambulatory ischemia were added to the Cox model, no significant impact on prognosis was found. Ventricular premature complexes carried no prognostic information. Thus, in patients with stable angina pectoris, ischemia during ambulatory monitoring showed independent prognostic importance regarding CV death. Ambulatory electrocardiographic monitoring and exercise testing provide complementary information, but only among patients with marked ischemia during exercise. Treatment reduced ambulatory ischemia, but the short-term treatment effects did not significantly influence prognosis.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chronic_Disease_MeSH P_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10569324
----K E
----T Effect of quinapril or metoprolol on circadian sympathetic and parasympathetic modulation after acute myocardial infarction.
----A Abnormal autonomic nervous system impairment in patients with acute myocardial infarction (AMI) has a circadian pattern with the greatest manifestation in the morning hours; it probably plays an important role in the pathogenesis of cardiac arrhythmias and acute ischemic syndromes. Angiotensin-converting enzyme inhibitors improve autonomic function in patients with AMI, but the circadian pattern of this effect has not been studied. Heart rate variability-normalized frequency domain indexes were assessed 5 days (baseline) after the onset of uncomplicated AMI and 30 days after therapy with quinapril (n = 30), metoprolol (n = 30), or placebo (n = 30) with a solid-state digital Holter monitor. Normal subjects (n = 30) were used as controls. Quinapril increased parasympathetic and decreased sympathetic modulation, and improved sympathovagal interactions manifested by an increase in normalized high-frequency power (HFP), and a decrease in normalized low-frequency power (LFP), and their ratio (LFP/HFP) during the entire 24-hour period (p<0.001), with maximal effect on the ratio (p<0.0001) between 02.00 to 04.00 A.M., 08.00 to 11.00 A.M., and 19.00 to 22.00 P.M. (delta% ratio -30%, -32%, and -26%, respectively). Metoprolol increased HFP and decreased LFP and the LFP/HFP ratio mainly between 08.00 A.M. to 12.00 noon, and 19.00 to 22.00 P.M. (delta% ratio -21%, and -12% respectively, p<0.001). Heart rate variability indexes in the placebo group and controls remained unchanged 30 days after the baseline study. In conclusion, quinapril increased parasympathetic, and decreased sympathetic and partially restored sympathovagal interaction in patients with uncomplicated AMI during the entire 24-hour period, with peak effect in the early and late morning and evening hours. Metoprolol had a similar effect during the late morning and evening hours, but at a lower level. These effects may prove beneficial in reducing cardiac arrhythmias and acute ischemic syndromes in past-AMI patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Isoquinolines_MeSH S_pharmacology_MeSH Isoquinolines_pharmacology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Parasympathetic_Nervous_System_MeSH S_drug_effects_MeSH Parasympathetic_Nervous_System_drug_effects_MeSH M_Prospective_Studies_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 10577635
----K I
----T Randomised trial of old and new antihypertensive drugs in elderly patients: cardiovascular mortality and morbidity the Swedish Trial in Old Patients with Hypertension-2 study.
----A BACKGROUND: The efficacy of new antihypertensive drugs has been questioned. We compared the effects of conventional and newer antihypertensive drugs on cardiovascular mortality and morbidity in elderly patients. METHODS: We did a prospective, randomised trial in 6614 patients aged 70-84 years with hypertension (blood pressure > or = 180 mm Hg systolic, > or = 105 mm Hg diastolic, or both). Patients were randomly assigned conventional antihypertensive drugs (atenolol 50 mg, metoprolol 100 mg, pindolol 5 mg, or hydrochlorothiazide 25 mg plus amiloride 2.5 mg daily) or newer drugs (enalapril 10 mg or lisinopril 10 mg, or felodipine 2.5 mg or isradipine 2-5 mg daily). We assessed fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease. Analysis was by intention to treat. FINDINGS: Blood pressure was decreased similarly in all treatment groups. The primary combined endpoint of fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease occurred in 221 of 2213 patients in the conventional drugs group (19.8 events per 1000 patient-years) and in 438 of 4401 in the newer drugs group (19.8 per 1000; relative risk 0.99 [95% CI 0.84-1.16], p=0.89). The combined endpoint of fatal and non-fatal stroke, fatal and non-fatal myocardial infarction, and other cardiovascular mortality occurred in 460 patients taking conventional drugs and in 887 taking newer drugs (0.96 [0.86-1.08], p=0.49). INTERPRETATION: Old and new antihypertensive drugs were similar in prevention of cardiovascular mortality or major events. Decrease in blood pressure was of major importance for the prevention of cardiovascular events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Mass_Index_MeSH M_Cerebrovascular_Accident_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Regression_Analysis_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH 
****** 10577448
----K E
----T Metoprolol CR/XL in patients with heart failure: A pilot study examining the tolerability, safety, and effect on left ventricular ejection fraction.
----A BACKGROUND: This study was designed to investigate the tolerability, safety, and effect on left ventricular function of a new long-acting preparation of metoprolol, metoprolol succinate (CR/XL). METHODS AND RESULTS: Sixty patients were randomly assigned with a 2:1 ratio, drug versus placebo, administered with a gradually increasing dose of 12.5 to 150 mg of blinded medication during an 8-week period and continued for 6 months. The average peak dose achieved was 99 mg and 132 mg in the metoprolol succinate and placebo groups, respectively. The drug was well tolerated and there was no significant difference in drug withdrawals, New York Heart Association class, or quality of life assessment. The increase in left ventricular ejection fraction measure at baseline and 6 months measured by radioisotopic ventriculography was greater in the metoprolol succinate group (27. 5% to 36.3%) than in the placebo group (26% to 27.9%) (P <.015). Examination of serial Holter electrocardiographic recordings indicate that metoprolol succinate therapy was associated with a significant (P <.05) decrease in total ventricular ectopy at 8 weeks of therapy and a decrease in ventricular couplets and nonsustained ventricular tachycardia at 8 through 26 weeks of therapy. No changes were observed in plasma norepinephrine during therapy except a transitory significant (P <.05) increase in N terminal proatrial natriuretic factor at 8 weeks in the metoprolol succinate group. CONCLUSIONS: This study indicates that treatment with metoprolol succinate for a 6-month period is safe and well tolerated and is associated with an increase in left ventricular ejection fraction and a decrease in ventricular ectopic beats.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Pilot_Projects_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10580184
----K E
----T Inflammatory and hemostatic markers in relation to cardiovascular prognosis in patients with stable angina pectoris. Results from the APSIS study. The Angina Prognosis Study in Stockholm.
----A Increased inflammatory activity and platelet activation have been associated with an increased risk of cardiovascular (CV) events in epidemiological studies, but their prognostic importance in patients with stable angina pectoris is less well established. The Angina Prognosis Study in Stockholm (APSIS), comprised 809 patients (2766 patient years) with stable angina pectoris on double-blind treatment with verapamil or metoprolol. Plasma levels of fibrinogen and orosomucoid (an acute phase reactant), white blood cell counts (WBC), platelet counts and the urinary excretion of beta-thromboglobulin (reflecting platelet secretion), were related to the risk of CV death (n=36), non-fatal myocardial infarction (MI) (n=30) or revascularization (n=99) in a subgroup of 782 patients. Verapamil and metoprolol had only minor effects on the inflammatory variables. In multivariate Cox regression analyses (adjusted for previous MI, hypertension, diabetes mellitus and smoking), fibrinogen and WBC were independent predictors of CV death or non-fatal MI, as well as the risk of revascularization. Orosomucoid did not carry any independent information. Platelet counts and urinary beta-thromboglobulin were not significantly related to CV prognosis. The treatment given did not significantly influence the prognostic impact of either fibrinogen or WBC. Fibrinogen and WBC were independent predictors of CV death or non-fatal MI as well as disease progression leading to revascularization in patients with stable angina pectoris. As fibrinogen is also an acute-phase reactant, the present findings indicate that inflammatory activity is involved in disease progression in stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_analysis_MeSH Fibrinogen_analysis_MeSH M_Hemostasis_MeSH M_Human_MeSH M_Inflammation_MeSH S_metabolism_MeSH Inflammation_metabolism_MeSH S_pathology_MeSH Inflammation_pathology_MeSH P_Leukocyte_Count_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Orosomucoid_MeSH S_analysis_MeSH Orosomucoid_analysis_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH M_beta-Thromboglobulin_MeSH S_analysis_MeSH beta-Thromboglobulin_analysis_MeSH 
****** 10589613
----K E
----T The hemodynamic effects of anesthetic induction in vascular surgical patients chronically treated with angiotensin II receptor antagonists.
----A The use of angiotensin II receptor subtype-1 antagonists (ARA), recently introduced as antihypertensive drugs, is becoming more prevalent. We studied the prevalence and severity of hypotension after the induction of general anesthesia in 12 patients treated with ARA until the morning of surgery. The hemodynamic response to induction was compared with that of patients treated with beta-adrenergic blockers (BB) and/or calcium channel blockers (CB) (BB/CB group, n = 45) and angiotensin-converting enzyme inhibitors (ACEI) (ACEI group, n = 27). A standardized anesthesia induction protocol was followed for all patients. Hypotension occurred significantly (p < or = 0.05) more often in ARA-treated patients (12 of 12) compared with BB/CB-treated patients (27 of 45) or with ACEI-treated patients (18 of 27). There was a significantly (P < or = 0.001) increased ephedrine requirement in the ARA group (21+/-3 mg) compared with the BB/CB group (10+/-6 mg) or the ACEI group (7+/-4 mg). Hypotension refractory to repeated ephedrine or phenylephrine administration occurred significantly (P < or = 0.05) more in the ARA group (4 of 12) compared with the BB/CB group (0 of 45) or the ACEI group (1 of 27), but it was treated successfully by using a vasopressin system agonist. Treatment with angiotensin II antagonism until the day of surgery is associated with severe hypotension after the induction of anesthesia, which, in some cases, can only be treated with an agonist of the vasopressin system. IMPLICATIONS: Hypotensive episodes occur more frequently after anesthetic induction in patients receiving Angiotensin II receptor subtype-1 antagonists under anesthesia than with other hypotensive drugs. They are less responsive to the vasopressors ephedrine and phenylephrine. The use of a vasopressin system agonist was effective in restoring blood pressure when hypotension was refractory to conventional therapy.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Anesthesia__General_MeSH S_adverse_effects_MeSH Anesthesia__General_adverse_effects_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH S_etiology_MeSH Hypotension_etiology_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Troponin_MeSH S_blood_MeSH Troponin_blood_MeSH P_Vascular_Surgical_Procedures_MeSH M_Vasoconstriction_MeSH S_drug_effects_MeSH Vasoconstriction_drug_effects_MeSH S_physiology_MeSH Vasoconstriction_physiology_MeSH 
****** 10588963
----K E
----T The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group.
----A BACKGROUND: Cardiovascular complications are the most important causes of perioperative morbidity and mortality among patients undergoing major vascular surgery. METHODS: We performed a randomized, multicenter trial to assess the effect of perioperative blockade of beta-adrenergic receptors on the incidence of death from cardiac causes and nonfatal myocardial infarction within 30 days after major vascular surgery in patients at high risk for these events. High-risk patients were identified by the presence of both clinical risk factors and positive results on dobutamine echocardiography. Eligible patients were randomly assigned to receive standard perioperative care or standard care plus perioperative beta-blockade with bisoprolol. RESULTS: A total of 1351 patients were screened, and 846 were found to have one or more cardiac risk factors. Of these 846 patients, 173 had positive results on dobutamine echocardiography. Fifty-nine patients were randomly assigned to receive bisoprolol, and 53 to receive standard care. Fifty-three patients were excluded from randomization because they were already taking a beta-blocker, and eight were excluded because they had extensive wall-motion abnormalities either at rest or during stress testing. Two patients in the bisoprolol group died of cardiac causes (3.4 percent), as compared with nine patients in the standard-care group (17 percent, P=0.02). Nonfatal myocardial infarction occurred in nine patients given standard care only (17 percent) and in none of those given standard care plus bisoprolol (P<0.001). Thus, the primary study end point of death from cardiac causes or nonfatal myocardial infarction occurred in 2 patients in the bisoprolol group (3.4 percent) and 18 patients in the standard-care group (34 percent, P<0.001). CONCLUSIONS: Bisoprolol reduces the perioperative incidence of death from cardiac causes and nonfatal myocardial infarction in high-risk patients who are undergoing major vascular surgery.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Diseases_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH S_prevention_&_control_MeSH Heart_Diseases_prevention_&_control_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_ultrasonography_MeSH Myocardial_Ischemia_ultrasonography_MeSH M_Perioperative_Care_MeSH M_Postoperative_Complications_MeSH S_epidemiology_MeSH Postoperative_Complications_epidemiology_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH P_Vascular_Surgical_Procedures_MeSH 
****** 10593636
----K E
----T Psychological risk factors may moderate pharmacological treatment effects among ischemic heart disease patients. Canadian Amlodipine/Atenolol in Silent Ischemia Study (CASIS) Investigators.
----A BACKGROUND: Numerous research findings support the proposed connection between such psychological characteristics as stress and hostility and the manifestation of disease. However, less evidence is available concerning the role(s) psychological factors might play in the process of disease recovery. METHODS: Eighty patients with known coronary disease and exercise-induced ischemia underwent treadmill exercise testing and 48-hour ambulatory electrocardiographic monitoring and completed a battery of standardized psychological tests assessing hostility, depression, and daily stress on four occasions during a 12-week pharmacological treatment study. After withdrawal of antiischemic drugs at baseline, patients returned for subsequent tests at 3-week intervals. During the second and third intervals, patients were prescribed one of two antiischemic medications, atenolol or amlodipine, or given a placebo. All patients were then placed on a combination treatment protocol for the 3 weeks before the final testing date. RESULTS: The combination treatment produced highly significant benefits across all measured cardiac variables (20.3% improvement in exercise performance, 13% reduction in reported angina, 64.0% reduction in the frequency of ischemic episodes; for all, p < .01). However, results showed that high baseline levels of daily stress were associated with reliably smaller treatment effects on measures of ischemia frequency and treadmill exercise time and with a significantly greater likelihood of reporting angina after treatment (r = -0.24, -0.25, and -0.33, respectively; p <.05). In addition, high baseline hostility predicted significantly smaller diastolic blood pressure improvements (r = -0.29, p < .05). CONCLUSIONS: These results indicate that psychological risk factors may have globally negative effects on the course of treatment and suggest particular factors that may warrant attention in trials targeting cardiac symptom reduction.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Depression_MeSH S_complications_MeSH Depression_complications_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hostility_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_psychology_MeSH Myocardial_Ischemia_psychology_MeSH M_Prospective_Studies_MeSH M_Psychiatric_Status_Rating_Scales_MeSH M_Regression_Analysis_MeSH M_Stress__Psychological_MeSH S_complications_MeSH Stress__Psychological_complications_MeSH M_Support__Non-U_S__Gov't_MeSH P_Type_A_Personality_MeSH 
****** 10592890
----K E
----T [Primary prevention of esophageal variceal rupture: endoscopic ligation or propranolol?]
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Comparative_Study_MeSH P_Endoscopy__Digestive_System_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Ligation_MeSH M_Middle_Aged_MeSH M_Primary_Prevention_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Rupture__Spontaneous_MeSH S_prevention_&_control_MeSH Rupture__Spontaneous_prevention_&_control_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10595953
----K E
----T Ventilatory and heart rate responses to exercise : better predictors of heart failure mortality than peak oxygen consumption.
----A BACKGROUND: An abnormally low chronotropic response and an abnormally high ventilatory response (V(E)/V(CO2)) to exercise are common in patients with severe heart failure, but their relative prognostic impacts have not been well explored. METHODS AND RESULTS: Consecutive patients with heart failure referred for metabolic stress testing who were not taking beta-blockers or intravenous inotropes (n=470) were followed for 1.5 years. The chronotropic index was calculated while peak V(O2) and V(E)/V(CO2) were directly measured. Chronotropic index and peak V(O2) were considered abnormal if in the lowest 25th percentiles of the patient cohort, whereas V(E)/V(CO2) was considered abnormal if in the highest 25th percentile. For comparative purposes, a group of 17 healthy controls underwent metabolic testing as well. Compared with controls, heart failure patients had markedly abnormal ventilatory and chronotropic responses to exercise. In the heart failure cohort, there were 71 deaths. In univariate analyses, predictors of death included high V(E)/V(CO2) low chronotropic index, low V(O2), low resting systolic blood pressure, and older age. Nonparametric Kaplan-Meier plots demonstrated that by dividing the population according to peak V(E)/V(CO2) and peak V(O2), it is possible to identify low, intermediate, and very high risk groups. In multivariate analyses, the only independent predictors of death were high V(E)/V(CO2) (adjusted relative risk [RR] 3.20, 95% CI 1.95 to 5.26, P<0.0001) and low chronotropic index (adjusted RR 1.94, 95% CI 1.18 to 3.19, P=0.0009). CONCLUSIONS: The ventilatory and chronotropic responses to exercise are powerful and independent predictors of heart failure mortality.
----P Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH M_Carbon_Dioxide_MeSH S_analysis_MeSH Carbon_Dioxide_analysis_MeSH M_Chronic_Disease_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Exercise_Test_MeSH P_Exertion_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH P_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Oxygen_MeSH S_analysis_MeSH Oxygen_analysis_MeSH M_Predictive_Value_of_Tests_MeSH M_Pulmonary_Gas_Exchange_MeSH P_Respiration_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH 
****** 10590490
----K I
----T The role of EP-guided therapy in ventricular arrhythmias: beta-blockers, sotalol, and ICD's.
----A Arrhythmic death can be reduced by antiarrhythmic drugs to a range of 24%. Electrophysiologic study by testing noninducibility of ventricular arrhythmia represents the classic method for evaluating the effectiveness of drug therapy.Several clinical studies have shown thaat sotalol suppresses VT induction and prevents arrhythmias recurrences at long term follow-up in 23% to 67% of patients. The efficacy of sotalol EP guided therapy in preventing VT/VF is not necessarily related to prevention of sudden death. In the ESVEM study the superiority of d,l-sotalol to other antiarrhythmic drugs was confirmed. The response to programmed ventricular stimulation was found to be strongly predictive for arrhythmia free state while the failure of sotalol therapy to suppress VT at the EP study was associated with an high recurrence rate (40%). However, EP study failes to predict freedom from sudden death. The beta-blocking activity of racemic sotalol may account for some of the observed survival benefit.Beta-blockers therapy reduces mortality in patients after myocardial infarction primarily by a reduction of sudden death. A reduction of death, worsening heart failure and life threatening ventricular arrhythmias was shown in a recent study on carvedilol. In the prospective study of Steinbeck the EP guided-therapy did not improve the overall outcome when compared to metoprolol. Suppression of inducible arrhythmias by antiarrhythmic drugs was associated with a better outcome. The effectiveness of defibrillator therapy in reducing overall mortality, has been uncertain since great clinical trials have been concluded. MADIT, AVID and CASH trials confirmed the superiority of ICD therapy over antiarrhythmic drugs therapy: ICD should be considered the first choice therapy in post-cardiac arrest patients.The ongoing BEST Trial will give us further responses about the interaction between EP study and metoprolol effect compared to ICD in patients post myocardial infarction also focusing on tolerability and compliance of the beta-blocking therapy in patients with low ejection fraction. In this study will be useful to optimize therapy in patients at high risk of sudden death.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Comparative_Study_MeSH P_Defibrillators__Implantable_MeSH M_Electrophysiology_MeSH S_methods_MeSH Electrophysiology_methods_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH M_Survival_Analysis_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Fibrillation_MeSH S_diagnosis_MeSH Ventricular_Fibrillation_diagnosis_MeSH S_mortality_MeSH Ventricular_Fibrillation_mortality_MeSH S_therapy_MeSH Ventricular_Fibrillation_therapy_MeSH 
****** 10590497
----K E
----T Other primary prevention trials-what is clinically and economically necessary?
----A There are a number of important primary prevention implantable cardioverter defibrillator (ICD) trials underway which will help define the role of the ICD in high risk patients. High risk is defined by low ejection fraction, although a number of electrical markers (e.g., the signal averaged ECG and invasive electrophysiologic test) are also under evaluation. The trials currently underway (including SCD-HEFT, MADIT II, and the CABG-PATCH substudy) are analyzing patients with either coronary or idiopathic cardiomyopathy who have an EF of 35% or under. Patients are randomized to either ICD therapy or no antiarrhythmic drug therapy. Maximal congestive heart failure therapy with ACE inhibitors and beta blockers is used in both arms of each trial. At the conclusion of these trials we should have a better understanding of which group of presumably high risk patients, if any, will benefit from the ICD. Another group of high risk patients that is being encountered more frequently: those who have a high risk diagnosis. These patients are present in such small numbers that a large randomized trial is impossible. As many of these patients are receiving ICDs, a national registry of firing rates will be helpful.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Cardiomyopathy__Congestive_MeSH S_economics_MeSH Cardiomyopathy__Congestive_economics_MeSH S_mortality_MeSH Cardiomyopathy__Congestive_mortality_MeSH S_therapy_MeSH Cardiomyopathy__Congestive_therapy_MeSH M_Coronary_Disease_MeSH S_economics_MeSH Coronary_Disease_economics_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Costs_and_Cost_Analysis_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Primary_Prevention_MeSH S_economics_MeSH Primary_Prevention_economics_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Survival_Analysis_MeSH 
****** 10603666
----K 1
----T [Clinical characteristics and follow-up of patients attending a hospital hypertension clinic. 10-year experience]
----A OBJECTIVE: To analyze the characteristics and control of hypertensive patients visited in a hospital hypertension clinic, dependent of the internal medicine department. METHODS: The study included 597 hypertensive patients, mean age 51.9 years (range 14-85), visited consecutively during the period 1989-1998. We applied the following initial protocol: Usual and orientated HBP anamnesis and physical examination, routine blood and urine test, standard electrocardiography and abdominal echocardiography. If necessary, we indicated other test or special explorations. After every visit, the data were stored into an electronic database, which we analyzed retrospectively to obtain the data of this study. RESULTS: Initial and final BP were: systolic BP 154 +/- 25 vs 141 +/- 21 mmHg, Dif. -12.9 (95% CI -14.8 a -11.0), and diastolic BP 96 +/- 12 vs 88 +/- 19 mmHg, Dif. -7.6 (95% CI -8.6 a -6.6). Four hundred and five patients (79.5%) presented I-II OMS stage and 121 (20.2%) III stage. One hundred and seventy-four cardiovascular events were registered. Hypercholesterolemia and obesity were present in 32% of the patients. Seventy-four (10.7%) had secondary HBP. ECA inhibitors were the antihypertensive drugs more used, either associated (58.9%) or as monotherapy (37%). Nine hundred patients (31.8%) presented optimal BP control (< 140/90 mmHg), and 27 (4.5%) refractory HBP. Weight and laboratory values (but uric acid) did not change significantly during the follow-up period. CONCLUSIONS: The patients showed a high prevalence of severe cardiovascular events, and associated risk factors. The 10% presented secondary HBP. About 31% of the patients reached optimal BP control.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_complications_MeSH Cardiovascular_Diseases_complications_MeSH M_Comparative_Study_MeSH M_Data_Interpretation__Statistical_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Outpatients_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH 
****** 10614147
----K 1
----T [Arterial hypertension and systolic left ventricular dysfunction: therapeutic approach]
----A Arterial hypertension is a cardinal precursor of congestive heart failure, and diastolic dysfunction is the most frequent mechanism for it. Systolic left ventricular dysfunction, although less frequent, has a worse prognosis. Most cases of systolic dysfunction in patients with hypertension is due to acute myocardial infarction, although other mechanisms can be involved. In some studies, non-ischemic hypertensive systolic dysfunction is the etiology of chronic heart failure in up to 10% of patients with dilated cardiomyopathy. Diastolic dysfunction and left ventricular hypertrophy are also associated with a higher risk of heart failure and systolic dysfunction. Given the poor prognosis of patients with congestive heart failure and dilated cardiomyopathy, it is fundamental to try to prevent the development of left ventricular dysfunction by means of a correct control of blood pressure, regression of left ventricular hypertrophy and prevention of coronary artery disease. When systolic dysfunction is established, angiotensin converting enzyme inhibitors are the treatment of choice; diuretics and digoxin can be added in patients with overt congestive heart failure. Recent studies suggest that other drugs, such as carvedilol and losartan, can be beneficial, but current evidence is still scarce.
----P Journal_Article 
----M M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Databases__Bibliographic_MeSH M_English_Abstract_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Meta-Analysis_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Systole_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_prevention_&_control_MeSH Ventricular_Dysfunction__Left_prevention_&_control_MeSH 
****** 10619579
----K E
----T The effect of weight loss intervention on antihypertensive medication requirements in the hypertension Optimal Treatment (HOT) study.
----A Obesity is a significant risk factor for hypertension and the cardiovascular sequelae of hypertension. Weight loss has been shown to be effective in lowering blood pressure in overweight individuals. The purpose of this study was to show the impact of a weight loss intervention on overall medication requirements for obese, hypertensive patients. This was a substudy of the Hypertension Optimal Treatment (HOT) study. HOT study patients who had a body mass index > or =27 kg/m2 were randomized to receive either the weight loss intervention, which included dietary counseling and group support, or to serve as the control group. Patients' weights and number of medication steps (per HOT protocol) required to achieve target diastolic blood pressure were measured at 3, 6, 12, 18, 24, and 30 months. Patients in the weight loss group lost significantly more weight than the control group only at 6 months (-3.2+/-4.3 v. -1.8+/-2.7 kg [mean +/- SD] for weight loss group versus control, respectively, P = .05). The weight loss group tended to regain weight after the first 6 months of the study. However, patients in the weight loss group used a significantly fewer number of medication steps than the control group at all time intervals except 3 months. Weight loss appears to be a useful tool in blood pressure management in patients who require medication to control their blood pressure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diet_MeSH M_Disease_Progression_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_therapy_MeSH Obesity_therapy_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH P_Weight_Loss_MeSH 
****** 10618300
----K E
----T Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators.
----A BACKGROUND: Ventricular septal defect (VSD) complicating acute myocardial infarction has been studied primarily in small, prethrombolytic-era trials. Our goal was to determine clinical predictors and angiographic and clinical outcomes of this complication in the thrombolytic era. METHODS AND RESULTS: We compared enrollment characteristics, angiographic patterns, and outcomes (30-day and 1-year mortality) of patients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial with and without a confirmed diagnosis of VSD. Univariable and multivariable analyses were used to assess relations between enrollment factors and the development of VSD. In all, 84 of the 41 021 patients (0.2%) developed VSD, a smaller percentage than reported in the prethrombolytic era. The median time from symptom onset to VSD diagnosis was 1 day. Enrollment factors most associated with this complication were advanced age, anterior infarction, female sex, and no previous smoking. The infarct artery was more often the left anterior descending and more likely to be totally occluded in patients who developed VSD. Mortality at 30 days was higher in patients with VSDs than in those without this complication (73.8% versus 6.8%, P<0.001). Patients with VSDs selected for surgical repair (n=34) had better outcomes than patients treated medically (n=35; 30-day mortality, 47% versus 94%). CONCLUSIONS: Compared with historical control subjects, patients who undergo thrombolysis within 6 hours of infarction onset may have a reduced risk of later VSD. If patients develop this mechanical complication, however, it typically occurs sooner than described in the prethrombolytic era. Despite improvements in medical therapy and percutaneous and surgical techniques, mortality with this complication remains extremely high.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH P_Coronary_Angiography_MeSH M_Coronary_Artery_Bypass_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Catheterization_MeSH M_Heart_Septal_Defects__Ventricular_MeSH S_complications_MeSH Heart_Septal_Defects__Ventricular_complications_MeSH S_radiography_MeSH Heart_Septal_Defects__Ventricular_radiography_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Risk_Factors_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thrombolytic_Therapy_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10624069
----K E
----T Control of tachycardia and hypertension following coronary artery bypass graft surgery: efficacy and haemodynamic effects of esmolol.
----A Hypertension following coronary artery bypass grafting is not uncommon, especially in patients having good left ventricular function. It is often accompanied by tachycardia. The purpose of this study is to determine the efficacy of esmolol in the treatment of tachycardia and hypertension immediately following cardiopulmonary bypass and to study other haemodynamic effects of esmolol. Thirty patients undergoing elective [corrected] coronary artery bypass grafting were included in this prospective study. Morphine-based anaesthetic technique along-with standard bypass techniques were used in all the patients. The study was performed in the operating room about 30-45 minutes after the termination of cardiopulmonary bypass. Patients having a heart rate of more than 90 bpm and systolic blood pressure of more than 130 mm Hg without any inotropic support were included and randomly assigned to esmolol or control group. Esmolol was administered in a bolus dose of 500 micrograms/kg followed by infusion of upto 100 micrograms/kg/min. The patients in the control group were administered comparable volumes of normal saline. Baseline haemodynamic measurements were obtained just before the administration of esmolol or normal saline and were repeated after 5, 10, 15, 30 and 45 min. The baseline measurement in both the groups showed that patients were maintaining a state of hyperdynamic circulation with high systolic blood pressure (esmolol group 148 +/- 15 mm Hg, control group 140 +/- 8 mm Hg; p = NS), heart rate (esmolol group 128 +/- 17 bpm, control group 127 +/- 17 bpm; p = NS) and cardiac index (esmolol group 3.1 +/- 1 L/min/m2, control group 3.3 +/- 0.5 L/min/m2; p = NS). Esmolol decreased systolic blood pressure (p < 0.001), heart rate (p < 0.01) and cardiac index (p < 0.05) at five minutes. These changes persisted throughout the study period. The left ventricular stroke work index decreased at five minutes (p < 0.05) and remained so till 30 minutes. The maximum fall in heart rate (15%) and systolic blood pressure (16%) was observed at 45 minutes. There were no haemodynamic changes in the control group except that cardiac index, stroke volume and left ventricular stroke work index increased at five minutes. We conclude that esmolol lowers the indices of cardiovascular work in patients who demonstrated hyperdynamic circulation. This was achieved by decreasing the heart rate and systolic blood pressure which was accompanied by decrease in cardiac index and left ventricular stroke work index.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiopulmonary_Bypass_MeSH P_Coronary_Artery_Bypass_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Tachycardia_MeSH S_drug_therapy_MeSH Tachycardia_drug_therapy_MeSH S_etiology_MeSH Tachycardia_etiology_MeSH M_Ventricular_Function__Left_MeSH 
****** 10423600
----K I
----T Quality of life before and during antihypertensive treatment: a comparative study of celiprolol and atenolol.
----A Hypertensive patients may be adversely affected by complications and other concomitant processes such as anxiety, sedation, and drug side effects. It has been suggested that some recently developed antihypertensive agents do not affect quality of life by causing adverse effects. We compared the effects of two antihypertensive drugs on quality of life: atenolol, a standard cardioselective beta-blocker, and celiprolol, one of a new class of selective beta-blockers with vasodilatory properties. One hundred thirty-two patients with mild-to-moderate hypertension were eligible to enter a 28-week, double-blind, parallel-group study. The study protocol consisted of a 4-week period on placebo and a 24-week period of dosage-adjusted treatment with either atenolol or celiprolol. We assessed both systolic and diastolic blood pressure and quality of life perception by a selected test battery that included the Bulpitt and Fletcher Quality of Life Questionnaire. Supine blood pressure fell from 167/101 (range 120/95 to 200/116) to 150/92 mm Hg (p < 0. 0001) during celiprolol treatment. This antihypertensive effect was at least as good with celiprolol as with atenolol. Quality of life perception was comparable for the two drugs although adverse effects were seen more frequently with atenolol than with celiprolol, particularly after prolonged treatment. Patient compliance was better for celiprolol than for atenolol. Our results show that the selective beta-blocker with vasodilatory property celiprolol is at least as effective as atenolol and that it is more advantageous in terms of some quality of life variables.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Celiprolol_MeSH S_adverse_effects_MeSH Celiprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10099062
----K E
----T Metoclopramide enhances labetalol-induced antihypertensive effect during handgrip in hypertensive patients.
----A The effects of metoclopramide, labetalol, and metoclopramide plus labetalol treatments on baseline cardiovascular parameters and isometric handgrip-induced changes were evaluated in 11 hypertensive subjects. Although all treatments were effective in reducing resting systolic (SBP) and diastolic (DBP) blood pressures, the combination of metoclopramide and labetalol appeared to provide a greater decrease (changes in SBP/DBP: 15/11 mm Hg, P < 0.05; from 149 +/- 4/95 +/- 4 mm Hg to 134 +/- 5/84 +/- 3 mm Hg) than did labetalol alone (changes in SBP/DBP: 10/9 mm Hg, P < 0.05; from 149 +/- 4/95 +/- 4 to 139 +/- 4/86 +/- 3 mm Hg). At 2 minutes, handgrip increased blood pressure on placebo (changes in SBP/DBP: 34/7 mm Hg, P < 0. 001). In the presence of metoclopramide and metoclopramide plus labetalol, however, handgrip induced lesser increases in blood pressure (changes in SBP/DBP: 23/7 mm Hg, P < 0.01, and 18/4 mm Hg, P < 0.01, for metoclopramide and metoclopramide plus labetalol treatments). We conclude that (1) metoclopramide lowers blood pressure in hypertensive patients; (2) metoclopramide attenuates blood pressure response to isometric handgrip; and (3) both compounds, labetalol and metoclopramide, seem to have a pharmacologic interaction concerning blood pressure decrease. A clinical significance is suggested for the metoclopramide effect.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH P_Hand_Strength_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Labetalol_MeSH S_pharmacology_MeSH Labetalol_pharmacology_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Male_MeSH M_Metoclopramide_MeSH S_pharmacology_MeSH Metoclopramide_pharmacology_MeSH S_therapeutic_use_MeSH Metoclopramide_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10099065
----K E
----T Nebivolol versus nifedipine in the treatment of essential hypertension: a double-blind, randomized, comparative trial.
----A The efficacy and acceptability of 5 mg nebivolol once daily, a long-acting, vasodilating cardioselective beta blocker that additionally facilitates the L-arginine/nitric oxide system, was assessed in a double-blind, randomized trial in comparison with 20 mg nifedipine retard twice daily in patients with essential hypertension. At 2 weeks of treatment, nebivolol was significantly more effective. Thereafter, both drugs effectively and similarly lowered systolic and diastolic pressures without orthostatic effect. Nebivolol had a trough-to-peak antihypertensive effect ratio of 90%. Nifedipine gave the expected side effects of headache, flushing, and edema. Nebivolol was well tolerated. Nebivolol slightly but significantly lowered heart rate. Neither drug adversely affected plasma levels of lipids.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10099075
----K E
----T Low-dose combination treatment for hypertension versus single-drug treatment-bisoprolol/hydrochlorothiazide versus amlodipine, enalapril, and placebo: combined analysis of comparative studies.
----A To assess the efficacy and safety of 2.5, 5, and 10 mg bisoprolol/6. 25 mg hydrochlorothiazide (HCTZ), 2.5, 5, and 10 mg amlodipine; and 5, 10, 20, and 40 mg enalapril in subjects (n = 541) with a sitting diastolic blood pressure of 95 to 114 mm Hg, data from two comparative studies were pooled. All drugs were titrated to a diastolic blood pressure 90 mm Hg or less. Both studies were double-blind, randomized, parallel dose escalation trials with similar designs and included three active treatments. The second study also had a placebo group. The mean change from baseline of systolic and diastolic blood pressure for placebo (n = 79) was -0. 1/-2.2 mm Hg; amlodipine (n = 154), -12.4/-10.3 mm Hg; enalapril (n = 155), -9.4/-8.2 mm Hg; and bisoprolol/HCTZ (n = 155), -14.0/-12.0. Overall efficacy analyses documented a statistically significant decrease in sitting diastolic blood pressure for bisoprolol/6.25 mg HCTZ compared with placebo, amlodipine, and enalapril. There was a significant reduction in sitting systolic blood pressure for bisoprolol/6.25 mg HCTZ compared with placebo and enalapril but not amlodipine. Also, there was a significant decrease in sitting heart rate for bisoprolol/6.25 mg HCTZ (-6.2 beats/min) compared with placebo (+0.1 beats/min), amlodipine (+1.2 beats/min), and enalapril (+0.5 beats/min). The control rate (diastolic blood pressure < or = 90 mm Hg) for bisoprolol/6.25 mg HCTZ (66.5%) was significantly better than for placebo (21.8%) and enalapril (47.1%) but not amlodipine (58.4%). Of those patients achieving and maintaining control, 49% of the bisoprolol/6.25 mg HCTZ subjects were on the lowest two doses compared with 30% of the amlodipine and 26% of the enalapril subjects. Percentages of patients reporting at least one drug-related adverse event through week 12 were 27%, 24%, 28%, and 25% for placebo, bisoprolol/6.25 mg HCTZ, amlodipine, and enalapril (not significant). Lower doses of two drugs in fixed combination can provide as good or better blood pressure control compared with higher doses of a single drug with similar tolerability and safety.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 10630736
----K E
----T Comparative effects of bisoprolol and nitrendipine on exercise capacity in hypertensive patients with regular physical activity.
----A The aim of this study was to evaluate the long-term effects of administering bisoprolol compared with nitrendipine on the duration of the exercise tolerated by male and female patients, aged 18-65 years, having mild to moderate hypertension and taking regular exercise. In this double-blind, randomized prospective study, 96 patients (85 men and 11 women, 48+/-10 years) formed two groups: 49 in the bisoprolol group, and 47 in the nitrendipine group. After a washout period of 14 days, either 10 mg of bisoprolol or 20 mg of nitrendipine was given daily over a treatment period of 12 weeks. During the treatment period, the stability of the physical training was monitored weekly by using a questionnaire. The results of two maximal triangular exercise tolerance tests (ETTs) on an ergometric bicycle performed at D0 under placebo and at D84 under active treatment were compared. No statistical difference was observed between both groups, concerning age, gender, morphologic characteristics, resting cardiovascular parameters, or physical training. Both groups maintained the same training level throughout the study. No significant differences between the groups were noted for duration of ETT [D0 892+/-284 s, D84, 919+/-267 s (NS) vs. D0 929+/-290 s, D84 904+/-324 s (NS)], or maximal work load [D0 190+/-49 W, D84 197+/-48 W (NS) vs. D0 198+/-49 W, D84 196+/-55 W (NS)]. On the other hand, both groups differed in maximal systolic blood pressure [D0 239+/-24 mm Hg, D84 215+/-22 mm Hg (p<0.001) vs. D0 237+/-24 mm Hg, D84 222+/-27 mm Hg (p<0.05)] (p = 0.05), and maximal pulse rate during exercise [141+/-18 vs. 163+/-17] (p<0.001), albeit not in maximal diastolic blood pressure [D0 113+/-13 mm Hg, D84 106+/-17 mm Hg (p<0.05) vs. D0 112+/-13 mm Hg, D84 104+/-15 mm Hg (p<0.05)]. The patient's own perception of the maximal effort (Borg scale) was not significantly different in either of the groups (placebo vs. treatment). Overall, in a population of hypertensive patients taking regular exercise, long-term treatment with bisoprolol produced no significant changes in the duration of peak effort, maximal workload, or the effort perceived by the patients themselves. The effects of regular exercise were comparable in both groups (bisoprolol or nitrendipine). Because previous studies have shown that dihydropyridines do not modify exercise performance in hypertensive patients, it may be concluded that the antihypertensive therapy with bisoprolol is well tolerated in a population of active hypertensive patients during dynamic exercise.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrendipine_MeSH S_therapeutic_use_MeSH Nitrendipine_therapeutic_use_MeSH M_Physical_Fitness_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10631628
----K E
----T Lack of pharmacokinetic interaction between sumatriptan and naproxen.
----A Sumatriptan is a 5HT1D agonist used in the treatment of migraine. Nonsteroidal anti-inflammatory drugs, beta-blockers, and calcium channel-blocking antagonists are used in the prophylaxis of migraine. Hence, there is a need to investigate the interaction of these prophylactic drugs with sumatriptan. The interaction of sumatriptan with propranolol, flunarizine, pizotifen, and butorphanol were reported earlier. Naproxen is shown to be effective in prophylactic treatment of migraine. In this study, the authors have investigated the circadian rhythm effect of naproxen on the pharmacokinetics of sumatriptan at 1000 and 2200 hours. Twelve healthy volunteers were treated with 100 mg sumatriptan succinate either alone or along with 500 mg naproxen orally at either 1000 or 2200 hours in a randomized Latin square design with a washout period of 10 days. Serum samples were collected at predetermined time intervals and analyzed for unchanged sumatriptan by high-performance liquid chromatography. The pharmacokinetic parameters were calculated by using model-independent methods. Naproxen had no statistically significant (p > 0.05) effect on any pharmacokinetic parameters of sumatriptan both at 1000 and 2200 hours treatment. The results of this study suggest that no alteration in the sumatriptan dosage will be necessary for migraine patients taking naproxen prophylactic therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Biological_Availability_MeSH M_Chromatography__High_Pressure_Liquid_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Cyclooxygenase_Inhibitors_MeSH S_blood_MeSH Cyclooxygenase_Inhibitors_blood_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Male_MeSH M_Naproxen_MeSH S_blood_MeSH Naproxen_blood_MeSH M_Serotonin_Agonists_MeSH S_blood_MeSH Serotonin_Agonists_blood_MeSH M_Sumatriptan_MeSH S_blood_MeSH Sumatriptan_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 10631632
----K E
----T Indicators of dysautonomia in severe Guillain-Barre syndrome.
----A This study sought to establish quantitative criteria for dysautonomia in artificially ventilated patients with Guillain-Barre syndrome (GBS). Such criteria would help to identify patients at risk for cardiovascular complications. This retrospective controlled clinical study compared hourly cardiovascular monitoring data from 36 successive, artificially ventilated GBS patients with that from 11 artificially ventilated control patients with myasthenia. Tolerance limits for daily means, extremes, and variations in heart rate (HR) and blood pressure (BP) were estimated from the most abnormal subgroups of the treatment days of our control patients. These exceeded previously suggested arbitrary cutoff values for dysautonomia. The range in systolic BP was increased in 27 GBS patients, despite an upper limit of normal (85 mmHg) that was double the value suggested in previous work. All 16 patients with mean systolic BP above 165 mmHg also had persistent tachycardia (mean HR > 125 bpm), or were treated with beta-blockers. This pattern of sympathetic hyperactivity was combined with probable vagal hyperactivity (bradycardia < 48 bpm) in 6 patients. Hypotension (minimal systolic BP < 85 mmHg) and unprovoked bradycardia indicated sympathetic hypoactivity in 3 patients. Except in one patient who suffered from asystole on his first day on the ICU, all episodes of bradycardia were preceded by increased daily systolic BP variation (> 85 mmHg), which thus proved to be a sensitive and prognostically valuable indicator of dysautonomia in GBS.
----P Journal_Article 
----M M_Autonomic_Nervous_System_Diseases_MeSH S_complications_MeSH Autonomic_Nervous_System_Diseases_complications_MeSH M_Blood_Pressure_MeSH M_Bradycardia_MeSH S_complications_MeSH Bradycardia_complications_MeSH M_Fever_MeSH S_complications_MeSH Fever_complications_MeSH M_Guillain-Barre_Syndrome_MeSH S_complications_MeSH Guillain-Barre_Syndrome_complications_MeSH S_drug_therapy_MeSH Guillain-Barre_Syndrome_drug_therapy_MeSH S_physiopathology_MeSH Guillain-Barre_Syndrome_physiopathology_MeSH S_therapy_MeSH Guillain-Barre_Syndrome_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Hypotension_MeSH S_complications_MeSH Hypotension_complications_MeSH M_Intensive_Care_MeSH M_Respiration__Artificial_MeSH M_Retrospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH M_Tachycardia_MeSH S_complications_MeSH Tachycardia_complications_MeSH 
****** 10634677
----K E
----T Heart Failure Society of America (HFSA) practice guidelines. HFSA guidelines for management of patients with heart failure caused by left ventricular systolic dysfunction--pharmacological approaches.
----A 
----P Guideline Journal_Article Practice_Guideline Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_classification_MeSH Cardiovascular_Agents_classification_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Systole_MeSH M_United_States_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 10636257
----K E
----T Hemodynamic comparison of twice daily metoprolol tartrate with once daily metoprolol succinate in congestive heart failure.
----A OBJECTIVES: To compare the hemodynamic effects of twice daily metoprolol tartrate (MT) and once daily metoprolol succinate (MS) in congestive heart failure patients. BACKGROUND: Adverse hemodynamic effects with MT demonstrated during initiation persist with drug readministration during chronic therapy. METHODS: Patients were randomly assigned to 6.25 mg MT or 25 mg MS orally and the dose was gradually increased to a target of 50 mg twice a day or 100 mg once a day, respectively. Hemodynamic measurements were obtained at baseline and after three months of therapy--both before and after drug readministration. RESULTS: Long term metoprolol therapy produced significant functional, exercise and hemodynamic benefits with no difference in response between either metoprolol preparation in the 27 patients (MT [14], MS [13]). When full dose metoprolol was readministered during chronic therapy, there were parallel adverse hemodynamic effects in both drug groups. Cardiac index decreased by 0.6 liters/min/m2 (p < 0.0001) with MT and by 0.5 liters/min/m2 (p < 0.0001) with MS. Systematic vascular resistance increased by 253 dyne-sec-cm(-5) (p < 0.001) with MT and by 267 dyne-sec-cm(-5) (p < 0.0005) with MS. Stroke volume index decreased by 7.0 ml/m2 (p < 0.0005) with MT and by 6.5 ml/m2 (p < 0.0001) with MS, while SWI decreased by 6.2 g-m/m2 (p < 0.0005) with MT and by 6.0 g-m/m2 (p < 0.001) with MS. CONCLUSION: Metoprolol tartrate and MS produce similar hemodynamic and clinical effects acutely and chronically despite the fourfold greater starting dose of MS used in this study. A more rapid initiation with readily available starting doses of MS may offer distinct advantages compared with MT in treating chronic heart failure patients with beta-adrenergic blocking agents.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 10642347
----K E
----T Influence of the I/D polymorphism of the angiotensin-converting enzyme gene on the outcome of microalbuminuria in essential hypertension.
----A The objective of the present study was to analyze the influence of the I/D polymorphism of the ACE gene on the outcome of microalbuminuria in essential hypertensive patients who were receiving antihypertensive treatment. One hundred thirty-six essential hypertensive patients who were <50 years old and had never previously received treatment with antihypertensive drugs were included in the study. During a 3-year period, patients received nonpharmacological treatment consisting of moderate salt restriction and a low-calorie diet they were obese, with or without a regimen of antihypertensive drugs based on beta-blockers or ACE inhibitors. Hydrochlorothiazide was added when necessary to maintain the blood pressure goal of <135/85 mm Hg. At the beginning of the study and at yearly intervals, systolic and diastolic blood pressures (SBP and DBP, respectively), 24-hour urinary albumin excretion (UAE), renal function, and biochemical profile measurements were made. The insertion/deletion (I/D) polymorphism of the ACE gene was determined through the use of polymerase chain reaction. The variables used in the statistical analysis were the measurements at the start of the study and the increase or decrease detected during the follow-up, estimated as individual specific regression line slope values. At baseline, no differences in blood pressure or UAE values were observed among genotypes. Likewise, the genotype or allele frequency was not significantly different between normoalbuminurics and microalbuminurics. After the 3 treatment years, significant reductions in SBP, DBP, and UAE were found (SBP 151.6+/-17.3 reduced to 137.2+/-14.3 mm Hg, P<0.001; DBP 96.6+/-8.9 reduced to 84.5+/-9.8 mm Hg, P<0.001; UAE 36.7+/-71.5 reduced to 28.3+/-78.6 mg/24 h, P<0. 05). The slopes of these parameters over time did not differ significantly among genotypes. The slope of SBP was the main factor related to the slope of logUAE (P<0.003). A significant positive correlation coefficient between the SBP and logUAE slopes was observed for the DD patients (r=0.57, P<0.0001) but was absent in patients carrying the I allele (II r=-0.03, P=NS; I/D r=0.01, P=NS). Follow-up studies should be used to achieve a better understanding of the impact of candidate gene polymorphisms on the development of hypertension-induced organ damage. Assessment of the I/D polymorphism of the ACE gene may identify subjects who require a greatly lowered blood pressure to prevent organ damage and to reduce hypertension-associated complications and death.
----P Journal_Article 
----M M_Adult_MeSH M_Albuminuria_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH S_genetics_MeSH Albuminuria_genetics_MeSH M_Alleles_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Blood_Pressure_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gene_Frequency_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_genetics_MeSH Peptidyl-Dipeptidase_A_genetics_MeSH P_Polymorphism_(Genetics)_MeSH 
****** 10650299
----K I
----T Predictors of medical events in patients enrolled in the cardiac insufficiency bisoprolol study (CIBIS): a study of the interactions between beta-blocker therapy and occurrence of critical events using analysis of competitive risks.
----A BACKGROUND: The risk of occurrence of medical events in a clinical trial is competitive in nature; that is, in a given patient the risk of having a critical event depends on the amount of time elapsed since random assignment and on the previous events that may have occurred in the patient. The purpose of this study was to examine the relations between baseline variables, the interactions between treatment, bisoprolol, or placebo, and the occurrence of critical events during the CIBIS trial, a mortality and morbidity trial of beta-blockade in patients with heart failure. METHODS AND RESULTS: A Cox model for censored data was used to analyze the relations between baseline variables, total deaths, permanent treatment withdrawals, nonlethal cardiovascular events, and their interactions with bisoprolol or placebo. We examined the influence of treatment on the occurrence of deaths, permanent treatment withdrawals, and nonlethal cardiovascular events by using the technique of event history analysis, which takes into account competitive risks between events. Compared with placebo, bisoprolol reduced mortality rates in patients with a left ventricular ejection fraction < or =20% (relative risk [RR] 0.49; 95% confidence interval [CI] 0.27 to 0.88; P =.02). In patients whose baseline heart rate was in the upper tertile of distribution, permanent treatment withdrawals were less frequent in patients randomly assigned to bisoprolol than in patients randomly assigned to placebo (RR 0.50; 95% CI 0.28 to 0.88; P =.02). Bisoprolol reduced the incidence of nonlethal cardiac events in patients in whom heart failure was present for at least 4 years (RR 0.44; 95% CI 0.27 to 0.71; P <.01). Event history analysis revealed that among patients who died under treatment after having at least 1 nonlethal cardiovascular event, 20 patients were treated with placebo but only 7 patients were treated with bisoprolol (RR 0.41; 95% CI 0.17 to 0.98; P <.05). CONCLUSIONS: Some patients with heart failure derive more benefit from beta-blocker therapy than others. In the CIBIS trial, they are those patients with the lower left ventricular ejection fractions and those who have nonlethal cardiovascular events but in whom beta-blocker therapy is not permanently discontinued.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Survival_Analysis_MeSH 
****** 10650302
----K E
----T Correlates of high HDL cholesterol among women with coronary heart disease.
----A BACKGROUND: The National Cholesterol Education Program (NCEP) has designated high-density lipoprotein cholesterol (HDL-C) > or =60 mg/dL a "negative" coronary heart disease (CHD) risk factor, but a substantial proportion of coronary events occur among women despite high HDL-C levels. METHODS AND RESULTS: The objective of this study was to characterize postmenopausal women with prevalent CHD despite HDL-C > or =60 mg/dL and to identify factors that may attenuate the protective effect of high HDL-C. We analyzed baseline data from a randomized, double-blind study of estrogen/progestin replacement therapy in 2763 postmenopausal women <80 years old with CHD. Demographics, CHD risk factors, medications, anthropometrics, and lipid levels were compared among women with low, normal, and high HDL-C by NCEP criteria with and without stratification by use of lipid-lowering medications. Independent correlates of high HDL-C were determined by logistic regression analysis. HDL-C > or =60 mg/dL was present in 20% of participants. Women with high HDL-C were older, better educated, had fewer CHD risk factors, lower triglyceride levels and total cholesterol/HDL-C ratio, and were more likely to report past estrogen and current calcium antagonist, niacin, and statin use. beta-Blocker, diuretic, and fibrate use was less common. Older age, alcohol consumption, niacin, and calcium antagonist use and prior estrogen use were independently associated with high HDL-C, whereas waist-to-hip ratio, smoking, triglyceride level, and beta-blocker and fibrate use were inversely associated (all P <.05). CONCLUSIONS: High HDL-C, as defined by the NCEP, occurred in 20% of women with CHD in this cohort without a concomitantly higher prevalence of other CHD risk factors. Redefinition of "high" HDL-C levels for women may be warranted.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH M_Double-Blind_Method_MeSH M_Estrogen_Replacement_Therapy_MeSH M_Female_MeSH M_Human_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Logistic_Models_MeSH M_Middle_Aged_MeSH M_Postmenopause_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10652967
----K I
----T Progression from hypertension to heart failure. Mechanisms and management.
----A Patients with hypertension are at increased risk of developing heart failure (HF), but the mechanisms by which hypertension leads to HF have not been clarified [although left ventricular hypertrophy (LVH) is clearly a predictor of an increased risk of HF]. Similarly, although antihypertensive therapy has been shown to reduce the risk of HF in hypertensive patients, it is not known how this benefit is produced and, currently, there is no clear evidence that any class of antihypertensive agent is more effective than any other in this respect. On theoretical grounds, beta-blockers would be expected to be ideal agents for the prevention of HF in hypertensive patients. In addition to control of blood pressure and regression of LVH, they have clear benefits on morbidity and mortality after myocardial infarction (MI), which probably plays a major role in the development of HF in hypertensive patients, and on the prognosis of HF itself. A reduction in long-term mortality after MI has been demonstrated only for non-selective beta-blockers. Carvedilol, a non-selective beta-blocker which also has other ancillary properties including alpha-1-receptor blockade and antioxidant effects and a favourable metabolic profile, may be an appropriate choice for the prevention of HF in hypertensive patients. This is reinforced by the salutary benefits of carvedilol for the reduction in the morbidity and mortality of HF itself.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10654500
----K E
----T The combination of propranolol and magnesium does not prevent postoperative atrial fibrillation.
----A BACKGROUND: Atrial fibrillation is a common complication of cardiovascular surgery. Beta-blockers have been shown to decrease the incidence of postoperative atrial fibrillation. However, the use of magnesium is more controversial. It was our hypothesis that adjunctive magnesium sulfate would improve the efficacy of beta-blockers alone in the prevention of postoperative atrial fibrillation. METHODS: We prospectively randomized 167 coronary artery bypass patients (mean age 61+/-10 years, 115 men) to receive propranolol alone (20 mg four times daily) or propranolol and magnesium (18 g over 24 hours). Magnesium was begun intraoperatively, and propranolol was started on admission to the intensive care unit. RESULTS: Using an intention-to-treat analysis, the incidence of postoperative atrial fibrillation was 19.5% in the propranolol-treated patients and 22.4% in propranolol + magnesium-treated patients (p = 0.65). Because combination therapy resulted in an excess of postoperative hypotension, which required withholding doses of propranolol, an on-treatment analysis was also performed. In this analysis, the incidence of atrial fibrillation was still not significantly different (18.5% in propranolol-treated patients and 10.0% in propranolol + magnesium-treated patients, p = 0.20). CONCLUSIONS: Adjunctive magnesium sulfate, in combination with propranolol, does not decrease the incidence of postoperative atrial fibrillation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Incidence_MeSH M_Infusions__Intravenous_MeSH M_Intraoperative_Care_MeSH M_Length_of_Stay_MeSH M_Magnesium_Sulfate_MeSH S_administration_&_dosage_MeSH Magnesium_Sulfate_administration_&_dosage_MeSH S_adverse_effects_MeSH Magnesium_Sulfate_adverse_effects_MeSH S_therapeutic_use_MeSH Magnesium_Sulfate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_chemically_induced_MeSH Postoperative_Complications_chemically_induced_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Single-Blind_Method_MeSH 
****** 10654875
----K E
----T Pharmacokinetics of bisoprolol and its effect on dialysis refractory hypertension.
----A The efficacy, safety, and pharmacokinetics of bisoprolol were investigated following oral administration once daily for 12 weeks in hyperreninemic patients with dialysis-refractory hypertension. Mean blood pressure rapidly fell from 132 to 112 mmHg in the 5.0-mg/day (n = 6) and from 142 to 128 mmHg in the 2.5-mg/day patients (n = 5), which were accompanied by a fall in plasma renin activity. On nondialysis days, Cmax and T1/2 were significantly higher in patients than in healthy control subjects. However, Cmax in the 2.5-mg/day patients was almost equal to that in healthy control subjects receiving 5.0 mg/day of bisoprolol. Plasma bisoprolol was dialyzable. During the course of the study, dialysis hypotension and bradycardia occurred in two patients receiving 5.0 mg/day of bisoprolol. In conclusion, a daily dose of 2.5 mg bisoprolol seems to be an adequate and relatively effective dose in our patients with dialysis-refractory hypertension.
----P Journal_Article 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Bisoprolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Renal_Dialysis_MeSH 
****** 10653828
----K I
----T Effects of metoprolol CR in patients with ischemic and dilated cardiomyopathy : the randomized evaluation of strategies for left ventricular dysfunction pilot study.
----A BACKGROUND: Metoprolol provides clinical benefits in patients with congestive heart failure (CHF). In this study, we investigated the effects of controlled-release metoprolol (metoprolol CR) on clinical status, on left ventricular (LV) volumes and function, and on neurohumoral activation in a large number of patients with CHF of mixed causes. METHODS AND RESULTS: Four hundred twenty-six patients with symptomatic CHF were randomized to receive metoprolol CR or placebo for 24 weeks. Metoprolol CR did not affect 6-minute walk distance, New York Heart Association functional class, or quality of life. However, there was a significant improvement in measures of LV function with an attenuation in the increase in LV end-diastolic (+23+/-65 mL [placebo] versus +6+/-61 mL, P=0.01) and LV end-systolic (+19+/-55 mL [placebo] versus -2+/-51 mL, P<0.001) volumes after 24 weeks of therapy. LV ejection fraction was unchanged (-0.05% or -0.005) in the placebo group but increased by 2. 4% in the metoprolol CR-treated patients (P=0.001). Patients receiving metoprolol CR had a greater decrease in angiotensin II (P=0.036) and renin (P=0.032) levels but an increase in N-terminal atrial natriuretic peptide and brain natriuretic peptide levels (P<0. 01). There were fewer deaths in the group receiving beta-blockers (3. 4% versus 8.1%), and there was a similar number of patients experiencing the composite outcomes of death or any hospitalization. CONCLUSIONS: When added to ACE inhibitors, angiotensin II receptor antagonists, or both, the use of metoprolol CR improves ventricular function, reduces activation of the renin-angiotensin systems, and results in fewer deaths.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_blood_MeSH Cardiomyopathy__Congestive_blood_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Delayed-Action_Preparations_MeSH M_Dopamine_MeSH S_blood_MeSH Dopamine_blood_MeSH M_Double-Blind_Method_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_blood_MeSH Myocardial_Ischemia_blood_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Pilot_Projects_MeSH M_Placebos_MeSH M_Quality_of_Life_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 10655195
----K 4
----T Comparison of the intraocular pressure lowering effect of latanoprost and a fixed combination of timolol-pilocarpine eye drops in patients insufficiently controlled with beta adrenergic antagonists. French Latanoprost Study Group, and the Swedish Latanoprost Study Group.
----A AIMS: To compare the effect on intraocular pressure (IOP) of latanoprost monotherapy and timolol-pilocarpine in patients with glaucoma or ocular hypertension with inadequately controlled IOP on topical beta adrenergic antagonists. METHODS: This was a multicentre, randomised, observer masked, 6 week study performed in France and Sweden. 23 centres enrolled 237 patients with glaucoma or ocular hypertension and an IOP of at least 22 mm Hg on treatment with topical beta adrenergic antagonists, alone or in combination. After a 21 day run in period on timolol 0.5% twice daily, patients were randomised either to latanoprost 0.005% once daily or to a fixed combination of timolol-pilocarpine twice daily. Changes in mean diurnal IOP from the baseline to the 6 week visit were determined with an analysis of covariance. RESULTS: Mean diurnal IOP was statistically significantly decreased from baseline in both groups (p<0.001). Switching to latanoprost treatment reduced mean diurnal IOP by 5.4 (SEM 0.3) mm Hg (ANCOVA -22%) and switching to timolol-pilocarpine treatment reduced mean diurnal IOP by 4.9 (0.4) mm Hg (-20%). Blurred vision, decreased visual acuity, decreased twilight vision, and headache were statistically significantly more frequent in the timolol-pilocarpine group. CONCLUSIONS: Latanoprost monotherapy was at least as effective as fixed combination timolol-pilocarpine twice daily treatment in reducing mean diurnal IOP in patients not adequately controlled on topical beta adrenergic antagonists. Latanoprost was better tolerated than timolol-pilocarpine regarding side effects. These results indicate that a switch to latanoprost monotherapy can be attempted before combination therapy is initiated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Miotics_MeSH S_therapeutic_use_MeSH Miotics_therapeutic_use_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Pilocarpine_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH M_Prostaglandins_F__Synthetic_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 10655253
----K 3
----T Long-term results of a clinical trial of nadolol with or without isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis.
----A It is clearly established that beta-blockers decrease the risk of a first variceal bleeding in cirrhosis. We have recently shown that the addition of isosorbide mononitrate to nadolol decreases the rate of variceal bleeding in patients with cirrhosis and varices, compared with nadolol alone, after a median follow-up of 30 months. It is not established if the long-term treatment with the combination continues to be beneficial. Therefore, we assessed the long-term effect of this combination on first variceal bleeding, complications, and death. One hundred forty-six cirrhotic patients with esophageal varices included in a previously published multicenter, randomized study comparing nadolol (40-160 mg/d) with the combination nadolol plus isosorbide mononitrate (10-20 mg 3 times per day) were followed up for up to 7 years (median follow-up, 55 months). The primary end-point was variceal bleeding of any severity. Twenty-four patients (16 in the nadolol group, and 8 in the combination group) experienced variceal bleeding (log rank test, P =.02). Cumulative risk of bleeding was 29% and 12%, respectively (95% CI for the difference, 1%-23%). Two and 4 patients, respectively, had bleeding from portal hypertensive gastropathy (log rank test, P =.20). Thirty and 25 patients, respectively, died during follow-up (log rank test, P =.13). Twelve and 10 patients, respectively, had de novo occurrence of ascites during follow-up (log rank test, P =.29). In conclusion, nadolol plus isosorbide mononitrate is significantly more effective than nadolol alone in the long-term use. Side effects are few, and no deleterious effects on ascites occurrence or on survival occur after long-term use of this combination.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Ascites_MeSH S_etiology_MeSH Ascites_etiology_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10666349
----K 5
----T Beta-blockers continue to surprise us.
----A 
----P Journal_Article Review Review__Tutorial 
----M P_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 10672977
----K E
----T Effects of labetalol treatment on the physiological and subjective response to smoked cocaine.
----A Adrenergic receptors mediate some of the physiological and possibly behavioral effects of cocaine. The purpose of this study was to investigate the effect of treatment with a peripherally acting adrenergic blocking drug labetalol on the cardiovascular and subjective response to repeated deliveries of smoked cocaine. In this double-blind, placebo-controlled, crossover study, 12 cocaine users were treated with a single 100 or 200 mg dose of labetalol, or placebo in each of three experimental sessions. Starting 2 h after the medication treatment, subjects received three doses of 0.4 mg/kg smoked cocaine, 30 min apart. Labetalol treatment significantly attenuated the cocaine-induced increases in heart rate and systolic blood pressure. This effect of labetalol on the cardiovascular response did not decrease with repeated cocaine deliveries. The subjective response to smoked cocaine deliveries was not affected by labetalol treatment. These results suggest that labetalol effectively attenuates the systolic blood pressure and heart rate increases induced by repeated doses of smoked cocaine, but does not alter subjective effects.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_Antagonists_MeSH S_pharmacology_MeSH Adrenergic_Antagonists_pharmacology_MeSH M_Behavior__Addictive_MeSH S_psychology_MeSH Behavior__Addictive_psychology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cocaine_MeSH S_administration_&_dosage_MeSH Cocaine_administration_&_dosage_MeSH S_antagonists_&_inhibitors_MeSH Cocaine_antagonists_&_inhibitors_MeSH M_Cocaine-Related_Disorders_MeSH S_psychology_MeSH Cocaine-Related_Disorders_psychology_MeSH M_Crack_Cocaine_MeSH M_Cross-Over_Studies_MeSH M_Dopamine_Uptake_Inhibitors_MeSH S_administration_&_dosage_MeSH Dopamine_Uptake_Inhibitors_administration_&_dosage_MeSH S_antagonists_&_inhibitors_MeSH Dopamine_Uptake_Inhibitors_antagonists_&_inhibitors_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Labetalol_MeSH S_pharmacology_MeSH Labetalol_pharmacology_MeSH M_Male_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 10673253
----K E
----T Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome.
----A BACKGROUND: beta-blockers are routinely prescribed in congenital long-QT syndrome (LQTS), but the effectiveness and limitations of beta-blockers in this disorder have not been evaluated. METHODS AND RESULTS: The study population comprised 869 LQTS patients treated with beta-blockers. Effectiveness of beta-blockers was analyzed during matched periods before and after starting beta-blocker therapy, and by survivorship methods to determine factors associated with cardiac events while on prescribed beta-blockers. After initiation of beta-blockers, there was a significant (P<0.001) reduction in the rate of cardiac events in probands (0.97+/-1.42 to 0.31+/-0.86 events per year) and in affected family members (0. 26+/-0.84 to 0.15+/-0.69 events per year) during 5-year matched periods. On-therapy survivorship analyses revealed that patients with cardiac symptoms before beta-blockers (n=598) had a hazard ratio of 5.8 (95% CI, 3.7 to 9.1) for recurrent cardiac events (syncope, aborted cardiac arrest, or death) during beta-blocker therapy compared with asymptomatic patients; 32% of these symptomatic patients will have another cardiac event within 5 years while on prescribed beta-blockers. Patients with a history of aborted cardiac arrest before starting beta-blockers (n=113) had a hazard ratio of 12.9 (95% CI, 4.7 to 35.5) for aborted cardiac arrest or death while on prescribed beta-blockers compared with asymptomatic patients; 14% of these patients will have another arrest (aborted or fatal) within 5 years on beta-blockers. CONCLUSIONS: beta-blockers are associated with a significant reduction in cardiac events in LQTS patients. However, syncope, aborted cardiac arrest, and LQTS-related death continue to occur while patients are on prescribed beta-blockers, particularly in those who were symptomatic before starting this therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Female_MeSH M_Human_MeSH M_Infant_MeSH M_Long_QT_Syndrome_MeSH S_congenital_MeSH Long_QT_Syndrome_congenital_MeSH S_drug_therapy_MeSH Long_QT_Syndrome_drug_therapy_MeSH S_physiopathology_MeSH Long_QT_Syndrome_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Nadolol_MeSH S_administration_&_dosage_MeSH Nadolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Nadolol_adverse_effects_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH 
****** 10673735
----K E
----T Does the Dundee Step Test predict outcome in treated hypertension? A sub-study protocol for the ASCOT trial. Anglo-Scandinavian Cardiac Outcome Trial.
----A Treated hypertensive subjects may remain five times more likely to die of cardiac and cerebrovascular diseases than normotensive subjects with equivalent resting blood pressure (BP) levels. Research evidence suggests that exercise BP is a better predictor of end-organ damage and mortality than resting BP, and data from our centre show that a significant proportion of treated hypertensives have uncontrolled BP during a 5-min Dundee Step Test. The prognostic usefulness of exercise BP has yet to be translated into clinical practice because of the lack of a suitable technique. The Dundee Step Test is being evaluated in the ASCOT (Anglo-Scandinavian Cardiac Outcome Trial) study, a 5-year follow-up multicentre, multinational trial comparing the effect of newer (amlodipine and perindopril) and older (bendroflumethiazide and atenolol) antihypertensive agents stratified according to cholesterol levels on cardiac outcome. If the value of the Dundee Step Test is proven, then it may be adopted into routine clinical practice for the assessment of exercise BP. This may result in the improved management of hypertension with a subsequent reduction in morbidity and mortality. The publication of this study protocol is meant to be a statement of on-going research which may stimulate interest among those with an interest in this area of research. Journal of Human Hypertension (2000) 14, 75-78.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Predictive_Value_of_Tests_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 10676671
----K E
----T A comparison of angiotensin-converting enzyme inhibitors, calcium antagonists, beta-blockers and diuretic agents on reactive hyperemia in patients with essential hypertension: a multicenter study.
----A OBJECTIVES: The purpose of this study was to compare the effect of different antihypertensive agents, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and diuretic agents on endothelial function. BACKGROUND: Endothelial dysfunction is a component of essential hypertension, and various antihypertensive drugs may be able to restore normal function. METHODS: Forearm blood flow (FBF) was measured in 296 patients with essential hypertension, including 46 untreated subjects using strain-gauge plethysmography during reactive hyperemia and after sublingual administration of nitroglycerin (NTG). Forty-seven normotensive subjects were similarly evaluated as control subjects. RESULTS: The FBF during reactive hyperemia in the 296 hypertensive patients was significantly less than that in age-matched normotensive subjects. The increase in FBF after administration of sublingual NTG was similar in both groups. Systolic and diastolic blood pressures and forearm vascular resistance were greater in the untreated group than in the four treated groups and did not differ with respect to the antihypertensive agent used. The maximal FBF response from reactive hyperemia was significantly greater in the ACE inhibitor-treated group than in the group treated with calcium antagonists, beta-blockers, diuretic agents, or nothing (40.5 +/- 5.2 vs. 32.9 +/- 5.8, 34.0 +/- 5.6, 32.1 +/- 5.9, and 31.9 +/- 5.8 ml/min per 100 ml tissue, p < 0.05, respectively). Reactive hyperemia was similar in the calcium antagonist, beta-blocker, diuretic and untreated groups, and changes in FBF after sublingual NTG administration were similar in all groups. The infusion of NG-monomethyl-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished the enhancement of reactive hyperemia in hypertensive patients treated with ACE inhibitors. CONCLUSIONS: These findings suggest that ACE inhibitors augment reactive hyperemia, an index of endothelium-dependent vasorelaxation, in patients with essential hypertension. This augmentation may be due to increases in NO.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Human_MeSH M_Hyperemia_MeSH S_physiopathology_MeSH Hyperemia_physiopathology_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_diagnostic_use_MeSH Nitroglycerin_diagnostic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 10678340
----K E
----T The evidence regarding the drugs used for ventricular rate control.
----A OBJECTIVE: Our goal was to determine what drugs are most efficacious for controlling the ventricular rate in patients with atrial fibrillation. SEARCH STRATEGY: We conducted a systematic review of the literature published before May 1998, beginning with searches of The Cochrane Collaboration's CENTRAL database and MEDLINE. SELECTION CRITERIA: We included English-language articles describing randomized controlled trials of drugs used for heart rate control in adults with atrial fibrillation. DATA COLLECTION/ANALYSIS: Abstracts of trials were reviewed independently by 2 members of the study team. We reviewed English-language abstracts of non-English-language publications to assess qualitative consistency with our results. MAIN RESULTS: Forty-five articles evaluating 17 drugs met our criteria for review. In the 5 trials of verapamil and 5 of diltiazem, heart rate was reduced significantly (P <.05), both at rest and with exercise, compared with placebo, with equivalent or improved exercise tolerance in 6 of 7 comparisons. In 7 of 12 comparisons of a beta-blocker with placebo, the beta-blocker was efficacious for control of resting heart rate, with evidence that the effect is drug specific, as nadolol and atenolol proved to be most efficacious. All 9 comparisons demonstrated good heart rate control with beta-blockers during exercise, although exercise tolerance was compromised in 3 of 9 comparisons. In 7 of 8 trials, digoxin administered alone slowed the resting heart rate more than placebo, but it did not significantly slow the rate during exercise in 4 studies. The trials evaluating other drugs yielded insufficient evidence to support their use, but those drugs may yet be promising. CONCLUSIONS: The calcium-channel blockers verapamil or diltiazem, or select beta-blockers are efficacious for heart rate control at rest and during exercise for patients with atrial fibrillation without a clinically important decrease in exercise tolerance. Digoxin is useful when rate control during exercise is less a concern.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Bias_(Epidemiology)_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH P_Evidence-Based_Medicine_MeSH M_Exercise_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Research_Design_MeSH S_standards_MeSH Research_Design_standards_MeSH M_Rest_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10680303
----K E
----T A comparison of esmolol & diltiazem for heart rate control during coronary revascularisation on beating heart.
----A This prospective study was done to compare the control of heart rate and haemodynamics during coronary artery revascularisation without cardiopulmonary bypass using either esmolol or diltiazem. Sixty adult patients with one or two vessel coronary artery disease, were randomly divided into 2 equal groups. Group A received a 500 micrograms/kg loading dose of esmolol followed by a 100 micrograms/kg/h infusion, for control of heart rate during surgical anastomosis of the coronary vessel. While Group B received 0.15 mg/kg diltiazem as a loading dose followed by a 5 mg/h infusion for heart rate control, during the anastomosis. It was seen that heart rate control was better in Group A, 51.4 (+/- 1.3) beats/min, than in Group B, 69.6 (+/- 3.9) beats/min but the decrease in heart rate was significant in both the groups at peak effect compared to respective predrug values. Group A patients had unchanged systemic resistance and pulmonary artery wedge pressure but mean pulmonary artery pressure and pulmonary vascular resistance were significantly raised. Group B patients had decreased systemic resistance, mean pulmonary artery pressure and pulmonary artery wedge pressure, and reduced right ventricular stroke work index. We concluded that although esmolol provided dramatically slower heart rates, during surgery, the resulting elevations in mean pulmonary artery pressure and pulmonary vascular resistance would require caution if used in patients with underlying right ventricular dysfunction from ischaemia or infarction. Diltiazem by virtue of its effects on systemic vascular resistance, cardiac output, and lowering of mean arterial pressure may be a better choice in hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Monitoring__Intraoperative_MeSH P_Myocardial_Revascularization_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 10682964
----K 3
----T The long-term safety and efficacy of brinzolamide 1.0% (azopt) in patients with primary open-angle glaucoma or ocular hypertension. The Brinzolamide Long-Term Therapy Study Group.
----A PURPOSE: Oral carbonic anhydrase inhibitors used to treat glaucoma have significant systemic side effects. Brinzolamide 1.0%, a new topical ocular carbonic anhydrase inhibitor, is effective apparently without significant systemic side effects. This study was performed to establish the long-term safety and efficacy of brinzolamide 1.0% two and three times daily for primary open-angle glaucoma and ocular hypertension. METHODS: An 18-month, multicenter, double-masked, parallel, controlled study was conducted. Patients were randomized to brinzolamide two or three times daily or timolol 0.5% twice daily in a 2:2:1 ratio (n = 150, 153, and 75, respectively). Intraocular pressure was measured at 8:00 AM at eligibility and months 1, 3, 6, 9, 12, 15, and 18. Efficacy was based on intraocular pressure reduction from baseline. Safety was also evaluated. RESULTS: All regimens produced clinically relevant and statistically significant (P<.05) intraocular pressure reductions from baseline. Mean changes in intraocular pressure trough measurements ranged from -2.7 to -3.9 mm Hg with brinzolamide twice-daily dosing and -2.8 to -3.8 mm Hg three times daily dosing compared with -4.7 to -5.6 mm Hg with timolol. The intraocular pressure reductions with brinzolamide two and three times daily were clinically and statistically equivalent. One hundred forty-four patients were discontinued from the study after randomization with the most common reasons being the occurrence of an adverse event (46), inadequate intraocular pressure control (23), patient decision unrelated to study medication (11), lost to follow-up (16), and noncompliance (9). Adverse events were nonserious and resolved without sequelae. There were no clinically relevant changes in safety parameters. Brinzolamide produced less ocular discomfort (burning/stinging) than timolol, and total carbonic anhydrase inhibition levels remained below that known to cause systemic side effects. CONCLUSION: Brinzolamide produced significant and equivalent reductions in intraocular pressure when dosed two and three times daily for 18 months. Brinzolamide was safe and well tolerated by patients, with minimal ocular discomfort.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_administration_&_dosage_MeSH Carbonic_Anhydrase_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH S_administration_&_dosage_MeSH Ophthalmic_Solutions_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Safety_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiazines_MeSH S_administration_&_dosage_MeSH Thiazines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Thiazines_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 10682563
----K 1
----T [Changes of plasma endothelin-1 in patients with congestive heart failure and the influence of metoprolol]
----A To investigate the alterations of plasma endothelin-1(ET-1) in patients with congestive heart failure(CHF) and the effects of metoprolol on it, plasma ET-1 and norepinephrine(NE) were measured in 43 patients using radioimmunoassay and high-performance liquid chromatography methods. Twenty-four patients were treated with metoprolol plus the routine therapy while the others were received the routine therapy only. The findings were that levels of plasma ET-1 and NE increased before the treatment, and decreased after the treatment with metoprolol for 1 month. There was no alteration of plasma ET-1 or NE in the control group.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH 
****** 10686705
----K E
----T Glycaemic and blood pressure controls achieved in a cohort of 318 patients with type 2 diabetes.
----A The aim of the study was to evaluate the current antihyperglycaemic and antihypertensive treatment schemes as well as the quality of metabolic control and blood pressure in a population with type 2 diabetes, in view of the United Kingdom Prospective Diabetes Study (UKPDS) data. 318 patients were included. 44% were treated with metformin and/or sulfonylurea. 44% received insulin in monotherapy or combined with oral drugs. HbA1c was 8.0 (7.9-9.4)% (median; percentiles 25-75). Chronic neurological and vascular (micro- and macroangiopathy) complications were present in 21-43% of patients and were related to glycaemic control. (Un)treated hypertension was found in 59% of patients. Main treatments were ACE-inhibitors (40%), calcium channel antagonists and diuretics (20%) and/or beta-blockers (18%). Systolic and diastolic blood pressure were 147 +/- 22 and 86 +/- 12 mm/Hg (mean +/- 1 SD). In conclusion, overall glycaemic control of a type 2 diabetic population remains slightly unsatisfactory in view of the UKPDS recommendations. In contrast, blood pressure control was adequate.
----P Journal_Article 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH M_Diabetic_Neuropathies_MeSH S_etiology_MeSH Diabetic_Neuropathies_etiology_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_analysis_MeSH Hemoglobin_A__Glycosylated_analysis_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Insulin_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Male_MeSH M_Metformin_MeSH S_therapeutic_use_MeSH Metformin_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Sulfonylurea_Compounds_MeSH S_therapeutic_use_MeSH Sulfonylurea_Compounds_therapeutic_use_MeSH 
****** 10687257
----K E
----T Comparison of trimetazidine with atenolol in patients with syndrome X: effects on diastolic function and exercise tolerance.
----A BACKGROUND: Trimetazidine has been shown to improve anginal symptoms without altering hemodynamic variables in patients with coronary artery disease. The aim of this study was to compare the effect of trimetazidine and atenolol upon symptoms, resting left ventricular filling dynamics and exercise tolerance. METHODS: Sixteen patients (3 males, 13 females, mean age 62 +/- 7 years) were randomized to receive trimetazidine for 2 weeks (20 mg 3 times daily) or atenolol (100 mg daily), according to a double-blind, randomized, cross-over, placebo-controlled design. At the end of each treatment period patients underwent symptom-limited exercise testing, an echocardiogram and a Doppler assessment of transmitral flow pattern. Daily life anginal symptoms were annotated on a diary throughout the study. Two patients discontinued trimetazidine because of severe palpitations and only 14 patients completed the study. RESULTS: Atenolol significantly reduced the number of anginal episodes as compared to placebo or trimetazidine (0.44 +/- 0.53, 4.8 +/- 4, 2.9 +/- 4.9, p < 0.01). On atenolol, the exercise test was negative in 8 patients, but none of the patients had a negative test while on trimetazidine. Atenolol increased both time to 1 mm ST segment depression (668 +/- 213 vs 838 +/- 81 s, p < 0.05) and Doppler-derived indices of ventricular filling (E/A ratio 0.87 +/- 0.20 vs 1.21 +/- 0.26, p < 0.05). CONCLUSIONS: These results confirm the beneficial effects of atenolol in improving symptoms, exercise performance and diastolic function in syndrome X patients. Trimetazidine did not exert any significant effect on any of the analyzed variables. Since trimetazidine has been previously shown to improve myocardial ischemia in patients with overt coronary artery disease to a similar extent of beta-blockers, it is likely that other mechanisms are responsible for angina in patients with syndrome X.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH S_drug_effects_MeSH Echocardiography__Doppler_drug_effects_MeSH S_methods_MeSH Echocardiography__Doppler_methods_MeSH S_statistics_&_numerical_data_MeSH Echocardiography__Doppler_statistics_&_numerical_data_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH S_methods_MeSH Exercise_Test_methods_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Syndrome_X_MeSH S_diagnosis_MeSH Syndrome_X_diagnosis_MeSH S_drug_therapy_MeSH Syndrome_X_drug_therapy_MeSH S_physiopathology_MeSH Syndrome_X_physiopathology_MeSH M_Trimetazidine_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10694188
----K E
----T Baseline reproducibility of B-mode ultrasonic measurement of carotid artery intima-media thickness: the European Lacidipine Study on Atherosclerosis (ELSA).
----A BACKGROUND AND OBJECTIVE: The European Lacidipine Study of Atherosclerosis (ELSA) is a prospective, randomized, double-blind, multi-national interventional trial to determine the effect of four-year treatment using the calcium antagonist lacidipine versus the beta-blocker atenolol on the progression of carotid atherosclerosis in 2259 asymptomatic hypertensive patients. B-mode ultrasound is used to measure the primary and secondary endpoints including the mean maximum intima-media thickness (IMT) of the carotid bifurcations and the common carotid arteries (CBM(max)), the mean maximum IMT of 12 standard carotid sites (M(max)) and the overall maximum IMT (T(max)). This paper reports the cross-sectional reproducibility of ultrasound measurements at baseline. METHOD: To evaluate measurement reliability, each patient is scanned twice at baseline and again at four annual visits, with 80% of the replicate scans performed by the same sonographer and 20% by a different sonographer; 50% of the replicate scans are read by the same reader and the other 50% by different readers. RESULTS: The overall coefficient of reliability (R) was 0.859 for CBM(max), 0.872 for M(max) and 0.794 for T(max). The reliability for CBM(max) was stable during the 1 3/4-year baseline period (R = 0.848 to 0.953) and was uniform among the 23 field centres (R = 0.798 to 0.926). Intra- and inter-reader reliability were 0.915 and 0.872 respectively, and intra-sonographer reliability was 0.866. CONCLUSION: The results demonstrate that by implementing standardized protocols and strict quality control procedures, highly reliable ultrasonic measurements of carotid artery IMT can be achieved in large multi-national trials.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Arteriosclerosis_MeSH S_drug_therapy_MeSH Arteriosclerosis_drug_therapy_MeSH S_ultrasonography_MeSH Arteriosclerosis_ultrasonography_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carotid_Arteries_MeSH S_ultrasonography_MeSH Carotid_Arteries_ultrasonography_MeSH M_Dihydropyridines_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Europe_MeSH M_Human_MeSH M_Observer_Variation_MeSH M_Prospective_Studies_MeSH M_Quality_Control_MeSH M_Reproducibility_of_Results_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultrasonography_MeSH S_instrumentation_MeSH Ultrasonography_instrumentation_MeSH S_standards_MeSH Ultrasonography_standards_MeSH S_statistics_&_numerical_data_MeSH Ultrasonography_statistics_&_numerical_data_MeSH 
****** 10692737
----K E
----T Treatment with carvedilol is associated with a significant reduction in microalbuminuria: a multicentre randomised study.
----A Patients with mild to moderate essential hypertension (n = 1570) were enrolled in a large, multicentre, randomised, open-label study designed to evaluate the safety and efficacy of different regimens of carvedilol. Reported here are the effects of carvedilol on microalbuminuria (MAU) in a subset of 876 patients who underwent MAU assessment (i.e. the Micral-Test) at baseline and at week 12. MAU was present at baseline in 245 (28%) of these patients. Despite different magnitudes of blood pressure reduction, improvements in MAU were similar in all groups (range 54-60%), with complete disappearance occurring in 48-55% of patients. The decrease in MAU did not correlate with the magnitude of blood pressure reduction, suggesting a possible renal protective effect exerted by carvedilol independent of blood pressure reduction mediated by beta-blockade and vasodilatation.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Albuminuria_MeSH S_drug_therapy_MeSH Albuminuria_drug_therapy_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Diseases_MeSH S_drug_therapy_MeSH Kidney_Diseases_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH 
****** 10695689
----K E
----T Relation of low body mass to death and stroke in the systolic hypertension in the elderly program. The SHEP Cooperative Research Group.
----A BACKGROUND: There are scant data on the effect of body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters) on cardiovascular events and death in older patients with hypertension. OBJECTIVE: To determine if low body mass in older patients with hypertension confers an increased risk of death or stroke. PATIENTS: Participants were 3975 men and women (mean age, 71 years) enrolled in 17 US centers in the Systolic Hypertension in the Elderly Program trial, a randomized, double-blind, placebo-controlled clinical trial of lowdose antihypertensive therapy, with follow-up for 5 years. MAIN OUTCOME MEASURES: Five-year adjusted mortality and stroke rates from Cox proportional hazards analyses. RESULTS: There was no statistically significant relation of death or stroke with BMI in the placebo group (P = .47), and there was a U- or J-shaped relation in the treatment group. The J-shaped relation of death with BMI in the treated group (P = .03) showed that the lowest probability of death for men was associated with a BMI of 26.0 and for women with a BMI of 29.6; the curve was quite flat for women across a wide range of BMIs. For stroke, men and women did not differ, and the BMI nadir for both sexes combined was 29, with risk increasing steeply at BMIs below 24. Those in active treatment, however, had lower death and stroke rates compared with those taking placebo. CONCLUSIONS: Among older patients with hypertension, a wide range of BMIs was associated with a similar risk of death and stroke; a low BMI was associated with increased risk. Lean, older patients with hypertension in treatment should be monitored carefully for additional risk factors.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Body_Mass_Index_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_MeSH M_Sex_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH M_Systole_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 10695358
----K 1
----T [The clinical course of end stage heart disease in 152 patients qualified for heart transplantation in a four year observation]
----A The aim of the study was to analyse the clinical course of pts with end stage disease (ESD) in the period of four years. The study population consisted of 152 pts (132 males, 20 females) at the age of 17-66 years (mean = 48.8 year SD = 9.1) primarily qualified to the heart transplantation (HTX). We analysed the ethiology of cardiac failure, the NYHA class of circulation insufficiency, frequency of occurrence of cardiac arrhythmias and conduction system disturbances in 24-hour ecg monitoring, and the pharmacotherapy efficacy. An ischemic ethiology of cardiac failure we found in 102 pts, cardiomyopathy (idiopathic, hypertrophic or postinfectious) in 46 and unoperable valvular disease--in 4. Ten pts were in II NYHA class, 112 in III, and 30 in IV. Left ventricular ejection fraction (echo assessed) ranged from 11% to 40%(mean = 24.9%), LVEDd = 46-111 mm (mean = 80.9 mm), LVESd = 34-83.5 mm(mean = 63 mm). We found IVa class by Lown ventricular arrhythmias (in Holter monitoring) in 38 pts and IVb in 78. Fifty six pts were treated with amiodarone, 10--with beta-blockers and 11 with sotalol. 19 pts were treated by permanent cardiac pacing during the waiting period, 2 ones--by PTCA, 2--by CABG, three ones--by dynamic cardiomyoplasty, and one--by partial aneurysmectomy. One pt was treated by CABG and automatic cardioverter-defibrilator implantation. In 5 cases HTX was delayed because of the positive effect of pharmacotherapy. In assessed period HTX were performed in 64 cases, 31 pts died and 43 are still waiting for the procedure. CONCLUSIONS: During the 4-year period HTX were performed in 42% of waiting pts. Mortality in this group was 38.2%. In 9 pts (5.9%) the alternative methods of surgical treatment were applicable. In 5 pts (3.9) the decision about HTX was delayed because of the positive change of the clinical status. This fact confirms the necessity of the waiting list verification.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Arrhythmia_MeSH S_diagnosis_MeSH Arrhythmia_diagnosis_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_epidemiology_MeSH Arrhythmia_epidemiology_MeSH M_Comorbidity_MeSH M_Disease_Progression_MeSH M_Electrocardiography__Ambulatory_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Heart_Transplantation_MeSH S_statistics_&_numerical_data_MeSH Heart_Transplantation_statistics_&_numerical_data_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_epidemiology_MeSH Myocardial_Ischemia_epidemiology_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH M_Waiting_Lists_MeSH 
****** 10694831
----K E
----T Induction of insulin resistance by beta-blockade but not ACE-inhibition: long-term treatment with atenolol or trandolapril.
----A The effects on glucose metabolism by the beta-blocker atenolol and the angiotensin-converting enzyme (ACE)-inhibitor trandolapril were investigated in a randomised double-blind parallel group study of patients with primary hypertension. Twenty-six patients were treated with 50-100 mg atenolol and 27 patients with 2-4 mg trandolapril o.d. Intravenous glucose tolerance tests, euglycaemic hyperinsulinaemic clamps and serum lipid measurements were performed after 8 and 48 weeks of active treatment. After 48 weeks insulin sensitivity was reduced by 23% by atenolol while it remained unchanged during trandolapril treatment (+0.5%, P = 0.0010 for difference between treatments, ANCOVA). The effect on triglycerides (+22% vs -8.5%) and high-density lipoprotein cholesterol (-13% vs +0.7%) also differed significantly between atenolol and trandolapril. Results after 8 weeks were similar. Glucose tolerance was not affected by either drug. Atenolol reduced diastolic blood pressure (DBP) better than trandolapril (-15.3 mm Hg vs -6.6 mm Hg for supine DBP after 48 weeks, P = 0.012). The difference in effect on insulin sensitivity between the drugs corresponded to 25% of the baseline values of insulin sensitivity, and persisted over 48 weeks of treatment. The choice of antihypertensive treatment could influence the risk of diabetes associated with treated hypertension. Journal of Human Hypertension (2000) 14, 175-180.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Body_Weight_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_MeSH S_physiology_MeSH Glucose_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Insulin_MeSH S_physiology_MeSH Insulin_physiology_MeSH P_Insulin_Resistance_MeSH M_Lipids_MeSH S_metabolism_MeSH Lipids_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Plasminogen_Activator_Inhibitor_1_MeSH S_blood_MeSH Plasminogen_Activator_Inhibitor_1_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 10694836
----K I
----T Bisoprolol and nifedipine retard in elderly hypertensive patients: effect on quality of life.
----A Subjects over the age 60 with sustained sitting diastolic pressures of 95-115 mm Hg were randomised to a regime based on bisoprolol (n = 368) or nifedipine retard (n = 379) for 24 weeks. The goal diastolic pressure was < or =90 mm Hg and to achieve this, double-blind medication could be doubled (5/10 mg bisoprolol, 40/80 mg nifedipine retard) or hydrochlorothiazide 25 mg (unblinded) could be added to the higher dose. In an intention-to-treat analysis, 309 subjects in both the bisoprolol and nifedipine retard treated group provided at least a baseline and a second quality of life assessment (82%). An excess of symptoms was observed in the nifedipine group for oedema of the legs, nocturia, constipation, racing heart and heart thumping. Fewer patients reported wheeze in the nifedipine group. For quality of life, there were no statistically significant differences between the two groups after 8 weeks. However, when analysing the results of the last available assessment (usually at 24 weeks) there were significant (P < 0.05) improvements in tension/anxiety, anger/ hostility, vigour/activity, and confusion/bewilderment, assessed by the Profile of Mood States (POMS) in patients receiving bisoprolol in comparison to those receiving nifedipine retard. The Sickness Impact Profile and objective tests of cognitive function did not differ statistically between the two groups. Quality of life was maintained at a good level on both treatments with advantages for bisoprolol in certain areas. Journal of Human Hypertension (2000) 14, 205-212.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Affect_MeSH S_drug_effects_MeSH Affect_drug_effects_MeSH M_Aged_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cognition_MeSH S_drug_effects_MeSH Cognition_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10698228
----K E
----T Predictors of improvement in left ventricular ejection fraction with carvedilol for congestive heart failure.
----A BACKGROUND: Beta-blocker therapy has been reported to improve survival and left ventricular ejection fraction (LVEF) in the setting of congestive heart failure (CHF). The magnitude and predictors of improved LVEF are unclear. METHODS: A total of 295 patients were enrolled in the study. Inclusion criteria were LVEF <35% at baseline and symptomatic (New York Heart Association class II to IV) CHF despite treatment with at minimum an angiotensin-converting enzyme inhibitor. Carvedilol was initiated at 3.125 mg twice daily and titrated to a target dose of 25 or 50 mg twice daily, depending on the patient's weight. Paired pretreatment baseline and 9 months with treatment follow-up quantitative LVEFs (assessed by resting radionuclide ventriculograms) were obtained in 161 (55 %) of the patients. RESULTS: LVEF improved from 25% +/- 6% at baseline to 36%+/-12% at follow-up (P<.001). Mean change in LVEF (deltaLVEF) was greater for nonischemic cardiomyopathy (NICM) (+14.5+/-2 LVEF points) than ischemic cardiomyopathy (deltaLVEF +/- 7.6+/-10 EF points, P = .001). The deltaLVEF was > or =21 LVEF points in 30% of the NICM group versus 10% of the ischemic cardiomyopathy group. Conversely, the deltaLVEF was unchanged to minimally improved (< or =5 LVEF points) in 21% of the NICM group versus 52% of the ischemic cardiomyopathy group. Multivariable analysis identified NICM and recent onset of congestive heart failure as correlates of improved LVEF. CONCLUSIONS: Carvedilol significantly improved LVEF, especially in patients with NICM and those with recent onset of CHF.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Failure__Congestive_radionuclide_imaging_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH 
****** 10702651
----K E
----T Beta-blockers after myocardial infarction: do benefits ever outweigh risks in asthma?
----A beta-Blockers are well documented to prolong life in patients after myocardial infarction (MI), yet patients who also have asthma are frequently and understandably denied this therapy. We reviewed the literature (via MEDLINE) for the past 35 years for beta-blocker-induced asthma, and reexamined potential beta-blocker use in the context of NIH guidelines for asthma classification and management. Because beta-blockers can cause fatal or life-threatening asthma, their use should be avoided in moderate to severe persistent asthmatics. Benefits of low-dose beta(1)-blockers (e.g. atenolol 50 mg daily) may outweigh risks in some patients with mild intermittent or well-controlled mild persistent asthma. Further study is needed to verify that low doses of beta(1)-blockers are effective in prolonging life after MI, and that use specifically in mild intermittent or mild persistent asthma per NIH classification is safe.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Asthma_MeSH S_complications_MeSH Asthma_complications_MeSH S_genetics_MeSH Asthma_genetics_MeSH M_Bronchial_Spasm_MeSH S_chemically_induced_MeSH Bronchial_Spasm_chemically_induced_MeSH S_drug_therapy_MeSH Bronchial_Spasm_drug_therapy_MeSH S_prevention_&_control_MeSH Bronchial_Spasm_prevention_&_control_MeSH M_Bronchodilator_Agents_MeSH S_therapeutic_use_MeSH Bronchodilator_Agents_therapeutic_use_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Polymorphism_(Genetics)_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__beta-1_antagonists_&_inhibitors_MeSH M_Risk_Assessment_MeSH 
****** 10709160
----K I
----T Lack of interaction between lansoprazole and propranolol, a pharmacokinetic and safety assessment.
----A Due to the prevalence of both gastrointestinal and cardiovascular diseases, it is likely that patients may be coprescribed gastric parietal cell proton pump inhibitors and beta-adrenergic antagonists. Therefore, the objectives of this phase I study were to assess the potential effects of the coadministration of lansoprazole on the pharmacokinetics of propranolol and to evaluate the safety of propranolol with concomitant lansoprazole dosing. In a double-blind fashion, 18 healthy male nonsmokers were initially randomized to receive either 60 mg oral lansoprazole, each morning for 7 days, or an identical placebo (period 1). On day 7, all subjects were concomitantly administered oral propranolol, 80 mg. After a minimum of 1 week following the last dose of either lansoprazole or placebo, subjects were crossed over to the opposite treatment for another 7 days (period 2). Subjects were again administered oral propranolol on day 7. During both treatment periods, blood samples for the determination of plasma propranolol and 4-hydroxy-propranolol were obtained just before the dose and at 0.5, 1, 2, 3, 4, 6, 8 12, 16, 20, and 24 hours postdose. Plasma propranolol and 4-hydroxy-propranolol concentrations were determined by using HPLC with fluorescence detection. The Cmax, tmax, AUC0-infinity, and t1/2 values for propranolol, as well as the AUC0-infinity for 4-hydroxy-propranolol, were calculated and compared between the lansoprazole and placebo regimens. The mean age of the 15 subjects who successfully completed the study was 31 years (range: 24-38 years), and their average weight was 174.8 pounds (range: 145-203 pounds). There were no statistically significant differences between the lansoprazole and placebo regimens for the propranolol Cmax, tmax, AUC0-infinity, and t1/2 values. Also, there were no statistically significant differences between regimens for the 4-OH-propranolol AUC0-infinity. Safety evaluations, which included adverse events, vital signs, clinical laboratory determinations, ECG, and physical examinations, revealed no unexpected clinically significant findings and did not suggest a drug-drug interaction. In conclusion, lansoprazole does not significantly alter the pharmacokinetics of propranolol, suggesting that it does not interact with the CYP2D6- or CYP2C19-mediated metabolism of propranolol. Modification of a propranolol dosage regimen in the presence of lansoprazole is not indicated, based on the pharmacokinetic analysis and the lack of a clinically significant alteration in the pharmacodynamic response.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Anti-Ulcer_Agents_MeSH S_adverse_effects_MeSH Anti-Ulcer_Agents_adverse_effects_MeSH S_pharmacology_MeSH Anti-Ulcer_Agents_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Male_MeSH M_Omeprazole_MeSH S_adverse_effects_MeSH Omeprazole_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Omeprazole_analogs_&_derivatives_MeSH S_pharmacology_MeSH Omeprazole_pharmacology_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Propranolol_pharmacokinetics_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Proton_Pumps_MeSH S_antagonists_&_inhibitors_MeSH Proton_Pumps_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10714728
----K I
----T Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group.
----A CONTEXT: Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored. OBJECTIVE: To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure. DESIGN: Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year. SETTING: Three hundred thirteen sites in 14 countries. PARTICIPANTS: Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy. INTERVENTIONS: Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001). MAIN OUTCOME MEASURES: Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients. RESULTS: The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P<.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P<.001), number of hospitalizations due to worsening heart failure (317 vs 451; P<.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P<.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively). CONCLUSIONS: In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10716137
----K E
----T The carvedilol hibernation reversible ischaemia trial, marker of success (CHRISTMAS) study. Methodology of a randomised, placebo controlled, multicentre study of carvedilol in hibernation and heart failure.
----A BACKGROUND: Carvedilol reduces mortality and improves symptoms and ejection fraction in ischemic heart failure, but its mode of action is not well defined and not all patients respond to treatment. The aim of the CHRISTMAS (Carvedilol Hibernation Reversible Ischaemia Trial, Marker of Success) study is to examine whether hibernation may be a significant factor determining this response. This paper describes the methodology and the rationale for the choice of the nuclear cardiology and echocardiography imaging techniques used in the study. METHODS AND RESULTS: The CHRISTMAS study is a double-blind, randomised, parallel group, multinational study of oral carvedilol versus placebo in patients with chronic stable heart failure due to left ventricular systolic dysfunction from coronary artery disease. The study aims to randomise 400 patients who are on optimal treatment. Two parallel groups will be randomised to carvedilol or placebo, namely 200 with hibernating myocardium at baseline and 200 matched patients without. The presence of hibernation is defined from a mismatch between regional contractile function and regional viability, measured by echocardiography (severe segmental asynergy) and nitrate prepared resting Tc99m-MIBI myocardial perfusion imaging (segmental activity >60%). The primary treatment-related end-point of the study is the comparison of the mean change, from baseline to the final visit, in radionuclide-determined left ventricular ejection fraction in patients on placebo with those on carvedilol, between the groups designated as hibernating and non-hibernating. Other end-points being examined include the prevalence of hibernation in heart failure, the relationship between the volume of hibernating myocardium and the ejection fraction response, the prevalence of reversible ischemia in heart failure, and the comparison of echo with gated SPECT. To date, 303 patients have been screened and 251 patients randomised in the study. The study aims to report in 2000. CONCLUSIONS: The CHRISTMAS study addresses the issue of whether the presence of hibernation is a predictor of the ejection fraction response to carvedilol in heart failure. It also examines the potential role of medical therapy in hibernation as well as a number of other end-points. The study may potentially lead to an important new role for nuclear cardiology in heart failure, and demonstrates important synergy between cardiac imaging and the pharmaceutical industry.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Heart_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Contraction_MeSH S_physiology_MeSH Myocardial_Contraction_physiology_MeSH M_Myocardial_Stunning_MeSH S_drug_therapy_MeSH Myocardial_Stunning_drug_therapy_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Technetium_Tc_99m_Sestamibi_MeSH S_diagnostic_use_MeSH Technetium_Tc_99m_Sestamibi_diagnostic_use_MeSH M_Tomography__Emission-Computed__Single-Photon_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 10718104
----K I
----T Felodipine/metoprolol: a review of the fixed dose controlled release formulation in the management of essential hypertension.
----A The main objective of fixed dose combination therapy for hypertension is to improve blood pressure (BP) control with lower, better tolerated dosages of 2 antihypertensives rather than higher dosages of a single agent. Felodipine and metoprolol lower BP via different, but complementary, mechanisms and controlled release formulations of these 2 drugs are available as a fixed dose combination, felodipine/metoprolol. In clinical trials in patients with hypertension, felodipine/metoprolol was significantly more effective than placebo and the respective monotherapies administered at the same dosages. Mean BP was reduced to < 155/90 mm Hg in patients treated with combination therapy and controlled in approximately 70% of patients. In one study that titrated dosages to effect, fewer felodipine/metoprolol than felodipine or metoprolol monotherapy recipients required dosage increases to achieve BP control (45 vs 60 and 67%, respectively). Data from double blind comparative studies show that the antihypertensive efficacy of felodipine/metoprolol 5 to 10/50 to 100 mg/day is significantly greater than that of enalapril monotherapy or captopril plus hydrochlorothiazide and equivalent to nifedipine/atenolol and amlodipine. In comparisons with enalapril, fewer felodipine/metoprolol than enalapril recipients required dosage titration to achieve BP control. Compared with amlodipine, felodipine/metoprolol significantly reduced mean 24-hour average BP (8.9/5.5 vs 14.4/9.5 mm Hg after 6 weeks; p < 0.001). Both treatments preserved diurnal rhythm. Long term follow-up studies show that the antihypertensive effect of felodipine/metoprolol occurs mostly during the first month of treatment with small additional decreases in BP being observed in the second and third months, and a relatively constant effect thereafter. According to a validated questionnaire, quality of life was relatively similar during 12 weeks treatment with felodipine/metoprolol, enalapril or placebo. In a retrospective pharmacoeconomic analysis conducted in Sweden, felodipine/metoprolol was more cost effective than enalapril as initial treatment for hypertension. Peripheral oedema, headache and flushing were the most commonly reported adverse events with felodipine/metoprolol and felodipine monotherapy, whereas dizziness, fatigue, headache and respiratory infection were more frequent with metoprolol monotherapy. Dose-dependent adverse events such as oedema may occur less often in patients taking lower dosages in combination than in those taking higher dosages of felodipine monotherapy. Thus, patients with hypertension treated with felodipine/metoprolol experience greater control of BP, with less need for dosage titration, than those treated with felodipine, metoprolol or enalapril monotherapy. Importantly this greater efficacy does not appear to be associated with a higher incidence of adverse events relative to monotherapy. Additionally, in short term studies felodipine/metoprolol had a similar (minimal) effect on QOL to enalapril monotherapy but was more cost effective.
----P Journal_Article Review Review__Tutorial 
----M M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_pharmacokinetics_MeSH Felodipine_pharmacokinetics_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH M_Quality_of_Life_MeSH 
****** 10718384
----K I
----T Variceal bleeding and portal hypertension.
----A Within the short span of half a century, the treatment of variceal bleeding has become highly differentiated, with multiple treatment options. Pharmacological therapy with beta-blockers is well established for preventing the first variceal bleeding. The utility of adding a vasodilator to beta-blockers needs to be studied further. Octreotide is widely used as an adjuvant to standard endoscopic treatment to prevent variceal rebleeding, and the utility of this approach has been validated in several randomized controlled trials. Band ligation is well established, and its popularity has increased with the introduction of multiple ligation devices. The technical simplicity and safety of band ligation has sparked interest in using this technique for primary prophylaxis of variceal bleeding. However, randomized trials have not shown any advantage for band ligation over beta-blocker therapy, and the high variceal recurrence rate after band ligation may eliminate any theoretical advantage. A synchronous combination of band ligation and sclerotherapy has not been shown to improve the results of band ligation alone, but a metachronous approach using sclerotherapy to treat recurrent varices after band ligation has shown beneficial results. Histoacryl remains the best treatment option for gastric varices, but band ligation and loop ligation have shown promising results, and should be considered when Histoacryl is not available. Balloon-occluded retrograde transvenous obliteration is a new radiological modality for gastric varices, and one that sounds promising. TIPS is well established as an alternative to elective endoscopic treatment. Compared with endoscopic treatment, TIPS has been shown to improve the survival rate in one randomized trial. However, the cost and complications of TIPS have restricted its use. The use of endoscopic ultrasound for Doppler studies of blood flow in portal hypertension is currently investigational, but it may gain a role in selecting the optimal treatment approach for the individual patient.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Enbucrilate_MeSH M_Endosonography_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Hemostasis__Endoscopic_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Ligation_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Sclerotherapy_MeSH 
****** 10738048
----K E
----T Hypertension and antihypertensive therapy as risk factors for type 2 diabetes mellitus. Atherosclerosis Risk in Communities Study.
----A BACKGROUND: Previous research has suggested that thiazide diuretics and beta-blockers may promote the development of type 2 diabetes mellitus. However, the results of previous studies have been inconsistent, and many studies have been limited by inadequate data on outcomes and by potential confounding. METHODS: We conducted a prospective study of 12,550 adults 45 to 64 years old who did not have diabetes. An extensive health evaluation conducted at base line included assessment of medication use and measurement of blood pressure with a random-zero sphygmomanometer. The incidence of new cases of diabetes was assessed after three years and after six years by measurement of serum glucose concentrations while the subjects were fasting. RESULTS: After simultaneous adjustment for age, sex, race, education, adiposity, family history with respect to diabetes, physical-activity level, other health-related behavior, and coexisting illnesses, subjects with hypertension who were taking thiazide diuretics were not at greater risk for the subsequent development of diabetes than were subjects with hypertension who were not receiving any antihypertensive therapy (relative hazard, 0.91; 95 percent confidence interval, 0.73 to 1.13). Likewise, subjects who were taking angiotensin-converting-enzyme inhibitors and calcium-channel antagonists were not at greater risk than those not taking any medication. In contrast, subjects with hypertension who were taking beta-blockers had a 28 percent higher risk of subsequent diabetes (relative hazard, 1.28; 95 percent confidence interval, 1.04 to 1.57). CONCLUSIONS: Concern about the risk of diabetes should not discourage physicians from prescribing thiazide diuretics to nondiabetic adults who have hypertension. The use of beta-blockers appears to increase the risk of diabetes, but this adverse effect must be weighed against the proven benefits of beta-blockers in reducing the risk of cardiovascular events.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_chemically_induced_MeSH Diabetes_Mellitus__Type_II_chemically_induced_MeSH S_epidemiology_MeSH Diabetes_Mellitus__Type_II_epidemiology_MeSH M_Diuretics__Thiazide_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Prospective_Studies_MeSH M_Regression_Analysis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 10721156
----K 1
----T [A critical analysis of the Hypertension Optimal Treatment (HOT) Study (appeared in Lancet 1998; 351: 1755-1762)]
----A In the HOT-study 18,790 patients in 26 countries (age 50-80 years, mean age 61.5 years) with hypertension (diastolic blood pressure between 100 and 115 mm Hg--mean value 105 mm Hg) were randomised into 3 groups with different target blood pressures (90 mm Hg, 85 mm Hg, 80 mm Hg). The basic treatment was with Felodipin (5 mg q. d.): if the target pressure was not achieved, further steps were initiated: either ACE-inhibitors or -blockers were added, in a third step the Felodipindose was increased to 100 mg and in a further step the doses of ACE-inhibitors or -blockers were doubled. If target pressure was still not achieved, a diuretic was added. Furthermore half of the patients in all groups received either placebo or 75 mg acetyl-salicylic acid. To prevent cardiovascular events the best benefit was shown, when a diastolic pressure of 82.6 mm Hg was reached. Acetyl-salicylic acid showed a further benefit in preventing myocardial infarction, but not in preventing strokes.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 10724047
----K I
----T Beta-adrenergic blocking agents in heart failure: benefits of vasodilating and non-vasodilating agents according to patients' characteristics: a meta-analysis of clinical trials.
----A BACKGROUND: In patients with heart failure, beta-adrenergic blocking agents reduce overall and cardiovascular mortality. This meta-analysis aimed at clarifying their effect on sudden death, the magnitude of their benefit according to the cause of heart failure, and whether there is any difference between vasodilating and nonvasodilating agents. METHODS: Randomized, clinical trials were included if they evaluated a beta-adrenergic blocking agent without intrinsic sympathomimetic activity, included a control group receiving placebo or standard treatment, evaluated mortality on an intention-to-treat basis, and lasted at least 8 weeks. RESULTS: Twenty-one trials with 5,849 patients (3,130 receiving beta-blockers) were included. Median length of treatment was 6 months. Most patients had mild or moderate heart failure and were treated with angiotensin-converting enzyme inhibitors, diuretics, and digitalis. The beta-blockers significantly reduced overall mortality, cardiovascular mortality, and mortality due to pump failure and sudden death by 34% to 39%. The decrease in overall mortality in patients with ischemic heart disease (IHD) (30%) was no different from that among patients with non-IHD (26%) (P = .08). The reduction in overall mortality was greater with vasodilating than with nonvasodilating agents (45% vs 27%; P = .007), particularly in patients without IHD (62%), compared with those with IHD (22%; P =.03). CONCLUSIONS: In patients with heart failure, beta-blockers reduce total and cardiovascular mortality at the expense of a decrease in mortality due to pump failure and sudden death. The magnitude of the benefit is similar in patients with IHD and in those with non-IHD. Vasodilating beta-blockers have a greater effect on overall mortality than nonvasodilating agents, particularly in patients with non-IHD.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10728951
----K E
----T Effectiveness of amiodarone as a single oral dose for recent-onset atrial fibrillation.
----A The efficacy of amiodarone has been proved in long-term maintenance of sinus rhythm (SR) in patients with paroxysmal atrial fibrillation (AF). The present study evaluates the efficacy and safety of a single oral dose of amiodarone in patients with recent-onset AF (<48 hours). Seventy-two patients were randomized to receive 30 mg/kg of either amiodarone or placebo. Conversion to SR was verified by 24-hour Holter monitoring. Ten patients were excluded because of SR in the beginning of monitoring or technical failure during Holter monitoring. The remaining study groups were comparable (n = 31 for each), except that in the placebo group beta blockers were more common. The patients receiving amiodarone converted to SR more effectively than those receiving placebo (p<0.0001). At 8 hours, approximately 50% of patients in the amiodarone group and 20% in the placebo group (Holter successful) had converted to SR, whereas after 24 hours the corresponding figures were 87% and 35%, respectively. The median time for conversion (8.7 hours for amiodarone and 7.9 hours for placebo) did not differ in the groups. Amiodarone was hemodynamically well tolerated, and the number of adverse events in the study groups was similar. Amiodarone as a single oral dose of 30 mg/kg appears to be effective and safe in patients with recent-onset AF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Comparative_Study_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10749962
----K E
----T The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group.
----A BACKGROUND: Patients with hypertension and renal-artery stenosis are often treated with percutaneous transluminal renal angioplasty. However, the long-term effects of this procedure on blood pressure are not well understood. METHODS: We randomly assigned 106 patients with hypertension who had atherosclerotic renal-artery stenosis (defined as a decrease in luminal diameter of 50 percent or more) and a serum creatinine concentration of 2.3 mg per deciliter (200 micromol per liter) or less to undergo percutaneous transluminal renal angioplasty or to receive drug therapy. To be included, patients also had to have a diastolic blood pressure of 95 mm Hg or higher despite treatment with two antihypertensive drugs or an increase of at least 0.2 mg per deciliter (20 micromol per liter) in the serum creatinine concentration during treatment with an angiotensin-converting-enzyme inhibitor. Blood pressure, doses of antihypertensive drugs, and renal function were assessed at 3 and 12 months, and patency of the renal artery was assessed at 12 months. RESULTS: At base line, the mean (+/-SD) systolic and diastolic blood pressures were 179+/-25 and 104+/-10 mm Hg, respectively, in the angioplasty group and 180+/-23 and 103+/-8 mm Hg, respectively, in the drug-therapy group. At three months, the blood pressures were similar in the two groups (169+/-28 and 99+/-12 mm Hg, respectively, in the 56 patients in the angioplasty group and 176+/-31 and 101+/-14 mm Hg, respectively, in the 50 patients in the drug-therapy group; P=0.25 for the comparison of systolic pressure and P=0.36 for the comparison of diastolic pressure between the two groups); at the time, patients in the angioplasty group were taking 2.1+/-1.3 defined daily doses of medication and those in the drug-therapy group were taking 3.2+/-1.5 daily doses (P<0.001). In the drug-therapy group, 22 patients underwent balloon angioplasty after three months because of persistent hypertension despite treatment with three or more drugs or because of a deterioration in renal function. According to intention-to-treat analysis, at 12 months, there were no significant differences between the angioplasty and drug-therapy groups in systolic and diastolic blood pressures, daily drug doses, or renal function. CONCLUSIONS: In the treatment of patients with hypertension and renal-artery stenosis, angioplasty has little advantage over antihypertensive-drug therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH P_Angioplasty__Balloon_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteriosclerosis_MeSH S_therapy_MeSH Arteriosclerosis_therapy_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Renovascular_MeSH S_drug_therapy_MeSH Hypertension__Renovascular_drug_therapy_MeSH S_therapy_MeSH Hypertension__Renovascular_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Renal_Artery_MeSH S_radiography_MeSH Renal_Artery_radiography_MeSH M_Renal_Artery_Obstruction_MeSH S_radiography_MeSH Renal_Artery_Obstruction_radiography_MeSH S_therapy_MeSH Renal_Artery_Obstruction_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10732887
----K E
----T Quality of life after coronary angioplasty or continued medical treatment for angina: three-year follow-up in the RITA-2 trial. Randomized Intervention Treatment of Angina.
----A OBJECTIVES: We sought to evaluate the impact of percutaneous transluminal coronary angioplasty (PTCA) and medical treatment on self-perceived quality of life among patients with angina. BACKGROUND: The second Randomized Intervention Treatment of Angina trial (RITA-2) implemented initial policies of PTCA or continued medical treatment in patients with angina, allowing assessment of long-term health consequences. METHODS: A total of 1,018 patients were randomly assigned (504 to PTCA and 514 to medical treatment). The short form 36 (SF-36) self-administered quality-of-life questionnaire was completed at randomization and three months, one year and three years later. To date, 98% of patients reached one year and 67% reached three years. RESULTS: The PTCA group had significantly greater improvements in physical functioning, vitality and general health at both three months and one year, but not at three years. These quality-of-life scores were strongly related to breathlessness, angina grade and treadmill exercise time both at baseline and at one year. The treatment differences in quality of life are explained by the PTCA group's improvements in breathlessness, angina and exercise time. The attenuation of treatment difference at three years is partly attributed to 27% of medically treated patients receiving nonrandomized interventions in the interim. For both groups, there were also improvements in ratings of physical role functioning, emotional role functioning, social functioning, pain and mental health, but for these the superiority of PTCA over medical treatment was less pronounced. After one year, 33% and 22% of the PTCA and medical groups, respectively, rated their health much better. CONCLUSIONS: Coronary angioplasty substantially improves patient-perceived quality of life, especially physical functioning and vitality, as compared with continued medical treatment. These differences are attributed to alleviation of cardiac symptoms (specifically, breathlessness and angina), but must be balanced against the small procedure-related risks of PTCA.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Activities_of_Daily_Living_MeSH S_classification_MeSH Activities_of_Daily_Living_classification_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_psychology_MeSH Coronary_Disease_psychology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10733260
----K I
----T Beta-blockers for congestive heart failure: what is the current consensus?
----A Despite the availability of angiotensin converting enzyme (ACE) inhibitors for patients with congestive heart failure (CHF), mortality and morbidity remains unacceptably high. CHF is thought to progress as a result of activation of endogenous neurohormonal systems which are activated by the initial myocardial injury. The 2 neurohormonal systems which seem to be important in CHF are the sympathetic nervous system (SNS), and the renin-angiotensin-aldosterone system (RAAS). While stimulation of the SNS has important circulatory support functions in the short term, long term activation appears to have deleterious effects on cardiac function and outcomes. The purpose of this article is to review the literature on the use of beta-blockers in patients with CHF. The published randomised clinical trials of beta-blockers in patients with CHF have shown very promising effects on mortality and morbidity. Several systematic overviews of these trials also suggest beneficial effects on mortality, hospitalisation for CHFE need for transplant, and ejection fraction. The effect of beta-blockers on exercise tolerance. New York Heart Association Function Class (NYHA-FC) and quality of life remain equivocal. The recent presentation of the results from several large-scale trials which were terminated early because of significant survival benefit, has removed any concern over the robustness of the mortality data. Available evidence suggests that a wide variety of patients with CHF, including the elderly, should be considered for beta-blocker therapy. Caution is warranted in the initiation and titration of therapy, as symptoms of CHF may transiently worsen. Whether all beta-blockers are equally efficacious remains unknown.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10735475
----K I
----T Bisoprolol prevents mortality and myocardial infarction after vascular surgery.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Diseases_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Reproducibility_of_Results_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH P_Vascular_Surgical_Procedures_MeSH S_adverse_effects_MeSH Vascular_Surgical_Procedures_adverse_effects_MeSH 
****** 10731399
----K E
----T Systematic review of the management of atrial fibrillation in patients with heart failure.
----A AIMS: To systematically review the management of atrial fibrillation (AF) in patients with heart failure. METHODS: Studies investigating the management of AF in patients with heart failure published between 1967 to 1998 were identified using MEDLINE, the Cochrane register and Embase databases. Reference lists from relevant papers and reviews were hand searched for further papers. RESULTS: Eight studies pertaining to acute and twenty-four pertaining to chronic AF were identified. For patients with acute AF ventricular rate control, anticoagulation and treatment of heart failure should be pursued simultaneously before cardioversion is attempted. Digoxin is relatively ineffective at controlling ventricular response and for cardioversion. Intravenous diltiazem is rapidly effective in controlling ventricular rate and limited evidence suggests it is safe. Amiodarone controls ventricular rate rapidly and increases the rate of cardioversion. There are insufficient data to conclude that immediate anti-coagulation, trans-oesophageal echocardiography to exclude atrial thrombi followed by immediate cardioversion is an appropriate strategy. Patients with chronic AF should be anti-coagulated unless contra-indications exist. It is not clear whether the preferred strategy should be cardioversion and maintenance of sinus rhythm with amiodarone or ventricular rate control of AF combined with anticoagulation to improve outcome including symptoms, morbidity and survival. Electrical cardioversion has a high initial success rate but there is also a high risk of early relapse. Amiodarone currently appears the most effective and safest therapy for maintaining sinus rhythm post-cardioversion. Digoxin is fairly ineffective at controlling ventricular rate during exercise. Addition of a beta-blocker reduces ventricular rate and improves symptoms. Whether digoxin is required in addition to beta-blockade for the control of AF in this setting is currently under investigation. If pharmacological therapy is ineffective or not tolerated then atrio-ventricular node ablation and permanent pacemaker implantation should be considered. CONCLUSION: There is a paucity of controlled clinical trial data for the management of AF among patients with heart failure. The interaction between AF and heart failure means that neither can be treated optimally without treating both. Presently treatment should be on a case by case basis.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Chronic_Disease_MeSH M_Clinical_Trials_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH P_Electric_Countershock_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Retrospective_Studies_MeSH 
****** 10737282
----K I
----T Regional and racial differences in response to antihypertensive medication use in a randomized controlled trial of men with hypertension in the United States. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A BACKGROUND: Stroke incidence and mortality rates are higher in the southeastern region of the United States, which is called the "Stroke Belt." We compared the response to antihypertensive medication use in patients from different US regions. METHODS: The short-term and 1-year efficacy of the antihypertensive medications hydrochlorothiazide, atenolol, diltiazem hydrochloride (sustained release), captopril, prazosin hydrochloride, and clonidine was compared by US region in a randomized controlled trial of 1,105 men with hypertension from 15 US Veterans Affairs medical centers. RESULTS: Compared with patients outside the Stroke Belt, patients inside the Stroke Belt achieved significantly lower treatment success rates of diastolic blood pressure control at 1 year with hydrochlorothiazide (63% vs 41%), atenolol (62% vs 46%), captopril (60% vs 30%), and clonidine (69% vs 43%); there were no differences in treatment success rates with diltiazem (70% vs 71%) or prazosin (54% vs 53%). When controlling for race, patients inside the Stroke Belt had significantly lower treatment success rates with hydrochlorothiazide (P = .003) and clonidine (P = .003), and the lower success rate with atenolol approached significance (P = .15). Regardless of region, blacks were less likely than whites to achieve treatment success with atenolol (P = .02) or prazosin (P = .03) and more likely with diltiazem (P = .05). There was a trend for blacks residing inside the Stroke Belt to have a lower treatment success rate than other race-region groups when treated with captopril (P = .07). Many regional and racial differences in diet, lifestyle, and other characteristics were observed. After adjustment for these characteristics by regression analysis, the effect of residing inside the Stroke Belt remained for captopril (P = .01) and clonidine (P = .01) and approached significance for hydrochlorothiazide (P = .10). CONCLUSIONS: Hypertension in patients residing inside the Stroke Belt responded less to the use of several antihypertensive medications and important differences were shown in a number of characteristics that may affect the control of blood pressure, compared with patients residing outside the Stroke Belt.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_African_Americans_MeSH S_statistics_&_numerical_data_MeSH African_Americans_statistics_&_numerical_data_MeSH M_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_European_Continental_Ancestry_Group_MeSH S_statistics_&_numerical_data_MeSH European_Continental_Ancestry_Group_statistics_&_numerical_data_MeSH M_Hospitals__Veterans_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Southeastern_United_States_MeSH S_epidemiology_MeSH Southeastern_United_States_epidemiology_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 10737284
----K E
----T Olive oil and reduced need for antihypertensive medications.
----A BACKGROUND: The blood pressure (BP) effects of changing the total fat intake and saturated-unsaturated fat ratio are still controversial, despite evidence that saturated fat-enriched diets are associated with higher BP levels. This double-blind, randomized crossover study evaluated a possible difference between antihypertensive effects of monounsaturated (MUFA) (extra-virgin olive oil) and polyunsaturated fatty acids (PUFA) (sunflower oil). METHODS: Twenty-three hypertensive patients were assigned randomly to MUFA or PUFA diet for 6 months and then crossed over to the other diet; effects were evaluated on the basis of daily antihypertensives needed. RESULTS: Diets high in MUFA and PUFA differed from the habitual diet for reduced total and saturated fats, whereas they differed from each other for MUFA (17.2% vs 10.5%) and PUFA content (3.8% vs 10.5%). Resting BP was significantly lower (P = .05 for systolic BP; P = .01 for diastolic BP) at the end of the MUFA diet compared with the PUFA diet. Blood pressure responses during sympathetic stimulation with the cold pressor test and isometric exercise were similar. Daily drug dosage was significantly reduced during the MUFA but not the PUFA diet (-48% vs - 4%, P<.005). All patients receiving the PUFA diet required antihypertensive treatment, whereas 8 of those receiving the MUFA diet needed no drug therapy. CONCLUSIONS: A slight reduction in saturated fat intake, along with the use of extra-virgin olive oil, markedly lowers daily antihypertensive dosage requirement, possibly through enhanced nitric oxide levels stimulated by polyphenols.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Cross-Over_Studies_MeSH M_Dietary_Fats__Unsaturated_MeSH S_administration_&_dosage_MeSH Dietary_Fats__Unsaturated_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Fatty_Acids__Monounsaturated_MeSH S_administration_&_dosage_MeSH Fatty_Acids__Monounsaturated_administration_&_dosage_MeSH M_Fatty_Acids__Unsaturated_MeSH S_administration_&_dosage_MeSH Fatty_Acids__Unsaturated_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_diet_therapy_MeSH Hypertension_diet_therapy_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitric_Oxide_MeSH S_blood_MeSH Nitric_Oxide_blood_MeSH M_Plant_Oils_MeSH S_administration_&_dosage_MeSH Plant_Oils_administration_&_dosage_MeSH M_Treatment_Outcome_MeSH 
****** 10734285
----K E
----T Minimum risk weights for comparing treatments in stratified binomial trials.
----A When comparing two treatments in a stratified trial with a binary endpoint, data are commonly analysed using a weighted averaging of the stratum-specific differences between proportions. Two popular sets of weights are the harmonic means of the stratum-specific sample sizes (SSIZE) and the reciprocals of the variances of the stratum-specific differences (INVAR). Either the SSIZE or INVAR weights are chosen and prespecified in the data analysis plan. We show that the 'wrong' choice between SSIZE and INVAR can result in a significantly inefficient analysis. To circumvent this potential problem, we propose a 'minimum risk' (MR) weighting strategy. The easy-to-compute MR weights are designed to yield more precise and less biased estimates of the overall treatment difference relative to the SSIZE and INVAR weights, respectively. We show, via a simulation study, that the proposed weights are an attractive compromise between the SSIZE and INVAR weights in terms of statistical power. Numerical examples are presented to illustrate the utility of the MR weights.
----P Journal_Article 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Bias_(Epidemiology)_MeSH P_Data_Interpretation__Statistical_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH P_Randomized_Controlled_Trials_MeSH P_Risk_MeSH M_Sample_Size_MeSH 
****** 10740140
----K E
----T Beta-blockade therapy in chronic heart failure: diastolic function and mitral regurgitation improvement by carvedilol.
----A BACKGROUND: In patients with chronic heart failure, the use of carvedilol therapy induces clinical and hemodynamic improvement. However, although the benefits of this beta-blocker have been established in patients with chronic heart failure, the mechanisms underlying them and the changes in left ventricular systolic function, diastolic function, and mitral regurgitation during long-term therapy remain unclear. OBJECTIVE: To identify the clinical and functional effects of carvedilol, focusing on diastolic function and mitral regurgitation variations. METHODS: Forty-five consecutive patients with chronic heart failure (ejection fraction 24% +/- 7%), 17 with dilated ischemic and 28 with nonischemic cardiomyopathy, were treated with carvedilol (mean dose 44 +/- 30 mg) and matched for clinical (New York Heart Association functional class and heart failure duration) and hemodynamic (cardiac index and pulmonary wedge pressure) characteristics to a control group. Clinical and echocardiographic variables were measured in the 2 groups at baseline and after 6 months and the results compared. RESULTS: After 6 months of treatment with carvedilol, left ventricular ejection fraction had increased from 24% +/- 7% to 29% +/- 9% (P <.0001); this change was caused by a reduction in end-systolic volume index (106 +/- 41 vs 93 +/- 37 mL/m(2); P <. 0001). Deceleration time of early diastolic filling increased (134 +/- 74 vs 196 +/- 63 ms; P <.0001). Seventeen of the 27 patients with demonstrated improvement of left ventricular diastolic filling moved from having a restrictive filling pattern to having a normal or pseudonormal left ventricular filling pattern. In the control group, no significant changes in deceleration time of early diastolic filling were found (139 +/- 74 vs 132 +/- 45 ms; P = not significant). The effective regurgitant orifice area decreased significantly in the carvedilol group but not in the control group. These changes were associated with a significant reduction of the mitral regurgitant stroke volume in the carvedilol group (50 +/- 25 vs 16 +/- 13 mL; P <.0001) but not in the control group (57 +/- 29 vs 47 +/- 24 mL; P = not significant). These changes of mitral regurgitation were closely associated with significant improvement of forward aortic stroke volume (r = -.57, P <.0001). These findings were not observed in patients in the control group. CONCLUSIONS: The results of this study show that long-term carvedilol therapy in patients with chronic heart failure was able to prevent or partially reverse progressive left ventricular dilatation. The effects on left ventricular remodeling were associated with a concomitant recovery of diastolic reserve and a decrease of mitral regurgitation, which have been demonstrated to be powerful prognostic predictors in such patients. Overall these findings provide important insights into the pathophysiologic mechanisms by which carvedilol improves the clinical course of patients with chronic heart failure.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Mitral_Valve_Insufficiency_MeSH S_diagnosis_MeSH Mitral_Valve_Insufficiency_diagnosis_MeSH S_drug_therapy_MeSH Mitral_Valve_Insufficiency_drug_therapy_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10746814
----K E
----T Effects of carvedilol on left ventricular regional wall motion in patients with heart failure caused by ischemic heart disease. Australia-New Zealand Heart Failure Research Collaborative Group.
----A BACKGROUND: Beta-blocker therapy has been shown to improve left ventricular (LV) ejection fraction and reduce LV volumes in patients with heart failure caused by ischemic heart disease. However, the possible mechanisms of this improvement and the effects of such treatment on regional wall motion have not been established. In a substudy of the Australia-New Zealand trial of carvedilol in patients with heart failure caused by ischemic heart disease, the effects of treatment on LV regional wall motion were assessed using 2-dimensional echocardiography. METHODS AND RESULTS: One hundred nineteen patients from 10 centers were included on this substudy. Patients were randomly assigned to treatment with carvedilol or placebo. Echocardiography was performed before randomization and after 6 and 12 months of treatment. LV regional wall motion was assessed using a semiquantitative scoring system. LV wall motion score index (WMSI) was reduced from 2.40 to 2.29 after 6 and 12 months in the carvedilol group and remained unchanged in the placebo group (2-tailed P = .005, carvedilol vs placebo). The percentage of myocardium with normal function also significantly improved with carvedilol treatment. CONCLUSIONS: Carvedilol improved LV regional WMSI in patients with heart failure caused by ischemic heart disease. These results indicate a mechanism by which beta-blocker therapy may benefit patients with heart failure and are consistent with an intrinsic improvement in LV function after treatment with carvedilol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10747343
----K E
----T Carvedilol for prevention of restenosis after directional coronary atherectomy : final results of the European carvedilol atherectomy restenosis (EUROCARE) trial.
----A BACKGROUND: In addition to its known properties as a competitive, nonselective beta and alpha-1 receptor blocker, carvedilol directly inhibits vascular myocyte migration and proliferation and exerts antioxidant effects that are considerably greater than those of vitamin E or probucol. This provides the basis for an evaluation of carvedilol for the prevention of coronary restenosis. METHODS AND RESULTS: In a prospective, double-blind, randomized, placebo-controlled trial, 25 mg of carvedilol was given twice daily, starting 24 hours before scheduled directional coronary atherectomy and continuing for 5 months after a successful procedure. The primary end point was the minimal luminal diameter as determined during follow-up angiography 26+/-2 weeks after the procedure. Of 406 randomized patients, 377 underwent attempted atherectomy, and in 324 (88.9%), a </=50% diameter stenosis was achieved without the use of a stent. Evaluable follow-up angiography was available in 292 eligible patients (90%). No differences in minimal luminal diameter (1.99+/-0.73 mm versus 2.00+/-0.74 mm), angiographic restenosis rate (23.4% versus 23.9%), target lesion revascularization (16.2 versus 14.5), or event-free survival (79.2% versus 79.7%) between the placebo and carvedilol groups were observed at 7 months. CONCLUSIONS: The maximum recommended daily dose of the antioxidant and beta-blocker carvedilol failed to reduce restenosis after successful atherectomy. These findings are in contrast to those of the Multivitamins and Probucol Trial, which raises doubts regarding the validity of the interpretation that restenosis reduction by probucol was via antioxidant effects. The relationship between antioxidant agents and restenosis remains to be elucidated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antioxidants_MeSH S_adverse_effects_MeSH Antioxidants_adverse_effects_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH P_Atherectomy__Coronary_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Failure_MeSH 
****** 10748304
----K E
----T Chronic beta-blocker treatment in patients with advanced heart failure. Effects on neurohormones.
----A BACKGROUND: To date, the use of beta-blockers in treating patients with chronic heart failure gains support, this since several large clinical trials reported reduced mortality after chronic beta-blockade. Part of these beneficial effects may result from inhibition of deleterious neurohormone activation that accompanies progression of chronic heart failure. The present study evaluates whether this neurohormone inhibition is preserved after chronic beta-blockade. METHODS: In a retrospective analysis the neurohormonal profiles of patients with moderate to severe chronic heart failure were studied from three treatment subgroups: (1) Without beta-blockers or ACE-inhibitors (n=15), (2) without beta-blockers, with ACE-inhibitors (n=324), (3) with beta-blockers and ACE-inhibitors (n=31). Patients were on beta-blockers for an average period of 3.8 years. Plasma samples were obtained under controlled conditions. RESULTS: Despite uneven group sizes, the groups were well matched for clinical characteristics. Plasma renin levels were significantly lower in patients treated adjunctively with beta-blockers. Plasma aldosterone and endothelin-I levels also tended to be lower after chronic beta-blockade, however, this did not reach statistical significance. CONCLUSIONS: Chronic adjunctive beta-blocker treatment shows significantly lower plasma renin levels when compared to single ACE-inhibition. This persistent reduction of plasma neurohormone activation may concomitantly reduce the chance of neurohormones to escape from inhibition.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH S_drug_effects_MeSH Atrial_Natriuretic_Factor_drug_effects_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH S_drug_effects_MeSH Endothelin-1_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Neuropeptides_MeSH S_blood_MeSH Neuropeptides_blood_MeSH S_drug_effects_MeSH Neuropeptides_drug_effects_MeSH M_Neurotransmitters_MeSH S_blood_MeSH Neurotransmitters_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH S_drug_effects_MeSH Renin_drug_effects_MeSH M_Retrospective_Studies_MeSH 
****** 10752168
----K 1
----T Effects of propranolol on the QT dispersion in congestive heart failure.
----A OBJECTIVE: Studies have shown that therapy with beta-blockers reduces mortality in patients with heart failure. However, there are no studies describing the effects of propranolol on the QT dispersion in this population. The objective of this study was to assess the electrophysiological profile, mainly QT dispersion, of patients with heart failure regularly using propranolol. METHODS: Fifteen patients with heart failure and using propranolol were assessed over a period of 12 months. Twelve-lead electrocardiograms (ECG) were recorded prior to the onset of beta-blocker therapy and after 3 months of drug use. RESULTS: A significant reduction in heart rate, in QT dispersion and in QTc dispersion was observed, as was also an increase in the PR interval and in the QT interval, after the use of propranolol in an average dosage of 100 mg/day. CONCLUSION: Reduction in QT dispersion in patients with heart failure using propranolol may explain the reduction in the risk of sudden cardiac death with beta-blocker therapy, in this specific group of patients.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Electrophysiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 10751738
----K E
----T Endometrial sonographic findings in asymptomatic, hypertensive postmenopausal women.
----A PURPOSE: In this retrospective study, the sonographically measured endometrial thickness in asymptomatic, hypertensive postmenopausal women was compared with that in normotensive postmenopausal women. METHODS: We reviewed clinical and sonographic data on 511 consecutive, unselected, asymptomatic postmenopausal women who attended our hospital for routine gynecologic examinations during a 6-month period. Two hundred nineteen patients (mean age, 60.2 years; age range, 49-81 years) were included in the study. Reasons for exclusion were: clinical data about hypertension were not available (n = 159); the patient had received or was receiving hormonal treatment (n = 78); the patient had undergone a hysterectomy (n = 25); and endometrial thickness could not be determined (n = 30). All patients had been examined using transvaginal or transabdominal sonography. Endometrial thickness was measured at the level of its maximum thickness in the uterine sagittal plane. RESULTS: Fifty-six (26%) of 219 patients were hypertensive. Of these 56 patients, 41 (73%) were receiving drug treatment. The mean endometrial thickness in the hypertensive patients receiving treatment [6.2 mm; 95% confidence interval (CI), 5.1-7.4 mm] was significantly greater than in both the untreated, hypertensive patients (4.3 mm; 95% CI, 3.1-5. 5 mm) (p = 0.008) and the normotensive patients (3.6 mm; 95% CI, 3. 4-3.8 mm) (p < 0.0001). Endometrial thickness was equal to or greater than 5 mm in 59% of the hypertensive patients receiving drug treatment compared with 40% of the untreated, hypertensive patients and 18% of the normotensive patients (p < 0.001). An endometrial stripe was sonographically detected in 22% of the hypertensive patients undergoing treatment, 7% of the hypertensive patients undergoing no treatment, and 1% of the normotensive patients (p < 0. 0001). CONCLUSIONS: Our data indicate that endometrial thickness, which can be determined sonographically, is frequently greater in asymptomatic, hypertensive postmenopausal women receiving antihypertensive drugs than in untreated hypertensive and normotensive patients. This conclusion could have clinical relevance when interpreting endometrial sonographic findings in asymptomatic, hypertensive postmenopausal patients.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Endometrium_MeSH S_anatomy_&_histology_MeSH Endometrium_anatomy_&_histology_MeSH S_drug_effects_MeSH Endometrium_drug_effects_MeSH S_ultrasonography_MeSH Endometrium_ultrasonography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH P_Postmenopause_MeSH M_Retrospective_Studies_MeSH 
****** 10759091
----K I
----T The effects of propranolol on cognitive function and quality of life: a randomized trial among patients with diastolic hypertension.
----A PURPOSE: We sought to determine whether propranolol has adverse effects on cognitive function, depressive symptoms, and sexual function in patients treated for diastolic hypertension. SUBJECTS AND METHODS: We performed a placebo-controlled trial among 312 men and women, 22 to 59 years of age, who had untreated diastolic hypertension (90 to 104 mm Hg). Patients were randomly assigned to treatment with propranolol (80 to 400 mg/day) or matching placebo tablets. Thirteen tests of cognitive function were assessed at baseline, 3 months, and 12 months. Five tests measured reaction time to, or accuracy in, interpreting visual stimuli; one test measured the ability to acquire, reproduce, and change a set of arbitrary stimulus-response sets; and seven tests measured memory or learning verbal information. Depressive symptoms and sexual function were assessed by questionnaires at baseline and 12 months. RESULTS: There were no significant differences by treatment assignment for 11 of the 13 tests of cognitive function at either 3 or 12 months of follow-up. Compared with placebo, participants treated with propranolol had slightly fewer correct responses at 3 months (33 +/- 3 [mean +/- SD] versus 34 +/- 2, P = 0.02) and slightly more errors of commission at 3 months (4 +/-5 versus 3 +/- 3, P = 0.04) and at 12 months (4 +/- 4 versus 3 +/- 3, P = 0.05). At 12 months, depressive symptoms and sexual function and desire did not differ by treatment assignment. CONCLUSIONS: Treatment of hypertension with propranolol had limited adverse effects on tests of cognitive function that were of questionable clinical relevance, and there were no documented adverse effects on depressive symptoms or sexual function. Selection of beta-blockers for treatment of hypertension should be based on other factors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cognition_MeSH S_drug_effects_MeSH Cognition_drug_effects_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH M_Diastole_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Sexual_Behavior_MeSH S_drug_effects_MeSH Sexual_Behavior_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 10759102
----K E
----T The search for high-yield, low-risk antihypertensive treatment.
----A 
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cognition_MeSH S_drug_effects_MeSH Cognition_drug_effects_MeSH M_Comorbidity_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Neuropsychological_Tests_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH M_Sexuality_MeSH S_drug_effects_MeSH Sexuality_drug_effects_MeSH 
****** 10758046
----K E
----T Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan.
----A BACKGROUND: Structural and functional alterations of the vasculature may contribute to complications of hypertension. Because angiotensin II may be pivotal in some of these vascular abnormalities, we tested the hypothesis that the angiotensin type 1 (AT(1)) receptor antagonist losartan, in contrast to the beta-blocker atenolol, would correct resistance artery abnormalities in patients with essential hypertension. METHODS AND RESULTS: Nineteen untreated patients with mild essential hypertension (47+/-2 years, range 30 to 65 years; 57% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for 1 year. Nine age/sex-matched normotensive subjects were also studied. Both treatments reduced blood pressure to a comparable degree (losartan, from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg, P<0.01; atenolol, from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg, P<0.01). Resistance arteries (luminal diameter 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. After 1 year of treatment, the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced (from 8.4+/-0.4% to 6.7+/-0.3%, P<0.01). Arteries from atenolol-treated patients exhibited no significant change (from 8. 3+/-0.3% to 8.8+/-0.5% after treatment). Endothelium-dependent relaxation (acetylcholine-induced) was normalized by losartan (from 82.1+/-4.9% to 94.7+/-1.1%, P<0.01) but not by atenolol (from 80. 4+/-2.7% to 81.7+/-4.6%). Endothelium-independent relaxation (by sodium nitroprusside) was unchanged after treatment. CONCLUSIONS: The AT(1) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension, whereas the beta-blocker atenolol had no effect.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Buttocks_MeSH S_blood_supply_MeSH Buttocks_blood_supply_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelium__Vascular_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH M_Vasodilation_MeSH 
****** 10761206
----K E
----T The sixth Carlos E. Rubio Memorial Lecture. Prevention and treatment of variceal hemorrhage.
----A The medical treatment of portal hypertension has experienced a marked progress in the past decade due to the introduction of effective portal hypotensive therapy. This has been possible because of the better understanding of the pathophysiological mechanisms leading to portal hypertension. A major step forward was the introduction of beta-blockers for the prevention of bleeding and rebleeding from gastroesophageal varices. Effective therapy requires the reduction of the hepatic venous pressure gradient (HVPG) to 12 mmHg or below, or at least by 20% of baseline values. Unfortunately, this is only achieved in 1/3 to 1/2 of patients. Combination therapy, associating isosorbide-5-mononitrate and propranolol or nadolol administration enhances the reduction in portal pressure and increases the number of patients in whom HVPG decreases by more than 20% of baseline values and below 12 mmHg. Randomized clinical trials (RCT's) do support the concept that combination therapy is more effective than propranolol or nadolol alone, significantly better than sclerotherapy, and probably than endoscopic banding ligation. Therapy may be complemented by the association of spironolactone. The main inconvenience of pharmacological therapy is that there is no non-invasive method available to detect non-responders to treatment. Failures of drug therapy should be managed endoscopically. Failures of endoscopic treatment require 'rescue' by means of TIPS or shunt surgery. Patients with advanced liver failure should be considered for orthotopic liver transplantation, and put into a waiting list if eligible. In the treatment of acute variceal bleeding pharmacological therapy offer the unique advantage of allowing to provide specific therapy immediately after arrival to hospital, or even during transferral to hospital by ambulance, since it does not require sophisticated equipment and highly qualified medical staff. Vasopressin has been abandoned because of its toxicity, although this can be reduced by the combined administration of transdermal nitroglycerin. Terlipressin has longer effects and is more effective and safer than vasopressin alone or in combination with nitroglycerin. It has proved to be effective and to decrease mortality from bleeding in double-blind studies. RCT's have shown that this drug is as effective and safer than emergency sclerotherapy. Therapy should be maintained for five days to prevent early rebleeding. Somatostatin is probably as effective as terlipressin. Octreotide is probably useful after endoscopic therapy but can not be recommended as first line treatment. Endoscopic injection sclerotherapy and endoscopic banding ligation are very effective, but require well trained medical staff. There is an increasing trend for initiating therapy with a pharmacological agent, followed by semi-emergency endoscopic therapy as soon as a well trained endoscopist is available (within 12-24 hours), while maintaining drug therapy for 5 days. Failures of medical therapy may be treated by a second session of endoscopic treatment, but if this fails TIPS of emergency surgery should be done. In high-risk situations, such as bleeding from gastric varices or in patients with advanced liver failure, the decision for TIPS or surgery should be done earlier, after failure of the initial treatment.
----P Lectures Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_administration_&_dosage_MeSH Aldosterone_Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_surgery_MeSH Hypertension__Portal_surgery_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Ligation_MeSH M_Liver_Transplantation_MeSH M_Lypressin_MeSH S_administration_&_dosage_MeSH Lypressin_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Lypressin_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Lypressin_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_administration_&_dosage_MeSH Nadolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Nitric_Oxide_Donors_MeSH S_administration_&_dosage_MeSH Nitric_Oxide_Donors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nitric_Oxide_Donors_therapeutic_use_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Sclerotherapy_MeSH M_Spironolactone_MeSH S_administration_&_dosage_MeSH Spironolactone_administration_&_dosage_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasoconstrictor_Agents_MeSH S_administration_&_dosage_MeSH Vasoconstrictor_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10760544
----K 5
----T Therapeutic relevance of pharmacogenetic factors in cardiovascular medicine.
----A The variability in the individual response to drugs may be due either to interindividual variations in the pharmacokinetics of the drugs or to the heterogeneity of the mechanism(s) underlying the diseases, or both. In both cases, genetic heterogeneity is involved in the metabolism of cardiovascular drugs and pathogenesis of inherited cardiovascular disorders. Molecular genetic technologies can now provide sensitive and efficient genetic testing, not only to identify polymorphic drug metabolism genes, but also to identify disease-associated genes for diagnosis and risk stratification of many hereditary cardiovascular diseases. In this review, we discuss the polymorphic metabolism of cardiovascular drugs and the molecular genetics of cardiovascular diseases in relation to the genes determining the responsiveness to a given drug.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_pharmacokinetics_MeSH Cardiovascular_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_genetics_MeSH Cardiovascular_Diseases_genetics_MeSH S_metabolism_MeSH Cardiovascular_Diseases_metabolism_MeSH M_Cytochrome_P-450_Enzyme_System_MeSH S_genetics_MeSH Cytochrome_P-450_Enzyme_System_genetics_MeSH S_metabolism_MeSH Cytochrome_P-450_Enzyme_System_metabolism_MeSH M_Human_MeSH M_Molecular_Biology_MeSH M_Pharmacogenetics_MeSH M_Polymorphism_(Genetics)_MeSH M_Potassium_Channel_Blockers_MeSH M_Sodium_Channel_Blockers_MeSH M_Variation_(Genetics)_MeSH M_Vasodilator_Agents_MeSH S_pharmacokinetics_MeSH Vasodilator_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10776828
----K 5
----T Pharmacological therapy for glaucoma: a review.
----A For some time the medical treatment of glaucoma has consisted of topical beta-blockers, adrenergic agents, miotics and oral carbonic anhydrase inhibitors (CAIs). However, the therapeutic arsenal available for the medical treatment of glaucoma has recently extended with new classes of ocular hypotensive agents i.e. prostaglandins, local CAIs and alpha2-adrenergic agents. Beta-blockers are still the mainstay in glaucoma treatment and are first line drugs. However, even if they are applied once daily, as with timolol in gel forming solution and levobunolol, the possible cardiopulmonary adverse effects of beta-blockers remain a cause for concern. When monotherapy with beta-blockers is ineffective in reducing intraocular pressure (IOP) or is hampered by adverse effects, a change of monotherapy to prostaglandins, local CAIs, alpha2-adrenergic agonists (brimonidine) or to dipivalyl epinephrine is advised. Prostaglandins, local CAIs and alpha2-adrenergic agonists, such as brimonidine, may in time become first line drugs because they reduce IOP effectively and until now systemic adverse effects have rarely been reported with these agents. The development of a pro-drug of either a local CAI or an alpha2-adrenergic agonist with a sustained and continuous effect on IOP level, which could be applied once a day is suggested. Because of these new developments, miotics, i.e. pilocarpine and carbachol, are recommended as second or third line drugs. The cholinesterase inhibitors are considered third line drugs as better agents with fewer local and systemic adverse effects have become available. Oral CAIs may be used temporarily in patients with elevated IOPs e.g. postsurgery or post-laser, or continuously in patients with glaucoma resistant to other treatment. Combining ocular hypotensive drugs is indicated when the target pressure for an individual patient cannot be reached with monotherapy. Combination therapy of beta-blockers is additive with prostaglandins, topical CAIs and miotics. Prostaglandins such as latanoprost can be combined with beta-blockers, adrenergic agents, local CAIs and miotics. Combinations with brimonidine or local CAIs need further investigation. Treatment of glaucoma with the new ocular hypotensive agents, either in monotherapy or combination therapy, may provide lower IOPs and delay or postpone the need for surgery.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Algorithms_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH S_epidemiology_MeSH Glaucoma_epidemiology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Parasympathomimetics_MeSH S_adverse_effects_MeSH Parasympathomimetics_adverse_effects_MeSH S_therapeutic_use_MeSH Parasympathomimetics_therapeutic_use_MeSH M_Sympathomimetics_MeSH S_adverse_effects_MeSH Sympathomimetics_adverse_effects_MeSH S_therapeutic_use_MeSH Sympathomimetics_therapeutic_use_MeSH 
****** 10783226
----K E
----T Myocardial integrated ultrasonic backscatter in patients with dilated cardiomyopathy: prediction of response to beta-blocker therapy.
----A BACKGROUND: Myocardial integrated backscatter (IB) imaging has been reported to be useful for ultrasonic tissue characterization and delineation of myocardial viability or fibrosis. beta-Blocker therapy has beneficial effects for patients with dilated cardiomyopathy (DCM), but there are no clear findings that indicate which patients with DCM will respond to this therapy. This study was performed to evaluate whether myocardial IB analysis can predict the response to beta-blocker therapy. METHODS AND RESULTS: We prospectively performed echocardiographic examination with IB analysis in 29 patients with DCM (20 men, 9 women) before starting bisoprolol therapy and in 15 normal subjects. Standard echocardiographic examination and IB analysis in the left ventricular wall in the 2-dimensional short-axis view were performed and the magnitude of cyclic variation (CV) of IB and calibrated myocardial IB intensity (subtracted pericardial) were obtained from the interventricular septum and the left ventricular posterior wall. Sixteen patients responded to bisoprolol therapy and 13 did not respond after 12 months of full-dose therapy. Calibrated myocardial IB intensity was lower in responders relative to nonresponders in both the interventricular septum (responders, -20.1 +/- 3.6 dB vs nonresponders, -9.8 +/- 5.1 dB, P <.0001; controls, -20.1 +/- 4.4 dB) and posterior wall (responders, -20.6 +/- 3.6 dB vs nonresponders, -14.6 +/- 4.2 dB, P =.0002; controls, -22.7 +/- 3.3 dB). Also, the lower the myocardial intensity in the interventricular septum or posterior wall, the better left ventricular systolic function improved after beta-blocker therapy. However, CV was lower in both DCM groups than in the controls, and CV in the interventricular septum was lower in nonresponders than in responders (responders, 4.0 +/- 4.1 dB vs nonresponders, -0.8 +/- 6. 1 dB, P <.02; controls, 8.3 +/- 2.4 dB). In addition, CV in the posterior wall showed no difference between the 2 DCM groups (responders, 5.6 +/- 1.3 dB vs nonresponders, 5.1 +/- 3.5 dB, P = not significant; controls, 9.6 +/- 2.5 dB). Also, the percent fibrosis on right ventricular endomyocardial biopsy specimens showed no distinctions between these 2 groups (responders, 25.1% +/- 16.1% vs nonresponders, 24.9% +/- 15.0%, P = not significant). CONCLUSIONS: These findings suggest that left ventricular myocardial IB data, especially IB intensity, provide useful information for predicting the response to beta-blocker therapy in patients with DCM. However, right ventricular endomyocardial biopsy findings do not appear to contribute to discriminating between the 2 groups.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Biopsy_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_pathology_MeSH Cardiomyopathy__Congestive_pathology_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH P_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Endocardium_MeSH S_pathology_MeSH Endocardium_pathology_MeSH M_Female_MeSH M_Fibrosis_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_pathology_MeSH Heart_Failure__Congestive_pathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH P_Image_Enhancement_MeSH P_Image_Processing__Computer-Assisted_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Necrosis_MeSH M_Prospective_Studies_MeSH M_Scattering__Radiation_MeSH M_Tissue_Survival_MeSH S_drug_effects_MeSH Tissue_Survival_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10789664
----K E
----T Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). ALLHAT Collaborative Research Group.
----A CONTEXT: Hypertension is associated with a significantly increased risk of morbidity and mortality. Only diuretics and beta-blockers have been shown to reduce this risk in long-term clinical trials. Whether newer antihypertensive agents reduce the incidence of cardiovascular disease (CVD) is unknown. OBJECTIVE: To compare the effect of doxazosin, an alpha-blocker, with chlorthalidone, a diuretic, on incidence of CVD in patients with hypertension as part of a study of 4 types of antihypertensive drugs: chlorthalidone, doxazosin, amlodipine, and lisinopril. DESIGN: Randomized, double-blind, active-controlled clinical trial, the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, initiated in February 1994. In January 2000, after an interim analysis, an independent data review committee recommended discontinuing the doxazosin treatment arm based on comparisons with chlorthalidone. Therefore, outcomes data presented herein reflect follow-up through December 1999. SETTING: A total of 625 centers in the United States and Canada. PARTICIPANTS: A total of 24,335 patients (aged > or = 55 years) with hypertension and at least 1 other coronary heart disease (CHD) risk factor who received either doxazosin or chlorthalidone. INTERVENTIONS: Participants were randomly assigned to receive chlorthalidone, 12.5 to 25 mg/d (n=15,268), or doxazosin, 2 to 8 mg/d (n=9067), for a planned follow-up of 4 to 8 years. MAIN OUTCOME MEASURES: The primary outcome measure was fatal CHD or nonfatal myocardial infarction (MI), analyzed by intent to treat; secondary outcome measures included all-cause mortality, stroke, and combined CVD (CHD death, nonfatal MI, stroke, angina, coronary revascularization, congestive heart failure [CHF], and peripheral arterial disease); compared by the chlorthalidone group vs the doxazosin group. RESULTS: Median follow-up was 3.3 years. A total of 365 patients in the doxazosin group and 608 in the chlorthalidone group had fatal CHD or nonfatal MI, with no difference in risk between the groups (relative risk [RR], 1.03; 95% confidence interval [CI], 0.90-1.17; P=.71). Total mortality did not differ between the doxazosin and chlorthalidone arms (4-year rates, 9.62% and 9.08%, respectively; RR, 1.03; 95% CI, 0.90-1.15; P=.56.) The doxazosin arm, compared with the chlorthalidone arm, had a higher risk of stroke (RR, 1.19; 95% CI, 1.01-1.40; P=.04) and combined CVD (4-year rates, 25.45% vs 21.76%; RR, 1.25; 95% CI, 1.17-1.33; P<.001). Considered separately, CHF risk was doubled (4-year rates, 8.13% vs 4.45%; RR, 2.04; 95% CI, 1.79-2.32; P<.001); RRs for angina, coronary revascularization, and peripheral arterial disease were 1.16 (P<.001), 1.15 (P=.05), and 1.07 (P=.50), respectively. CONCLUSION: Our data indicate that compared with doxazosin, chlorthalidone yields essentially equal risk of CHD death/nonfatal MI but significantly reduces the risk of combined CVD events, particularly CHF, in high-risk hypertensive patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH 
****** 10800794
----K E
----T Ineffectiveness and potential proarrhythmia of atrial pacing for atrial fibrillation prevention after coronary artery bypass grafting.
----A BACKGROUND: Atrial pacing is often used empirically to suppress atrial ectopy and prevent atrial fibrillation after coronary artery bypass grafting. METHODS: To determine whether atrial overdrive pacing reduces atrial fibrillation and atrial ectopy after coronary artery bypass grafting, 100 patients were randomized to no atrial pacing (Control) versus AAI pacing at 10 beats/min or more above the resting heart rate (Paced), started by postoperative day 1 and continued through day 4. Major end points were new atrial fibrillation and frequency of atrial ectopy during the first 4 days after coronary artery bypass grafting. RESULTS: Atrial fibrillation occurred by day 4 in 13 of 51 (25.5%) Paced and in 14 of 49 (28.6%) Control patients, p = 0.90. Control patients who developed atrial fibrillation had significantly more atrial ectopy than those who did not. Atrial ectopy was paradoxically more frequent in the Paced group (2,106+/-428 versus 866+/-385 per 24 hours, p = 0.0001). Loss of capture, sensing, and consistent atrial pacing occurred frequently during atrial pacing. CONCLUSIONS: Contrary to prevailing opinion and practice, postoperative atrial overdrive pacing significantly increases atrial ectopy and does not reduce the likelihood of atrial fibrillation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH P_Cardiac_Pacing__Artificial_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Feasibility_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10803490
----K E
----T Progress report on the Nordic diltiazem study (NORDIL): an outcome study in hypertensive patients.
----A NORDIL--the Nordic Diltiazem Study (NORDIL)--is a prospective, randomized, open blinded-endpoint (PROBE), multicenter, parallel-group morbidity/mortality outcome study in hypertensive patients designed to compare an intervention strategy based on the calcium antagonist diltiazem with a strategy based on conventional antihypertensive drug treatment (diuretics or beta-adrenergic blockers). Patient recruitment was started in Norway and Sweden in September 1992, and ended on December 15, 1996, when 10.896 male and female patients, aged 50-74 years, with essential hypertension had been randomized. In this paper we describe the baseline data of the patient cohort and blood pressures achieved in the two treatment groups during the early part of the study. The patient cohort consists of 5294 males and 5602 females with a mean age of 59.6 and 60.3 years, respectively. Concomitant disorders and risk factors in the cohort are: smoking 22%, ischemic heart disease 3.0%, previous myocardial infarction (MI) 2.0%, previous stroke 1.5%, diabetes mellitus 7.0%, and renal impairment 0.3%. There were no differences between the treatment groups in these respects. The blood pressure treatment goal is a target diastolic blood pressure of < or =90 mmHg or a 10% diastolic blood pressure reduction from the inclusion pressure. In the treatment group randomized to a diltiazem-based treatment strategy, blood pressure was 174/106 mmHg at baseline and 156/90 mmHg after 12 months of follow-up on active treatment. In the group randomized to a conventional treatment strategy, baseline blood pressure at randomization was 173/106 mmHg and 153/90 mmHg after 12 months on active therapy. The NORDIL study will terminate on October 31, 1999 and the final results should be available by mid-2000.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cohort_Studies_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Scandinavia_MeSH M_Treatment_Outcome_MeSH 
****** 10803042
----K E
----T [Clinical study of the month. The STOP-2 study of arterial hypertension in the elderly]
----A After the demonstration of the efficacy of beta-blockers or diuretics versus placebo to prevent cardiovascular complications in elderly hypertensive patients in the first STOP-Hypertension study in 1991, a Swedish group published at the end of 1999 the STOP-2 Hypertension study. The latter randomised trial showed in a similar population that the cardiovascular protection of more recent antihypertensive agents such as calcium antagonists and angiotensin-converting-enzyme inhibitors is similar to that of the conventional antihypertensive drugs used in the first study. In fact, the degree of blood pressure control appears to be more important than the type of antihypertensive drugs used, and this conclusion is reinforced by the observation that numerous patients should rapidly be treated by more than one antihypertensive agent to reach blood pressure targets.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10801996
----K E
----T Usefulness of carvedilol in unstable angina pectoris.
----A The safety and efficacy of adding oral carvedilol (25 mg twice daily) to standardized treatment of unstable angina was assessed in a multicenter, randomized, double-blind, placebo- controlled trial on 116 patients with acute unstable angina. Patients were monitored in an intensive care unit and underwent 48-hour Holter monitoring to assess transient ischemia. Carvedilol as adjunctive therapy resulted in a significant reduction of median heart rate (65 vs 75 beats/min, p <0.05), mean systolic blood pressure (133 vs 130 mm Hg, p <0.05), and mean rate-pressure product (8,337 vs 10,042, p <0.05). Carvedilol reduced the ischemic burden during 48 hours of treatment by 75% (49 vs 204 minutes), including a 36% reduction of patients with ischemic episodes (p <0.05), a 66% reduction of the mean number of ischemic episodes (8 vs 24, p <0.05), and a 76% reduction in the mean duration of ischemic episodes (50 vs 205 minutes, p <0.05). Side effects occurred in 8 of 59 patients (13.6%) in the carvedilol group and in 5 of 54 patients (8.8%) given placebo. Although not significant, the early onset of maximal blood pressure reduction and the delayed effect on heart rate were closely correlated to drug-induced hypotension and bradycardia in the carvedilol group. Thus, carvedilol as an adjunctive to standardized treatment effectively reduces heart rate and blood pressure, and thus the ischemic burden in patients with unstable angina pectoris, but requires close monitoring of patients at risk for bradycardia or hypotension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Acute_Disease_MeSH M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH S_physiopathology_MeSH Angina__Unstable_physiopathology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10806607
----K E
----T Effect of metoprolol and verapamil administered separately and concurrently after single doses on liver blood flow and drug disposition.
----A Nine healthy males participated in a double-blind, placebo-controlled, randomized, crossover study to determine the effects of verapamil and metoprolol administered alone and concurrently on blood flow through the hepatic artery and portal and hepatic veins and to detect a possible drug interaction between the two agents. Single oral doses of placebo/placebo, metoprolol (50 mg)/placebo, verapamil (80 mg)/placebo, or verapamil/metoprolol were separated by at least 14 days. Liver blood flow through individual hepatic vessels was measured up to 8 hours after dosage administration using a duplex Doppler ultrasound technique. Cardiac output, heart rate, blood pressure, stroke volume, and total peripheral resistance were measured for 3 hours after drug doses were given. In 5 subjects, pharmacokinetic parameters for total drug as well as S- and R-enantiomers were also measured. Verapamil given alone caused a rapid and intense increase in liver blood flow (hepatic artery = 50%, portal vein = 42%, hepatic vein = 55%) 0.75 to 1 hour after administration because of a decrease in total peripheral resistance and an increase in heart rate, stroke volume, and cardiac output. Metoprolol given alone caused a slow but prolonged decrease in liver blood flow (maximum decrease: hepatic artery = -54%, portal vein = -21%, hepatic vein = -27%) 4 hours after administration because of a decrease in heart rate and cardiac output. When the two agents were given together, a composite of the changes noted after separate administration was noted: a brief peak increase in liver blood flow at 0.33 to 1 hour followed by a slow, prolonged decrease that reached its maximum decline 4 to 5 hours postdose. During the combined phase, metoprolol and its enantiomers had an increased AUC and Cmax, while verapamil and its enantiomers had an increased AUC and t1/2. These pharmacokinetic changes were consistent with the magnitude and time course of liver blood flow changes through the hepatic artery and portal or hepatic veins.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Area_Under_Curve_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hepatic_Artery_MeSH S_drug_effects_MeSH Hepatic_Artery_drug_effects_MeSH S_physiology_MeSH Hepatic_Artery_physiology_MeSH M_Hepatic_Veins_MeSH S_drug_effects_MeSH Hepatic_Veins_drug_effects_MeSH S_physiology_MeSH Hepatic_Veins_physiology_MeSH M_Human_MeSH M_Liver_MeSH S_blood_supply_MeSH Liver_blood_supply_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Male_MeSH M_Metoprolol_MeSH S_blood_MeSH Metoprolol_blood_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Portal_Vein_MeSH S_drug_effects_MeSH Portal_Vein_drug_effects_MeSH S_physiology_MeSH Portal_Vein_physiology_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Verapamil_MeSH S_blood_MeSH Verapamil_blood_MeSH S_pharmacokinetics_MeSH Verapamil_pharmacokinetics_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH 
****** 10806014
----K E
----T Prognostic implications of results from exercise testing in patients with chronic stable angina pectoris treated with metoprolol or verapamil. A report from the Angina Prognosis Study In Stockholm (APSIS).
----A AIMS: To evaluate the prognostic implications of results from exercise testing, and of antianginal treatment among patients with chronic stable angina pectoris. MATERIAL AND METHODS: Out of 809 patients in the Angina Prognosis Study In Stockholm (APSIS), 731 (511 men) performed evaluable exercise tests before and after 1 month on double-blind treatment with metoprolol or verapamil. During a median follow-up of 40 months, 32 patients suffered a cardiovascular death and 29 a non-fatal myocardial infarction. RESULTS: Prognostic implications of results from exercise tests were assessed in a multivariate Cox model which included sex, previous myocardial infarction, hypertension and diabetes mellitus. Maximal ST-segment depression, especially if >/=2 mm and occurring after exercise, as well as exercise duration independently predicted cardiovascular death. Similar results were obtained for the combined end-point of cardiovascular death+myocardial infarction. Among patients with a positive exercise test at baseline, verapamil reduced the maximal ST-depression more markedly than metoprolol (P<0. 01). However, when the treatment given and treatment effects on ST-segment depression were added to the Cox model, no impact on prognosis could be detected for either cardiovascular death alone or combined with myocardial infarction. Anginal pain carried no prognostic information. CONCLUSION: Marked ST-segment depression during and after exercise, and a low exercise capacity independently predicted an adverse outcome in patients with stable angina pectoris, whereas anginal symptoms had no predictive value. Short-term treatment effects on ischaemia did not seem to influence prognosis. Post-exercise ischaemia should be examined carefully when evaluating patients with stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chronic_Disease_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10808734
----K 1
----T [Effects of nitrates and beta-blockers on platelet aggregation in patients with coronary heart disease]
----A Our study aimed at evaluating an effect of the selected nitrates and beta adrenoceptor blockers on platelet aggregation in patients (pts) with coronary artery disease (CAD). The study included 168 male patients (M), aged between 33 and 72 years (mean age 51 +/- 7). 61 M given isosorbide dinitrate were divided into three groups: in the group I and II an effect of the drug on the platelet aggregation following a single 10 mg (I) and 20 mg (II) dose has been evaluated; in group III an effect of the drug after a two-week treatment has been evaluated. 14 male patients (group IV) were given 5-mononitrate 40 mg daily for two weeks. 85 male patients, treated with propranolol have also been divided into three groups. In group V and group VII an effect of propranolol on platelet aggregation following a single dose of 40 mg and 80 mg has been evaluated respectively. In the group VII an outcome of a two-week propranolol therapy has been assessed. Eleven patients (group VIII) received nadolol in a dose of 40-80 mg daily for two weeks. Platelet aggregation induced by adenosine diphosphate (ADP) in concentration of 1 mM/ml and 5 mM/ml (groups I, II, III, V, VI, VII) and only of 1 microM/ml (groups IV, VIII) was evaluated with Born's method. In patients with CAD only isosorbide dinitrate inhibits platelet aggregation. This effect has been noted following a single dose as well as a two-week treatment. Other drugs (5-mononitrate, propranolol, nadolol) transiently increase platelet aggregation, but became either ineffective after two-week therapy (5-mononitrate, nadolol) or increase (propranolol) platelet aggregation. Tendency to inhibit (sorbonit) or to increase (propranolol) platelet aggregation has been more pronounced with higher concentration of aggregating factor.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Dose-Response_Relationship__Drug_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_pharmacology_MeSH Isosorbide_Dinitrate_pharmacology_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10808740
----K 1
----T [An influence of cardiovascular risk factors and pharmacotherapy on the long-term results in women undergoing coronary artery bypass]
----A This study aimed at analysing an effect of the coronary risk factors and pharmacotherapy on the long-term outcome in women following the coronary artery by-pass. In 1004-1997, 253 female patients, aged between 33 and 82 years (mean [+/- SD] 57.0 +/- 8 years) were treated surgically. The follow-up period lasted for 7 to 60 months (mean 32.0 +/- 14 months). Ten patients (3.9%) died. Answers to the questionnaire and personal interviews assessed physical fitness based on CCS classification, pharmacotherapy, and presence of risk factors. According to CCS scale, significant improvement has been seen in 195 (82.6%; p < .0001) patients. Health state did not change in 34 (14.4%) patients, and deteriorated in 7 (3.0%). Analysisn coronary risk factors, hypertension proved prevailing (60.3%), followed by diabetes mellitus (25.5%) and obesity (22.9%). Eleven percent of patients returned to cigarettes smoking after surgery. Postoperatively, 74.1% of patients received nitrates as a constant, medication, 58.2%--beta-blockers, 53.4%--ACE inhibitors, and 19.8% of patients received calcium antagonists. Lipid abnormalities have been treated in 49.1% of patients whereas antiplatelet therapy has been carried out in 74.1%. Only 9.9% of patients received hormones. The lower CCS class before surgery, the more significant improvement after it. As pharmacotherapy was used according to the European guidelines, an improvement in the long-term outcome required some modifications in patients' life style.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 10811588
----K E
----T Prediction of 1-year survival after thrombolysis for acute myocardial infarction in the global utilization of streptokinase and TPA for occluded coronary arteries trial.
----A BACKGROUND: When a patient survives thrombolysis for acute myocardial infarction, little information from large studies exists from which to estimate prognosis during follow-up visits. METHODS AND RESULTS: Baseline, in-hospital, and later survival data were collected from 41 021 patients enrolled in Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries, a randomized trial of 4 thrombolytic-heparin regimens with standard aspirin and beta-blockade. Cox proportional hazards models were developed to predict 1-year survival in 30-day survivors (n=37 869) from baseline clinical and ECG factors and in-hospital factors; a combined model then was developed (C-index 0.800). The model was simplified into a nomogram to predict individual outcomes (C-index 0.754). Factors reflecting demographics (advanced age, lighter weight), larger infarctions (higher Killip class, lower blood pressure, faster heart rate, longer QRS duration), cardiac risk (smoking, hypertension, prior cerebrovascular disease), and arrhythmia were important predictors of death between 30 days and 1 year. Black race was associated with a substantial increase in risk after considering other factors. Revascularization was associated with reduced risk between 30 days and 1 year. CONCLUSIONS: When evaluating a patient who has survived acute infarction treated with thrombolysis, clinicians can estimate the likelihood of survival from factors easily measured during admission. Although many risk factors clearly relate to age, left ventricular dysfunction, or clinical instability, black race is an unexplained risk factor requiring further examination.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Streptokinase_MeSH S_therapeutic_use_MeSH Streptokinase_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH 
****** 10819408
----K E
----T Frequency-domain heart rate variability in 24-hour Holter recordings: role of spectral method to assess circadian patterns and pharmacological autonomic modulation.
----A Different spectral methodologies for heart rate variability were recently shown to provide the same qualitative results in the context of passive tilt test. However, the impact of the method and the use of normalized power units in long-term ECG monitoring is still debated. Autoregressive and Fast Fourier transform (FFT) spectral approaches were applied to assess circadian modulation and the effect of beta-blocker administration in mild hypertensive patients who underwent continuous ambulatory ECG recording (n = 44, 51 +/- 12 years, 30 men). Spectral analysis was applied to 5-minute sequences and spectral parameters representative of each circadian period (24 hour, day, night) were calculated. In baseline recordings, FFT spectral method provided a smaller estimate of total and very low frequency powers. On the contrary, low- and high-frequency components were systematically larger with FFT. Circadian variations were in favor of an increased overall nocturnal variability but of a reduced low frequency normalized power with both spectral methods. Chronic oral administration of beta-blocker induced an increase of all spectral components except for an unchanged low-frequency normalized power, independently from the spectral approach. In spite of quantitative differences, the qualitative assessment of circadian patterns and beta-blockade effect by autoregressive- and FFT-based spectral analyses is equivalent. The low-frequency component of heart rate variability cannot be considered a reliable direct marker of sympathetic activity in long-term ambulatory ECG recording.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH P_Circadian_Rhythm_MeSH P_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Fourier_Analysis_MeSH P_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Signal_Processing__Computer-Assisted_MeSH 
****** 10821360
----K E
----T Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group.
----A BACKGROUND: We undertook a prospective systematic overview based on data from individual patients from five long-term randomised trials that assessed inhibitors of angiotensin-converting enzyme (ACE) in patients with left-ventricular dysfunction or heart failure. METHODS: Three of the trials enrolled patients within a week after acute myocardial infarction. Data were combined by use of the Peto-Yusuf method. FINDINGS: Overall 12,763 patients were randomly assigned treatment or placebo and followed up for an average of 35 months. In the three post-infarction trials (n=5,966), mortality was lower with ACE inhibitors than with placebo (702/2995 [23.4%] vs 866/2971 [29.1%]; odds ratio 0.74 [95% CI 0.66-0-83]), as were the rates of readmission for heart failure (355 [11.9%] vs 460 [15.5%]; 0.73 [0.63-0.85]), reinfarction (324 [10.8%] vs 391 [13.2%]; 0.80 [0.69-0.94]), or the composite of these events (1049 [35.0%] vs 1244 [41.9%]; 0.75 [0.67-0.83]; all p<O.001). For all five trials the ACE inhibitor group had lower rates of death than the placebo group (1,467/6,391 [23.0%] vs 1,710/6,372 [26.8%]; 0.80 [0.74-0.87]) and lower rates of reinfarction (571 [8.9%] vs 703 [11.0%]; 0.79 [0.70-0.89]), readmission for heart failure (876 [13.7%] vs 1202 [18.9%]; 0.67 [0.61-0.74]), and the composite of these events (2161 [33.8%] vs 2610 [41.0%]; 0.72 [0.67-0.78]; all p<0.0001). The benefits were observed early after the start of therapy and persisted long term. The benefits of treatment on all outcomes were independent of age, sex, and baseline use of diuretics, aspirin, and beta-blockers. Although there was a trend towards greater reduction in risk of death or readmission for heart failure in patients with lower ejection fractions, benefit was apparent over the range examined.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 10821361
----K E
----T Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial--the Losartan Heart Failure Survival Study ELITE II.
----A BACKGROUND: The ELITE study showed an association between the angiotensin II antagonist losartan and an unexpected survival benefit in elderly heart-failure patients, compared with captopril, an angiotensin-converting-enzyme (ACE) inhibitor. We did the ELITE II Losartan Heart Failure Survival Study to confirm whether losartan is superior to captopril in improving survival and is better tolerated. METHODS: We undertook a double-blind, randomised, controlled trial of 3,152 patients aged 60 years or older with New York Heart Association class II-IV heart failure and ejection fraction of 40% or less. Patients, stratified for beta-blocker use, were randomly assigned losartan (n=1,578) titrated to 50 mg once daily or captopril (n=1,574) titrated to 50 mg three times daily. The primary and secondary endpoints were all-cause mortality, and sudden death or resuscitated arrest. We assessed safety and tolerability. Analysis was by intention to treat. FINDINGS: Median follow-up was 555 days. There were no significant differences in all-cause mortality (11.7 vs 10.4% average annual mortality rate) or sudden death or resuscitated arrests (9.0 vs 7.3%) between the two treatment groups (hazard ratios 1.13 [95.7% CI 0.95-1.35], p=0.16 and 1.25 [95% CI 0.98-1.60], p=0.08). Significantly fewer patients in the losartan group (excluding those who died) discontinued study treatment because of adverse effects (9.7 vs 14.7%, p<0.001), including cough (0.3 vs 2.7%).
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 10818057
----K E
----T Hypokalemia associated with diuretic use and cardiovascular events in the Systolic Hypertension in the Elderly Program.
----A The treatment of hypertension with high-dose thiazide diuretics results in potassium depletion and a limited benefit for preventing coronary events. The clinical relevance of hypokalemia associated with low-dose diuretics has not been assessed. To determine whether hypokalemia that occurs with low-dose diuretics is associated with a reduced benefit on cardiovascular events, we analyzed data of 4126 participants in the Systolic Hypertension in the Elderly Program (SHEP), a 5-year randomized, placebo-controlled clinical trial of chlorthalidone-based treatment of isolated systolic hypertension in older persons. After 1 year of treatment, 7.2% of the participants randomized to active treatment had a serum potassium <3.5 mmol/L compared with 1% of the participants randomized to placebo (P<0.001). During the 4 years after the first annual visit, 451 participants experienced a cardiovascular event, 215 experienced a coronary event, 177 experienced stroke, and 323 died. After adjustment for known risk factors and study drug dose, the participants who received active treatment and who experienced hypokalemia had a similar risk of cardiovascular events, coronary events, and stroke as those randomized to placebo. Within the active treatment group, the risk of these events was 51%, 55%, and 72% lower, respectively, among those who had normal serum potassium levels compared with those who experienced hypokalemia (P<0.05). The participants who had hypokalemia after 1 year of treatment with a low-dose diuretic did not experience the reduction in cardiovascular events achieved among those who did not have hypokalemia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH M_Diuretics__Sulfamyl_MeSH S_administration_&_dosage_MeSH Diuretics__Sulfamyl_administration_&_dosage_MeSH S_adverse_effects_MeSH Diuretics__Sulfamyl_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypokalemia_MeSH S_chemically_induced_MeSH Hypokalemia_chemically_induced_MeSH S_physiopathology_MeSH Hypokalemia_physiopathology_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 10818061
----K E
----T Influence of diabetes and type of hypertension on response to antihypertensive treatment.
----A The aim of our investigation was to determine whether the presence of additional risk factors or type of hypertension (diastolic or isolated systolic) influences blood pressure (BP) response to treatment. The International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) study is a double-blinded outcome comparison of calcium channel blockade with diuretics in high-risk patients aged 55 to 80 years. Dynamic randomization between nifedipine once daily and hydrochlorothiazide/amiloride was performed to ensure that approximately equal numbers of patients in the 2 groups had each of the major cardiovascular risk factors. Patients with isolated systolic hypertension were also separately randomized. Atenolol or enalapril was the mandatory second-line drug. In 5669 patients who completed the 18-week titration, BP fell from 172+/-15/99+/-9 mm Hg (mean+/-SD) while receiving placebo to 139+/-12/82+/-7 mm Hg. Twenty-six percent of patients required 2 drugs, and 4% required 3 drugs. Patients with diabetes were the most resistant to treatment, requiring second and third drugs 40% and 100% more frequently than patients without diabetes and achieving marginally the highest final BP, for any risk group, of 141+/-13/82+/-8 mm Hg. Age, smoking, gender, hypercholesterolemia, left ventricular hypertrophy, and existing atherosclerosis had little (<1 mm Hg) or no influence on BP at the end of titration, but all except smoking slightly reduced the initial response of either systolic or diastolic BP. Patients with isolated systolic hypertension were slightly more responsive than average to treatment. Our findings suggest that in patients at high absolute risk of cardiovascular complications from hypertension, the risk factors themselves do not prevent the recommended BP targets from being achieved.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_physiopathology_MeSH Diabetes_Mellitus_physiopathology_MeSH M_Diastole_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH 
****** 10820942
----K E
----T Nebivolol: a new beta blocker on the horizon.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_administration_&_dosage_MeSH Benzopyrans_administration_&_dosage_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_administration_&_dosage_MeSH Ethanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10826457
----K E
----T Placebo-associated blood pressure response and adverse effects in the treatment of hypertension: observations from a Department of Veterans Affairs Cooperative Study.
----A BACKGROUND: The use of placebo in clinical trials has been vigorously debated. Placebo control may be useful in disease states, such as stage 1 and stage 2 hypertension as defined by the Sixth Report of the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure (JNC VI), in which response rates for placebo are high or close to response rates for effective therapies, or when established interventions have significant adverse effects. OBJECTIVE: To compare rates for the control of blood pressure and adverse effects of placebo vs active treatment in patients with stage 1 and stage 2 hypertension. METHODS: This study is a randomized controlled trial evaluating the blood pressure response and adverse effects of placebo vs 6 active treatments administered in 15 Veterans Affairs hypertension centers. The 1292 subjects of the Veterans Affairs Cooperative Study receiving single-drug therapy for hypertension were randomly allocated to receive treatment with 1 of 6 active drugs (n= 1105) or placebo (n=187). Treatment success was defined as maintaining a diastolic blood pressure of less than 95 mm Hg for at least 1 year. We compared treatment success rates for the control of blood pressure and adverse effects of placebo vs active treatment. Using the Kaplan-Meier method, we also compared rates of discontinuation from placebo vs active drug treatment over time as a result of adverse drug effects and blood pressure exceeding safety limits. RESULTS: At the end of the titration phase, 58 patients who were treated with placebo (31%) achieved a goal diastolic blood pressure lower than 90 mm Hg and 57 (30%) achieved success at 1 year. Older white patients who received placebo had a success rate of 38% vs 23% to 27% for the other age-race subgroups. The rates of discontinuation as a result of adverse drug effects were 13% for patients receiving placebo vs 12% for patients receiving active treatment (P=.40). The rates of discontinuation for blood pressure being too high were 14% for patients receiving placebo vs 7% for patients receiving active treatment (P=.01). CONCLUSIONS: Placebo control provides an important benchmark for both efficacy and adverse effects. It continues to have an appropriate place in certain therapeutic trials, particularly those involving the treatment of stage 1 and stage 2 hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Placebo_Effect_MeSH P_Veterans_MeSH 
****** 10826461
----K E
----T Medical therapy, symptoms, and the distress the cause: relation to quality of life in patients with angina pectoris and/or hypertension.
----A BACKGROUND: Adverse events during drug therapy can be assessed through measurement of 2 features: their frequency and their severity. Their severity, in turn, can be measured by assessing the distress that they cause. Our goal was to relate the magnitude of the distress induced by treatment with calcium-channel blocking agents to the change in quality of life assessed through psychosocial instruments in patients treated with calcium-channel blocking agents, either for hypertension or for angina pectoris. METHODS: Four hundred seventy-five patients with angina pectoris were randomized to double-blind treatment with PPR (physiological pattern release) verapamil hydrochloride, amlodipine besylate, amlodipineatenolol combination, or placebo. In addition, 557 hypertensive patients were randomized either to PPR verapamil or nifedipine GITS (gastrointestinal system). Both studies were double-blind. RESULTS: Significant differences in treatment of angina pectoris or hypertension, were not found between the regimens. Overall quality of life also failed to show a significant difference in either group. In both groups, however, remarkable concordance was found between the degree of distress associated with specific symptoms and a change in quality of life. An unchanged, stable symptom distress was associated with a significant improvement in the quality of life of about 0.1 SD. Improvement or erosion of symptom distress represented by 1 step was associated with a 0.1- to 0.2-SD change. The extreme change in symptom distress was associated with a substantially larger change in global quality of life. CONCLUSIONS: The magnitude of symptom distress or relief associated with symptoms in 2 patient populations correlated strongly with a shift in quality of life. The assessment of distress associated with symptoms provides valuable additional information on drug therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Adverse_Drug_Reaction_Reporting_Systems_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10826499
----K I
----T Defective suppression of the aldosterone biosynthesis during stroke permissive diet in the stroke-prone phenotype of the spontaneously hypertensive rat.
----A Previous studies have shown that short-term high salt intake unmasks blunted plasma aldosterone suppression in stroke-prone spontaneously hypertensive rats (SHRsp). The aim of this study was to evaluate the response of aldosterone biosynthesis and production to a sustained exposure to the stroke-permissive Japanese-style diet (JD) in young stroke-prone and stroke-resistant SHRs. For this purpose, 6-week old male rats from both strains were divided into 2 dietary groups and received regular diet (SHR = 37, SHRsp = 32) or the JD and 1% saline to drink (SHR = 34, SHRsp = 30) for 4 weeks. All measurements were carried out at the end of the dietary periods. After JD, plasma aldosterone levels were significantly decreased in SHR (from 357.8 +/- 57 to 163.3 +/- 31.5 pg/ml, p < 0.05) but markedly increased in SHRsp (from 442 +/- 56.5 to 739 +/- 125.7 pg/ml, p < 0.05). Consistently, the adrenal aldosterone synthase expression was reduced by JD in SHR (p < 0.05), whereas it was even slightly raised by JD in SHRsp so that, at the end of JD, aldosterone synthase mRNA was 5-fold higher in SHRsp than in SHR. Urinary sodium excretion (mEq/24h) achieved lower levels in SHRsp, so that fractional excretion of sodium was 80.2 +/- 9% in SHR and 40.3 +/- 8% in SHRsp (p < 0.05) in balance studies performed at the end of JD. These different responses of mineralocorticoid biosynthesis and urinary sodium excretion to JD were not accounted for by different adaptations of the renin-angiotensin and atrial natriuretic peptide systems, of serum potassium levels, or of adrenal 11beta-hydroxylase expression in the two strains. Systolic blood pressure was comparable in both strains throughout the experiment. These results demonstrate enhanced aldosterone biosynthesis, associated with reduced urinary excretion of sodium in response to JD in SHRsp before the onset of stroke. This abnormality may play a role in the higher susceptibility to stroke of this model.
----P Journal_Article 
----M M_Aldosterone_MeSH S_biosynthesis_MeSH Aldosterone_biosynthesis_MeSH M_Animals_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Japan_MeSH M_Male_MeSH M_Rats_MeSH M_Rats__Inbred_SHR_MeSH M_Renin_MeSH S_metabolism_MeSH Renin_metabolism_MeSH M_Sodium_Chloride__Dietary_MeSH S_administration_&_dosage_MeSH Sodium_Chloride__Dietary_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10826501
----K I
----T Endothelin-1 induces interleukin-6 release via activation of the transcription factor NF-kappaB in human vascular smooth muscle cells.
----A The potent vasoconstrictor peptide endothelin-1 (ET-1) has been implicated in the pathophysiology of atherosclerosis and its complications. Since inflammation of the vessel wall is a hallmark of atherosclerosis, the purpose of the present study was to investigate the influence of ET-1 on cytokine production in human vascular smooth muscle cells (SMC) as a marker of inflammatory cell activation. ET-1 (100 pM - 1 microM) stimulated interleukin-6 (IL-6) secretion from human vascular SMC in a concentration-dependent manner. The ET-A-receptor antagonist BQ-123 (10 microM), but not the ET-B-receptor antagonist BQ-788, inhibited IL-6 release. ET-1 also transiently increased IL-6 mRNA compatible with regulation of IL-6 release at the pretranslational level. Electrophoretic mobility shift assays demonstrated time- and concentration-dependent activation of the proinflammatory transcription factor nuclear factor-kappaB (NF-kappaB) in ET-1-stimulated human vascular SMC. A decoy oligodeoxynucleotide bearing the NF-kappaB binding site inhibited ET-1-stimulated IL-6 release to a great extent suggesting that this transcription factor plays a key role for cytokine production elicited by ET-1. Moreover, the antioxidant pyrrolidine dithiocarbamate (10 microM) inhibited ET-1-induced IL-6 release indicating involvement of reactive oxygen species in ET-1 signaling. ET-1-stimulated IL-6 secretion was also suppressed by diphenylene iodonium (40 microM), an inhibitor of flavon-containing enzymes such as NADH/NADPH oxidase. The results demonstrate the ability of ET-1 to induce an inflammatory response in human vascular SMC. These observations may contribute to a better understanding of the role of ET-1 in inflammatory activation of the vessel wall during atherogenesis.
----P Journal_Article 
----M M_Antioxidants_MeSH S_pharmacology_MeSH Antioxidants_pharmacology_MeSH M_Cells__Cultured_MeSH M_Endothelin-1_MeSH S_pharmacology_MeSH Endothelin-1_pharmacology_MeSH M_Human_MeSH M_Interleukin-6_MeSH S_genetics_MeSH Interleukin-6_genetics_MeSH S_secretion_MeSH Interleukin-6_secretion_MeSH M_Muscle__Smooth__Vascular_MeSH S_cytology_MeSH Muscle__Smooth__Vascular_cytology_MeSH S_drug_effects_MeSH Muscle__Smooth__Vascular_drug_effects_MeSH S_metabolism_MeSH Muscle__Smooth__Vascular_metabolism_MeSH M_NF-kappa_B_MeSH S_physiology_MeSH NF-kappa_B_physiology_MeSH M_Receptors__Endothelin_MeSH S_physiology_MeSH Receptors__Endothelin_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10827148
----K E
----T Isosorbide mononitrate and propranolol compared with propranolol alone for the prevention of variceal rebleeding.
----A The aim of this study was to test the effectiveness of isosorbide-5-mononitrate (IM) as an adjunct to propranolol (PR) in the prevention of variceal rebleeding. Ninety-five cirrhotic patients with variceal bleeding were randomly assigned to treatment with PR + IM (46 patients) or PR alone (49 patients). Eighteen patients in the PR + IM group and 28 in the PR group had rebleeding during the 2 years after randomization. The actuarial probability of rebleeding 2 years after randomization was lower in the PR + IM group (40.4% vs. 57.4%) but the difference was not significant (P =. 09). However, the decrease in the risk of rebleeding reached statistical significance after stratification according to age, i.e. less than 50 versus >/=50 years old, (P =.03) or by adding an additional year of follow-up (P =.05). No significant difference was found in rebleeding index and survival. The multivariate Cox analysis indicated first, that both treatment (P =.03) and age (P =. 001) were factors predictive of rebleeding and second, that PR + MI reduced the risk of rebleeding by half (relative risk: 0.51, 95% confidence interval: 0.28-0.95). Seven patients in the PR + MI group and 1 patient in the PR group had to discontinue one of the drugs because of adverse events (P =.03). These results suggest that the addition of IM improves the efficacy of PR alone in the prevention of variceal rebleeding in cirrhotic patients. However no beneficial effects were observed on other parameters reflecting the efficacy of treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Proportional_Hazards_Models_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10829361
----K 3
----T Doxazosin in elderly patients with hypertension.
----A Hypertension constitutes a major cardiovascular risk factor of high prevalence in the elderly, and reducing elevated blood pressure has been shown to be of significant benefit in decreasing the incidence of cardiovascular and cerebrovascular disease in this patient population. Elderly patients are more likely to have comorbid disorders, such as dyslipidaemia, diabetes, renal disease, atherosclerosis and, for males, benign prostatic hyperplasia (BPH). Therefore, when choosing an antihypertensive agent for elderly patients, it is particularly important to ensure that treatment does not exacerbate comorbid conditions and does not interact deleteriously with any concurrent medication that the patient is taking. The alpha 1-adrenoceptor antagonist, doxazosin, has been shown to be an effective, well-tolerated antihypertensive therapy in elderly male patients and does not exacerbate--and in some cases improves--some other common disorders. Doxazosin has been shown to be effective in reducing the symptoms of BPH in elderly patients whose blood pressure is well controlled by concomitant antihypertensive medication. In addition, improvements in the symptoms of BPH as well as reductions in blood pressure have been observed in elderly men with mild-to-moderate hypertension. Doxazosin has been shown to have positive effects on lipid profiles and glycaemic control, which make it an attractive choice of therapy for elderly patients with hypertension and diabetes or dyslipidaemia. In addition, doxazosin is administered once daily, either in the morning or the evening, which may aid compliance, an important consideration in the elderly.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Doxazosin_MeSH S_administration_&_dosage_MeSH Doxazosin_administration_&_dosage_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 10832808
----K E
----T Influence of hydrophilic and lipophilic beta-blockers on heart rate, ventricular repolarization and their interrelationship in normal subjects.
----A BACKGROUND: It has been hypothesized that hydrophilic and lipophilic beta-blockers have different antiarrhythmic properties because only the latter seem to reduce the rate of sudden death in post-myocardial infarction patients as well as animal models which seem to be independent of their effect on autonomic nervous system modulation. The aim of this study was to evaluate the different effects of a hydrophilic (nadolol) and lipophilic (metoprolol) beta-blocker on ventricular repolarization in normal subjects. METHODS: Seventeen normal subjects entered this randomized, single-blind cross-over study designed to compare the effects of nadolol (80 mg/day) and slow-release metoprolol (200 mg/day) on dynamic ventricular repolarization. The RR intervals, the QT evaluated at the apex (QT apex) and at the end (QT end) of the T wave before and after correction for heart rate, the standard deviation of QT apex and QT end, and the slope of the QT/RR linear relationship (QTa-slope and QTe-slope) were studied using the ELATEC system (ELA Medical, Mountrouge, France), and an evaluation was made of their reproducibility and the effects of each beta-blocker. RESULTS: The most reproducible parameters were QT apex, corrected QT apex and the QTe-slope. Nadolol was associated with a greater adrenergic blockade than metoprolol (lengthening of RR interval +25 +/- 7 and +17 +/- 8% respectively, p = 0.0003) and a lower effect on ventricular repolarization (reduction of corrected QT apex -0.6 +/- 3 and -2.5 +/- 2.1% respectively, p < 0.01; reduction of QTe-slope -5 +/- 16 and -15 +/- 15% respectively, p = 0.03). CONCLUSIONS: At the dosages used in the study, metoprolol showed lower adrenergic blockade but greater effect on ventricular repolarization than nadolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiology_MeSH Heart_Ventricles_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Nadolol_MeSH S_pharmacology_MeSH Nadolol_pharmacology_MeSH M_Reproducibility_of_Results_MeSH M_Single-Blind_Method_MeSH 
****** 10834451
----K E
----T Retrospective analysis showing less cardiac events in post-myocardial infarction patients treated with metoprolol. Secondary Prevention Group.
----A This analysis was carried out to clarify the capacity of metoprolol to prevent cardiac events in Japanese post-myocardial infarction patients during a follow-up period of 16.3 months. Cardiac events occurred in 44 of 650 patients treated without beta-blockers (6.8%) and in 13 of 432 patients treated with metoprolol (3.0%), which represents a significant decline in the incidence of cardiac events among patients receiving metoprolol (p<0.01, odds ratio 0.43, 95% confidence interval 0.23-0.80). Because this was a retrospective analysis, there were unavoidable differences in the backgrounds of the patients in the 2 groups. Subgroup analyses, each focusing on a specific patient characteristic, were therefore performed. These showed that metoprolol effectively reduced cardiac events in many subgroups. Furthermore, multivariate analysis carried out to exclude any modification based on the differences in patient background confirmed metoprolol to be effective in reducing subsequent cardiac events in post-myocardial infarction patients. A large, randomized, placebo-controlled clinical trial needs to be performed in the Japanese population to confirm the present result.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_standards_MeSH Adrenergic_beta-Antagonists_standards_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Drug_Evaluation_MeSH S_statistics_&_numerical_data_MeSH Drug_Evaluation_statistics_&_numerical_data_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Incidence_MeSH M_Japan_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_standards_MeSH Metoprolol_standards_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 10835905
----K 1
----T [Side effects during dobutamine stress echocardiography: analysis of 582 studies]
----A The purpose of the study was to assess the safety, adverse effects and complications of the dobutamine stress echocardiography (ED). 582 patients without previous infarction were prospectively studied with ED. There were 196 female and 368 male, age varied from 27 to 74 years, mean 52. Dobutamine was given in stepwise increasing doses from 5 to 40 mcg/kg/min. Mean maximal dose achieved was 33 mcg/kg/min. Atropine was added in 253 (43%) cases. Significant coronary artery disease was present in 323 patients (53%). There were no death, no myocardial infarction or episodes of sustained ventricular tachycardia as a result of ED. The test was terminated when following conditions were revealed: target heart rate (28.9%), maximal established dose achieved (25.3%), left ventricular asynergy (19.6%), angina pectoris (10.8%), increase of systolic blood pressure above 220 mm Hg (2.6%), hypotension (7.6%), nonsustained ventricular tachycardia (1.7%). The most common non-cardiac side effects were skin tingling (19.8%), atypical chest pain(16.3%), palpitations (13.9%) and headache (7.9%). The most side effects were usually well tolerated, without the need for test cessation. The ED was terminated only in 4 (0.6%) patients because of non-cardiac side effects including nausea (0.3%) and headache (0.3%). We conclude that ED may be safely performed in routine clinical practice. Side effects were rare and usually minor. Most severe ischemic pain was relieved by test interruption and sublingual nitro-glycerine or short acting beta-blocker administration.
----P Case_Reports Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Atropine_MeSH S_diagnostic_use_MeSH Atropine_diagnostic_use_MeSH M_Cardiotonic_Agents_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH M_Dobutamine_MeSH S_adverse_effects_MeSH Dobutamine_adverse_effects_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Parasympatholytics_MeSH S_diagnostic_use_MeSH Parasympatholytics_diagnostic_use_MeSH M_Prospective_Studies_MeSH 
****** 10839554
----K 5
----T Combination antihypertensive drugs: recommendations for use.
----A The recommendation for first-line therapy for hypertension remains a beta blocker or diuretic given in a low dosage. A target blood pressure of less than 140/90 mm Hg is achieved in about 50 percent of patients treated with monotherapy; two or more agents from different pharmacologic classes are often needed to achieve adequate blood pressure control. Single-dose combination antihypertension therapy is an important option that combines efficacy of blood pressure reduction and a low side effect profile with convenient once-daily dosing to enhance compliance. Combination antihypertensives include combined agents from the following pharmacologic classes: diuretics and potassium-sparing diuretics, beta blockers and diuretics, angiotensin-converting enzyme (ACE) inhibitors and diuretics, angiotensin-II antagonists and diuretics, and calcium channel blockers and ACE inhibitors.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH M_Drug_Combinations_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH 
****** 10841241
----K I
----T Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter.
----A BACKGROUND: Despite the high success rate of radiofrequency (RF) ablation, pharmacologic therapy is still considered the standard initial therapeutic approach for atrial flutter. OBJECTIVE: We prospectively compared the outcome at follow-up of patients with atrial flutter randomly assigned to drug therapy or RF ablation. METHODS: Patients with at least two episodes of symptomatic atrial flutter in the last four months were randomized to regimens of either antiarrhythmic drug therapy or first-line RF ablation. After institution of therapy, end points included recurrence of atrial flutter, rehospitalization and quality of life. RESULTS: A total of 61 patients entered the study, 30 of whom were randomized to drug therapy and 31 to RF ablation. After a mean follow-up of 21 +/- 11 months, 11 of 30 (36%) patients receiving drugs were in sinus rhythm, versus 25 of 31 (80%) patients who underwent RF ablation (p < 0.01). Of the patients receiving drugs, 63% required one or more rehospitalizations, whereas post-RF ablation, only 22% of patients were rehospitalized (p < 0.01). Following RF ablation, 29% of patients developed atrial fibrillation which was seen in 53% of patients receiving medications (p < 0.05). Sense of well being (pre-RF 2.0 +/- 0.3 vs. post-RF 3.8 +/- 0.5, p < 0.01) and function in daily life (pre-RF 2.3 +/- 0.4 vs. post-RF 3.6 +/- 0.6, p < 0.01) improved after ablation, but did not change significantly in patients treated with drugs. CONCLUSION: In a selected group of patients with atrial flutter, RF ablation could be considered a first-line therapy due to the better success rate and impact on quality of life, the lower occurrence of atrial fibrillation and the lower need for rehospitalization at follow-up.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Flutter_MeSH S_drug_therapy_MeSH Atrial_Flutter_drug_therapy_MeSH S_surgery_MeSH Atrial_Flutter_surgery_MeSH P_Catheter_Ablation_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10841254
----K E
----T Beta-blockers and ventricular arrhythmias in dilated cardiomyopathy.
----A 
----P Comment Letter 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH M_Heart_Ventricles_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 10837379
----K 4
----T A comparison of latanoprost and dorzolamide in patients with glaucoma and ocular hypertension: a 3 month, randomised study. Ireland Latanoprost Study Group.
----A AIMS: To compare the effects on intraocular pressure (IOP) and side effects of monotherapy with either latanoprost or dorzolamide in patients with glaucoma or ocular hypertension. METHODS: 224 patients with open angle glaucoma or ocular hypertension were recruited to a 3 month open labelled study. Previous glaucoma medications were washed out and the patients were randomised to receive either latanoprost 0.005% once daily or dorzolamide 2% three times daily. RESULTS: Of 224 patients 213 were included in the analysis of efficacy. After 3 months, latanoprost reduced mean baseline diurnal IOP from 27.2 (SD 3.0) mm Hg by 8.5 (3.3) mm Hg. The corresponding figures for dorzolamide were 27.2 (3.4) and 5.6 (2.6) mm Hg. The difference of 2.9 mm Hg (95% CI: 2.3-3.6) was highly significant (p<0.001, ANCOVA). Latanoprost reduced IOP at peak by 8.6 mm Hg (32%) compared with 6.2 mm Hg (23%) for dorzolamide, and the difference of 2.4 mm Hg was significant (p<0.001, ANCOVA). The corresponding figures at trough were 8.1 mm Hg (31%) for latanoprost and 4.7 mm Hg (17%) for dorzolamide, a significant difference of 3.4 mm Hg (p<0.001, ANCOVA). Both drugs were well tolerated systemically and locally. CONCLUSION: Latanoprost was superior to dorzolamide in reducing the IOP, judged both from the effect on IOP at peak and trough and by the effect on diurnal IOP.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Sulfonamides_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH 
****** 10840011
----K E
----T Local pulse pressure and regression of arterial wall hypertrophy during long-term antihypertensive treatment.
----A BACKGROUND: Local pulse pressure (PP) is an independent determinant of carotid artery wall thickness, stronger than mean blood pressure (BP). The present study was designed to assess whether a beta-adrenoceptor antagonist-based or an ACE inhibitor-based treatment was able to reduce carotid artery wall hypertrophy through a reduction in carotid PP rather than by lowering mean BP and whether the influence of local PP reduction could also be detected at the site of a muscular artery, the radial artery. METHODS AND RESULTS: Ninety-eight essential hypertensive patients were randomized to 9 months of double-blind treatment with either celiprolol or enalapril. Arterial parameters were determined with high-resolution echo-tracking systems. PP was measured locally with applanation tonometry and independently of mean BP. After 9 months of treatment, mean BP, carotid PP, and intimal-medial thickness (IMT) decreased significantly, with no difference between the 2 groups. The reduction in carotid PP but not in mean BP was a major independent determinant of the reduction in carotid IMT. Radial artery IMT and PP decreased significantly with both treatments. However, the reduction in radial artery IMT was not related to the changes in radial artery PP. CONCLUSIONS: The regression of carotid artery wall hypertrophy during long-term antihypertensive treatment was dependent on the reduction in local PP rather than on the lowering of mean BP. The effect of PP lowering on IMT reduction was observed at the site of an elastic artery but not at the site of a muscular artery.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH P_Blood_Pressure_MeSH M_Carotid_Arteries_MeSH S_pathology_MeSH Carotid_Arteries_pathology_MeSH M_Celiprolol_MeSH S_administration_&_dosage_MeSH Celiprolol_administration_&_dosage_MeSH M_Elasticity_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Hypertrophy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10840295
----K E
----T Endoscopic sclerotherapy plus propranolol versus propranolol alone in the primary prevention of bleeding in high risk cirrhotic patients with esophageal varices: a prospective multicenter randomized trial.
----A BACKGROUND: Analysis of primary prevention studies of the use of beta-blockers has shown clear reductions in variceal bleeding in cirrhotic patients with varices. In contrast, the usefulness of prophylactic endoscopic sclerotherapy, alone or in combination with propranolol, in the management of these patients is still under investigation. The present study compared the efficacy of combined sclerotherapy and propranolol versus propranolol alone in the primary prevention of hemorrhage in cirrhotic patients with varices and high (greater than 18 mm Hg) intraesophageal variceal pressure. METHODS: Patients were randomly assigned to propranolol (42 patients) or to propranolol plus sclerotherapy (44 patients). The mean duration of follow-up was 26.8 +/- 7.7 and 24.6 +/- 9.8 months, respectively. RESULTS: During this period 23% of the patients in the combination group experienced at least 1 episode of bleeding due to varices or congestive gastropathy as compared with 14% in the propranolol group (not significant). Twenty-three patients (52%) in the combination group developed complications as compared with 8 (19%) in the propranolol group (p = 0.002). The mortality rate was similar in both groups (14% and 18%, respectively). The only independent factor predictive of survival was the level of serum albumin. CONCLUSIONS: Endoscopic sclerotherapy should not be used for the primary prevention of hemorrhage in cirrhotic patients at high risk of variceal bleeding who are undergoing treatment with propranolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH P_Esophagoscopy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Manometry_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Sclerotherapy_MeSH S_methods_MeSH Sclerotherapy_methods_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 10853616
----K E
----T Gender differences in labetalol kinetics: importance of determining stereoisomer kinetics for racemic drugs.
----A STUDY OBJECTIVE: To evaluate the impact of gender on labetalol kinetics. DESIGN: Part of a randomized, crossover study. SETTING: Academic medical center. PATIENTS: Nineteen hypertensive patients (14 men, 5 women; 6 blacks, 13 whites). INTERVENTIONS: Participants had labetalol dosages titrated to a specific antihypertensive response, then underwent ambulatory blood pressure monitoring (ABPM) and a pharmacokinetic study. Labetalol plasma concentrations were measured by high-performance liquid chromatography (HPLC) and labetalol stereoisomer ratios were determined in a single plasma sample by chiral HPLC, both with fluorescence detection. MEASUREMENTS AND MAIN RESULTS: Labetalol concentrations were 80% higher in women (area under the concentration-time curve [AUC]/dose x 1000: 6.79 +/- 2.11 in women vs 3.82 +/- 1.37 hr/L in men, p<0.05), yet both genders had a similar antihypertensive response by 24-hour ABPM. Dose-corrected AUC (AUC/dose x 1000) for labetalol's stereoisomers in women and men, respectively, were S,R-labetalol 7.55 +/- 1.47 and 4.83 +/- 1.54 hr/L (p<0.05), S,S-labetalol 8.23 +/- 2.93 and 4.65 +/- 1.78 hr/L (p<0.05), R,S-labetalol 6.99 +/- 3.30 and 4.25 +/- 2.35 hr/L (p=0.11), and R,R-labetalol 3.91 +/- 2.57 and 3.55 +/- 3.08 hr/L (NS). CONCLUSION: The higher labetalol concentration in women than in men was explained largely by differences in inactive and alpha1-blocking stereoisomers. However, concentrations were similar between genders for the beta-blocking stereoisomer (R,R-labetalol), possibly explaining the similarity in antihypertensive response to the drug. This study highlights the importance of determining stereoisomer kinetics for agents administered as racemates, particularly when relating concentrations to pharmacologic response.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Labetalol_MeSH S_pharmacokinetics_MeSH Labetalol_pharmacokinetics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sex_Characteristics_MeSH M_Stereoisomerism_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 10853626
----K E
----T Update on the interaction between aspirin and angiotensin-converting enzyme inhibitors.
----A We summarized recent published literature regarding the significance of an interaction between aspirin and angiotensin-converting enzyme (ACE) inhibitors in patients with various cardiovascular diseases. A MEDLINE search (January 1998-July 1999) was performed and abstracts from the 1999 American College of Cardiology and 1998 American Heart Association annual scientific sessions were reviewed to identify pertinent studies. Material for discussion was identified through a MEDLINE search from January 1996-July 1999 and through cited references. The results of several studies added to our understanding of the clinical ramifications of an aspirin-ACE inhibitor interaction, but also introduced questions. These studies are largely contradictory, but do reiterate the possibility of an interaction, if only in certain subsets of patients. Low dosages (< or = 100 mg/day) of aspirin appear to be safer in this regard than higher dosages. The frequency and severity of the interaction and possible predisposing factors await future research.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Aspirin_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH M_Clinical_Trials_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Interactions_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 10853498
----K 1
----T [Quality of antihypertensive drug prescription in a health area]
----A OBJECTIVE: To find the compliance with previously established criteria on the quality of prescription of medication for hypertension. DESIGN: Retrospective and concurrent evaluation study of scientific and technical quality, with processing data, using as data source the clinical history. SETTING: Primary care teams in a Madrid Health Area. PARTICIPANTS: 873 clinical histories of hyper-intense patients in treatment with diuretics, beta-blockers, ACE inhibitors and/or calcium antagonists were chosen through systematic probabilistic sampling with a randomised start. MEASUREMENTS AND MAIN RESULTS: Data on age, sex, recording of treatment, linked pathologies and situations conditioning the choice of medicine were gathered. Information on the defined use criteria of the various pharmacological groups was also collected. 1145 drugs were used on 873 patients. Most common were the thiazide diuretics (36%), followed by ACE inhibitors (34.4%), calcium antagonists (21%) and beta-blockers (8.6%). 72% of the patients were undergoing one single therapy. 89.7% of the cases (95% CI, 87.43-91.59) had the treatment correctly recorded in the clinical record. Of the 721 hyperintense patients over 59 years old, 70.3% (95% CI, 66.81-73.60) fitted the defined criterion for use of diuretics. 48.7% fitted the ACE inhibitor criteria defined (CI, 43.71-53.78); 85.7% the beta-blocker criteria (CI, 76.85-91.69); and 58.7% the calcium antagonist criteria (95% CI, 52.17-64.9). CONCLUSIONS: The fit of the use of diuretics with the defined quality criterion is acceptable, while in the cases of ACE inhibitors and calcium antagonists the quality of prescription could be improved, while the use of beta-blockers is minimal.
----P Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Catchment_Area_(Health)_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Prescriptions__Drug_MeSH S_standards_MeSH Prescriptions__Drug_standards_MeSH M_Retrospective_Studies_MeSH M_Spain_MeSH 
****** 10855730
----K E
----T Blood pressure level and relation to other cardiovascular risk factors in male hypertensive patients without clinical evidence of ischemic heart disease.
----A Arterial hypertension is accompanied by increased morbidity and mortality and constitutes a substantial part of medical care. Antihypertensive intervention reduces the cardiovascular morbidity and mortality. The aims of the study were to evaluate the relationship between cardiovascular risk factors and the blood pressure (BP), and to evaluate the percentage of patients who had achieved a BP level as recommended by the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). BP was evaluated in relation to age, body mass index, duration of hypertension, cholesterol and triglyceride level, smoking status, information of regular exercise, a family history of ischemic heart disease (IHD) and drug treatment, in 220 men treated for arterial hypertension. In the univariate analyses we found a higher systolic blood pressure (SBP) with older age, higher SBP in smoking patients and lower SBP in patients with regular exercise. In a multivariate model age (p = 0.0004), smoking status (p = 0.01) and regular exercise (p= 0.06) were independently associated with SBP. There was a lower diastolic blood pressure (DBP) with older age, and age was independently associated with DBP. Office SBP was above 140 mmHg in 83% and above 160 mmHg in 44% of patients. During ambulatory blood pressure monitoring (AMBP), SBP was above 135 mmHg in 40% and above 155 mmHg in 15% of patients. In addition to male sex and hypertension there was a high percentage of other cardiovascular risk factors--43% was smoking, 21% had a family history of IHD, 77% had a se-cholesterol above 5.5 mmol/l and 48% had a se-triglyceride above 1.6 mmol/l. In a consecutive group of asymptomatic male treated hypertensive patients SBP is independently associated with age and smoking status, and DBP with age. A high percentage of the patients do not have a well controlled BP, and a high percentage have additional risk factors such as smoking, hypercholesterolaemia, hypertriglyceridaemia and a family history of IHD. This means that there is room for much improvement in the control of hypertension.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH P_Blood_Pressure_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH M_Exercise_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10857839
----K E
----T Effects of systemic beta-blocker therapy on the efficacy and safety of topical brimonidine and timolol. Brimonidine Study Groups 1 and 2.
----A PURPOSE: To determine the impact of coadminstration of systemic beta-blockers on the ocular hypotensive efficacy and safety of topical timolol, a nonselective, beta-blocker, and that of brimonidine, an alpha2-selective adrenergic agonist, in patients with glaucoma or ocular hypertension. DESIGN: Post hoc evaluation of data collected from two prospective, multicenter, randomized, double-masked, parallel-group, actively-controlled, 12-month clinical trials. PARTICIPANTS: Of the 926 subjects with ocular hypertension or glaucoma that were enrolled in the two prospective trials, 66 (7.1%) were concurrently maintained on systemic beta-blocker therapy. Of these patients, 34 had been assigned to the brimonidine group and 32 to the timolol group. METHODS: Subjects instilled into each eye either 1 drop of brimonidine 0.2% or timolol 0.5% twice daily for 1 year. Study subjects within medication treatment groups were classified as to their use or nonuse of concurrent systemic beta-blockers, and mean intraocular pressure (IOP) reduction, adverse events, heart rate, and blood pressure were compared. MAIN OUTCOME MEASURES: Mean IOP reduction from baseline was the primary efficacy variable. Adverse events and mean changes in heart rate and blood pressure from baseline were the primary safety variables. RESULTS: Timolol-treated subjects concurrently taking systemic beta-blockers had smaller decreases in IOP, a greater mean change in systolic (at week 2, months 1, 2, 6, and 9; P < or = 0.001) and diastolic blood pressure (months 2 and 6; P < or = 0.02), and a significantly greater mean decrease in heart rate (month 6; P = 0.004) compared with timolol subjects not taking systemic beta-blockers. By contrast, there was a modest enhancement of IOP-lowering efficacy at trough and no effect on blood pressure or heart rate in brimonidine-treated subjects who were concurrently receiving systemic beta-blocker therapy compared with brimonidine subjects not receiving systemic beta-blockers. CONCLUSIONS: Concurrent systemic beta-blocker therapy had no deleterious effect on ocular hypotensive efficacy and no impact on systemic safety parameters with topical brimonidine, whereas efficacy was reduced and systemic safety parameters were impacted with topical timolol. Ocular hypotensive agents other than beta-blockers, such as the alpha2 agonist brimonidine, may be a more appropriate first-line therapy for ocular hypertension and glaucoma patients concurrently taking systemic beta-blockers.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Administration__Topical_MeSH M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Quinoxalines_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 10856394
----K E
----T Treatment of heart failure with celiprolol, a cardioselective beta blocker with beta-2 agonist vasodilatory properties. The CELICARD Group.
----A Treatment with beta blockers results in improvement in functional status, and reduces mortality in patients with heart failure. A number of differences in the results noted could be due to additional properties of the specific beta blockers studied: absence of cardioselectivity, and existence of a vasodilator effect and of an associated antioxidant effect. We studied the effects of celiprolol, a cardioselective beta blocker with a stimulant effect on beta2 receptors. One hundred thirty-two patients presenting with chronic heart failure of various etiologies, with an ejection fraction of <40% and New York Heart Association cardiac functional status grades II and III were included in a randomized, double-blind, placebo-controlled study. The maximum dose of celiprolol (100 mg) was attained after 1 month. The study lasted 1 year. The primary evaluation criterion was functional class as evaluated using the Goldman questionnaire. There was no difference in efficacy between the 2 treatment groups in terms of functional class (p = 0.56). With regard to the secondary evaluation criteria, an improvement in DiBianco functional score was seen with celiprolol (p = 0.03), as well as a significant reduction in heart rate (p = 0.01). Ejection fraction increased in both groups (p = 0.15). There was no difference regarding improvement in left ventricular volume as determined at echocardiography or in exercise capacity. The safety profile of celiprolol was excellent. There was no difference in terms of cardiovascular mortality (2 receiving celiprolol vs 4 placebo), onset of arrhythmias (2 receiving celiprolol vs 3 placebo), worsening of heart failure (26 receiving celiprolol vs 23 placebo), or noncardiovascular adverse events (9 receiving celiprolol vs 14 placebo). The absence of a significant efficacy of celiprolol, a beta blocker with vasodilator properties, but exerting stimulation of beta2 receptors, suggests an unfavorable role of this latter property in heart failure. However, the safety profile of celiprolol was excellent. This beta blocker may consequently be used for its other indications, hypertension and angina, in patients presenting with altered cardiac function.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Celiprolol_MeSH S_adverse_effects_MeSH Celiprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10856401
----K I
----T Effectiveness of carvedilol alone versus carvedilol + pimobendan for severe congestive heart failure. For the Keio Interhospital Cardiology Study (KICS) Group.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Pyridazines_MeSH S_pharmacology_MeSH Pyridazines_pharmacology_MeSH S_therapeutic_use_MeSH Pyridazines_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10860176
----K 5
----T Beta-blockers, angiotensin-converting enzyme inhibitors, and calcium antagonists in treatment of elderly patients with acute myocardial infarction.
----A Administration of beta-blockers reduces mortality among old persons during and after acute myocardial infarction. The American College of Cardiology/American Heart Association guidelines recommend that persons without contraindications to use of beta-blockers should be administered beta-blockers within a few days of myocardial infarction (if administration is not initiated acutely) and that their administration should be continued indefinitely. These guidelines also recommend the use of angiotensin converting enzyme inhibitors in treating persons within the first 24 h of suspected onset of acute myocardial infarction with ST-segment elevation in two or more anterior precordial leads or with congestive heart failure in the absence of significant hypotension or other contraindications to use of ACE inhibitors; and persons during and after convalescence from acute myocardial infarction with congestive heart failure associated with an abnormal left ventricular ejection fraction (LVEF) or with asymptomatic left ventricular systolic dysfunction with a LVEF < 40%. These guidelines state that there are no class I indications for using calcium antagonists after myocardial infarction. If patients have persistent angina pectoris after myocardial infarction despite treatment with beta-blockers and nitrates or hypertension inadequately controlled by other drugs, administration of a nondihydropyridine calcium antagonist such as verapamil or diltiazem should be added to the therapeutic regimen if the LVEF is normal. If the LVEF is abnormal, administration of amlodipine or felodipine should be added to the therapeutic regimen.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Practice_Guidelines_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10861116
----K 1
----T [A randomized controlled study of ligustrazine in combination with propranolol for prevention of recurrent esophageal varices bleeding]
----A OBJECTIVE: To assess the efficacy of Ligustrazine in combination with propranolol in the prevention of recurrent esophageal varices bleeding following liver cirrhosis, and its act mechanism. METHODS: A prospective controlled study was conducted on 74 patients, in whom 38 belonged to treatment group, and 36 to control group. By detecting the portal system hemodynamics in patients with portal hypertension and esophageal varices using color Doppler ultrasound technique, the therapeutic efficacy and safety were investigated. Meanwhile the blood pressure, heart rate, hepatic and renal function were dynamically observed. RESULTS: After four weeks administration of the drugs, the flow of portal vein and splenic vein, the diameter of portal vein and splenic vein in the treatment group were significantly decreased with the values of 1152.36A387.46 ml/min, 529.35A326.31 ml/min, 1.36A0.28 cm, and 0.94A0.19 cm, respectively. No adverse effect was observed on the system circulation and the liver function. In the follow-up period of two years, the rebleeding rate and mortality rate in the placebo group were higher than that in the treatment group, but patients with liver cirrhosis Grade C in the two groups were not significant different. CONCLUSION: Low dose ligustrazine plus propranolol is a safe and effective therapy in preventing recurrent esophageal varices bleeding, and worth further trial.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Prospective_Studies_MeSH M_Pyrazines_MeSH S_administration_&_dosage_MeSH Pyrazines_administration_&_dosage_MeSH M_Recurrence_MeSH 
****** 10862571
----K E
----T Stamps in Cardiology. Hypertension.
----A 
----P Historical_Article Journal_Article 
----M M_Blood_Pressure_Determination_MeSH S_history_MeSH Blood_Pressure_Determination_history_MeSH S_nursing_MeSH Blood_Pressure_Determination_nursing_MeSH M_History_of_Medicine__20th_Cent__MeSH M_Human_MeSH P_Philately_MeSH M_United_Nations_MeSH M_West_Indies_MeSH 
****** 10868496
----K E
----T Comparison of the long-term efficacy of implantable defibrillators and sotalol for documented spontaneous sustained ventricular tachyarrhythmias secondary to coronary artery disease.
----A BACKGROUND: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. AIM: To compare the mortality in patients treated with ATPICD and sotalol for documented spontaneous sustained ventricular tachyarrhythmias occurring late after previous myocardial infarction. METHODS: In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol. RESULTS: The two groups were well-matched for age, type of presenting arrhythmia, severity of coronary artery disease and ventricular function. At 36 months Kaplan-Meier estimates of mortality from ventricular tachyarrhythmia were 0% with ATPICD and 15% with sotalol (p=0.03). Kaplan-Meier estimates of total mortality at 36 months were 12% with ATPICD and 25% with sotalol (p=0.09). Multivariate analysis showed hazard ratio of 7.9 (p=0.06) for death from ventricular tachyarrhythmia in patients treated with sotalol compared to ATPICD.CONCLUSIONS: While no difference in total mortality was demonstrated, treatment with ATPICD is probably superior to sotalol for preventing deaths due to ventricular tachyarrhythmia.
----P Journal_Article 
----M M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH P_Defibrillators__Implantable_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Retrospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Survival_Analysis_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 10867087
----K E
----T Use of resources, quality of life, and clinical outcomes in patients with and without new Q waves after thrombolytic therapy for acute myocardial infarction (from the GUSTO-I trial).
----A Previous reports indicate that patients who do not develop Q waves after thrombolytic therapy are a different population with a better long-term survival than those who do develop Q waves. However, the use of resources, quality of life, and health status of this population have not been fully evaluated. Using data from the Economics and Quality of Life subset of the Global Utilization of Streptokinase and tPA for Occluded Arteries study, we examined 30-day and 1-year mortality, use of resources, and quality-of-life measures among 1,830 of 3,000 patients with acute myocardial infarction and ST-segment elevation treated with thrombolytic therapy. At hospital discharge, 555 patients (30.2%) had not developed Q waves. These patients had lower mortality than patients with Q waves at 30 days (1.6% vs 4.5%, p <0.01) and at 1 year (4.7% vs 6.8%, p <0.04). Recurrent chest pain and dyspnea were similar at 30 days and 1 year. Patients without Q waves had significantly more angiography and trends toward higher readmission, revascularization, and use of calcium antagonists at 30 days. Angiography, revascularization, readmission, and quality of life were equivalent from 30 days to 1 year, with no sign of late instability. Logistic regression analysis showed an association between in-hospital revascularization and better survival and quality of life at 1 year. Conversely, there was no association between in-hospital use of calcium antagonists and outcome to explain the lower mortality in non-Q-wave patients. The absence of Q waves after thrombolytic therapy is a marker of success, implying better prognosis and equivalent quality of life, use of resources, and health status than for patients with Q-wave acute myocardial infarction and no sign of long-term unstable clinical course.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH S_utilization_MeSH Coronary_Angiography_utilization_MeSH P_Electrocardiography_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Health_Status_MeSH M_Human_MeSH M_Length_of_Stay_MeSH S_statistics_&_numerical_data_MeSH Length_of_Stay_statistics_&_numerical_data_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH M_Patient_Readmission_MeSH M_Prognosis_MeSH P_Quality_of_Life_MeSH M_Recurrence_MeSH M_Streptokinase_MeSH S_therapeutic_use_MeSH Streptokinase_therapeutic_use_MeSH M_Survival_Rate_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH 
****** 10867093
----K E
----T Clinical characteristics of patients intolerant to VVIR pacing.
----A The incidence and clinical predictors of the development of intolerance to VVIR pacing have not been extensively studied in prospective long-term randomized trials comparing different pacing modes. The frequency and clinical factors predicting intolerance to ventricular pacing are controversial. The Pacemaker Selection in the Elderly (PASE) Trial enrolled 407 patients aged >/=65 years in a 30-month, single-blind, randomized, controlled comparison of quality of life and clinical outcomes with ventricular pacing and dual-chamber pacing in patients undergoing dual-chamber pacemaker implantation for standard clinically accepted indications. We reviewed the clinical, hemodynamic, and electrophysiologic variables at the time of pacemaker implantation in 204 patients enrolled in the PASE trial and randomized to the VVIR mode, some of whom subsequently required crossover (reprogramming) to DDDR pacing. During a median follow-up of 555 days, 53 patients (26%) crossed over from VVIR to DDDR pacing. A decrease in systolic blood pressure during ventricular pacing at the time of pacemaker implantation (p = 0.001), use of beta blockers at the time of randomization (p = 0.01), and nonischemic cardiomyopathy (p = 0.04) were the only variables that predicted crossover in the Cox multivariate regression model. After reprogramming to the dual-chamber mode, patients showed improvement in all aspects of quality of life, with significant improvements in physical and emotional role. The high incidence of crossover from VVIR to DDDR pacing along with significant improvements in quality of life after crossover to DDDR pacing strongly favors dual-chamber pacing compared with single-chamber ventricular pacing in elderly patients requiring permanent pacing.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Blood_Pressure_MeSH M_Bradycardia_MeSH S_physiopathology_MeSH Bradycardia_physiopathology_MeSH S_therapy_MeSH Bradycardia_therapy_MeSH M_Cardiac_Pacing__Artificial_MeSH S_adverse_effects_MeSH Cardiac_Pacing__Artificial_adverse_effects_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH M_Comparative_Study_MeSH M_Dyspnea_MeSH S_etiology_MeSH Dyspnea_etiology_MeSH S_physiopathology_MeSH Dyspnea_physiopathology_MeSH S_prevention_&_control_MeSH Dyspnea_prevention_&_control_MeSH M_Edema_MeSH S_etiology_MeSH Edema_etiology_MeSH S_prevention_&_control_MeSH Edema_prevention_&_control_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Foot_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Syncope_MeSH S_etiology_MeSH Syncope_etiology_MeSH S_physiopathology_MeSH Syncope_physiopathology_MeSH S_prevention_&_control_MeSH Syncope_prevention_&_control_MeSH 
****** 10872552
----K E
----T beta2-adrenoceptor gene polymorphisms and blood pressure variations in East Anglian Caucasians.
----A OBJECTIVE: The amino-terminal polymorphisms, Arg16Gly and Gln27Glu, of the beta2-adrenergic receptor (beta2AR) have been shown to affect regulation of the receptor expression by an agonist in cell culture studies. The Arg16Gly polymorphism has also been recently shown to be associated with essential hypertension. We therefore evaluated whether the amino-terminal polymorphisms of beta2AR are associated with hypertension in a Caucasian population. SUBJECTS AND METHODS: We performed an association study in 298 hypertensive patients and an equal number of age-matched normotensive controls from the East Anglian region, with blood pressure assessed categorically and quantitatively. We also examined the influence of the amino-terminal polymorphisms on blood pressure response to beta-blockade in 144 of the patients randomly assigned to this class of drug. Genotyping of the Arg16Gly polymorphism was undertaken by a newly designed mismatched polymerase chain reaction (PCR) and digestion with Nde I, whereas the Gln27Glu polymorphism was genotyped by PCR followed by Fnu4H I cleavage. RESULTS: We found no differences in the genotype or allele frequencies of the beta2AR polymorphisms between hypertensive and normotensive participants. There was also no association between the beta2AR genotypes and variations in either basal blood pressure or the blood pressure response to a beta-blocker. CONCLUSION: These findings suggest that the amino-terminal polymorphisms of the beta2AR gene are unlikely to constitute major susceptibility for essential hypertension in the East Anglian population.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Alleles_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_England_MeSH M_European_Continental_Ancestry_Group_MeSH S_genetics_MeSH European_Continental_Ancestry_Group_genetics_MeSH M_Female_MeSH M_Gene_Frequency_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Polymorphism_(Genetics)_MeSH S_physiology_MeSH Polymorphism_(Genetics)_physiology_MeSH M_Receptors__Adrenergic__beta_MeSH S_genetics_MeSH Receptors__Adrenergic__beta_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH P_Variation_(Genetics)_MeSH 
****** 10872566
----K I
----T The efficacy and tolerability of losartan versus atenolol in patients with isolated systolic hypertension. Losartan ISH Investigators Group.
----A OBJECTIVE: To compare the efficacy and tolerability of angiotensin II (Ang II) antagonist losartan and the beta-blocker atenolol in the treatment of patients with isolated systolic hypertension (ISH) after 16 weeks of treatment. METHODS: A double-blind, randomized, multi-country study was carried out in 273 patients with ISH. Patients with a sitting systolic blood pressure (SiSBP) of 160-205 mmHg, and a sitting diastolic blood pressure (SiDBP) < 90 mmHg at screening and at placebo baseline were subjected to a 4-week placebo period and then randomly grouped to receive 50 mg losartan or 50 mg atenolol once daily for 16 weeks. At 8 and 12 weeks, patients not controlled (SiDBP > or = 160 mmHg) were given additional treatment of 12.5 mg hydrochlorothiazide (HCTZ) once daily. RESULTS: Similar significant reductions in SiSBPs (mean +/- SD) were obtained with 50 mg losartan and 50 mg atenolol, from 173.7 +/- 10.3 and 173.5 +/- 10.7 mmHg at baseline to 149.0 +/- 15.5 and 148.2 +/- 15.3 mmHg after 16 weeks of losartan or atenolol treatment respectively. Sixty-seven percent of the losartan-treated and 64% of the atenolol-treated patients remained on monotherapy throughout the study. Only 1.5% of the losartan-treated patients withdrew because of a clinical adverse event (CAE) compared with 7.2% in the atenolol-treatment group (P= 0.035). Drug-related CAEs were observed significantly more frequently with atenolol than with losartan treatment (20.3 versus 10.4%; P = 0.029). CONCLUSION: It is concluded that 50 mg losartan and 50 mg atenolol produced comparable reductions in SiSBP in patients with ISH but losartan was better tolerated. This is the first demonstration of the therapeutic value of selective Ang II receptor blockade with losartan in the treatment of ISH.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 10877373
----K 5
----T Clinical success and quality of life with brimonidine 0.2% or timolol 0.5% used twice daily in glaucoma or ocular t hypertension: a randomized clinical trial. Brimonidine Outcomes Study Group I.
----A PURPOSE: To compare the clinical success rates and quality of life impact of brimonidine 0.2% with timolol 0.5% in newly diagnosed patients naive to glaucoma therapy. METHODS: A prospective, multicenter, randomized, double-masked, clinical effectiveness trial in which the clinical outcomes of twice daily brimonidine tartrate 0.2% were compared with those of timolol maleate 0.5% in patients with glaucoma and' ocular hypertension was conducted. Two hundred nineteen patients were enrolled--111 in the brimonidine group and 108 in the timolol group. Patients instilled their study medications twice daily for 4 months. Factors for determining clinical success were reduction of intraocular pressure (IOP), safety, and adverse events. Quality of life effects were assessed with the SF-36 Health Survey and Glaucoma Disability Index questionnaires. RESULTS: Clinical success was 71% (75/106) with brimonidine and 70% (73/105) with timolol as initial treatment. The overall mean decrease in IOP was 6.5 mm Hg with brimonidine and 6.2 mm Hg with timolol. Few patients reported a specific adverse event and, with the exception of a slightly higher rate of ocular burning and stinging in the brimonidine group, there were no significant between-group differences. No significant chronotropic effects on the heart were seen with brimonidine, while small but significant mean decreases in heart rate were seen at months 1 and 4 with timolol. Mean systolic and diastolic blood pressure remained relatively stable in both groups. Quality of life remained stable, with no significant between-group differences. CONCLUSIONS: As a first-line agent for the treatment of glaucoma and ocular hypertension, brimonidine has clinical effectiveness equivalent to timolol, but with less chronotropic effect on the heart. Brimonidine is a viable alternative to timolol for first-line therapy in glaucoma and ocular hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH S_administration_&_dosage_MeSH Ophthalmic_Solutions_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Prospective_Studies_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10873979
----K E
----T Effects of glaucoma medications on the cardiorespiratory and intraocular pressure status of newly diagnosed glaucoma patients.
----A AIMS: To evaluate the short term cardiovascular, respiratory, and intraocular pressure (IOP) effects of four glaucoma medications in newly diagnosed glaucoma patients. METHODS: 141 newly diagnosed glaucoma patients were recruited and underwent a full ocular, cardiovascular, and respiratory examination, including an electrocardiogram (ECG) and spirometry. They were prescribed one of four topical glaucoma medications and reviewed 3 months later. One eye of each patient was randomly chosen for analysis, performed using analysis of variance and the chi(2) test. RESULTS: Latanoprost had the greatest mean IOP lowering effect in both the primary open angle glaucoma (POAG) (p = 0.005) and the "presumed" normal tension glaucoma (NTG) groups (p = 0.33), reducing the IOP by 8.9 mm Hg and 4.1 mm Hg respectively. Timolol was associated with lowered pulse rates and reductions in the spirometry measurements. 41% of patients using brimonidine complained of systemic side effects and over 55% of patients using betaxolol complained of ocular irritation. 28% of patients required an alteration in their glaucoma management. CONCLUSIONS: Latanoprost appears to be a useful primary treatment for glaucoma patients, in view of superior IOP control and a low incidence of local and systemic side effects. Timolol causes a reduction in measurements of respiratory function, a concern in view of the potential subclinical reversible airways disease in the elderly glaucoma population. Brimonidine is associated with substantial, unpredictable systemic side effects and betaxolol causes ocular irritation and weak IOP control. Spirometry is advised in all patients receiving topical beta blocker therapy to control their glaucoma.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Betaxolol_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Forced_Expiratory_Volume_MeSH S_drug_effects_MeSH Forced_Expiratory_Volume_drug_effects_MeSH M_Glaucoma_MeSH S_complications_MeSH Glaucoma_complications_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lung_Diseases__Obstructive_MeSH S_complications_MeSH Lung_Diseases__Obstructive_complications_MeSH M_Male_MeSH M_Ophthalmic_Solutions_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Prostaglandins__Synthetic_MeSH S_therapeutic_use_MeSH Prostaglandins__Synthetic_therapeutic_use_MeSH M_Pulse_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Vital_Capacity_MeSH S_drug_effects_MeSH Vital_Capacity_drug_effects_MeSH 
****** 10878693
----K E
----T Difference in blood pressure, but not in heart rate, between measurements performed at a health centre and at a hospital by one and the same physician.
----A Background: Blood pressure (BP) has been found to vary between examiners, for example it is often higher when measured by a physician than by a nurse. Whether the location for the physician-measured BP is also a source of variation has, however, not been studied. Hence, we found it of interest to find out if the location used for examination was of any significance.Objective: To explore if BP and/or heart rate measured in the same subjects by the same general practitioner in the health centre and at the hospital, differed.Method: Twenty-five hypertensive and 25 age-matched normotensive middle-aged men had their office BP and heart rate recorded by one and the same female general practitioner (IE) who was well known to them, at both the health centre before ambulatory BP equipment was attached to the subject and at the clinical physiological department before an exercise test. The hypertensive patients performed an exercise test and ambulatory BP was measured before and after being treated.Results:The hypertensive patients' office BP was lower at the health centre than at the hospital, both when they were untreated and after they were treated. The difference (systolic/diastolic (s.d.)) was 9.4/6.0 (7.4/2.7) mm Hg (P < 0.001 for systolic and diastolic BP), when they were untreated. Corresponding figures when they were treated were 5.4/4.0 (9.4/4.7) mm Hg, a significant difference in diastolic BP (P < 0.001). The normotensive subjects also had a lower office BP at the health centre than at the hospital. The difference (systolic/diastolic (s.d. ) was 1.8/5.3 (7.0/5.0) mm Hg (P < 0.001 for diastolic BP). Heart rate did not differ between recordings in the health centre and in the hospital, either in the hypertensives or in the normotensives. Conclusion: Office BP differed significantly between measurements performed in the health centre and at the hospital. Hence, being examined at a hospital seemed to be a stronger stimuli in most patients than to be examined in a health centre. When diagnosing or evaluating treatment in hypertension, this may have implications. Journal of Human Hypertension (2000) 14, 355-358
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Ambulatory_Care_Facilities_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_Determination_MeSH S_psychology_MeSH Blood_Pressure_Determination_psychology_MeSH S_standards_MeSH Blood_Pressure_Determination_standards_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH P_Environment_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Hospitals_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Reference_Values_MeSH M_Sweden_MeSH 
****** 10894441
----K E
----T Circadian heart rate response to chronotherapy versus conventional therapy in patients with hypertension and myocardial ischemia.
----A BACKGROUND: Changes in heart rate (HR) may contribute to the higher incidence of cardiovascular events in the morning. HYPOTHESIS: The objectives of this analysis were to assess HR patterns in two populations (patients with chronic stable angina or stage I to III hypertension) and to compare the effects of various antianginal and antihypertensive treatments on HR. METHODS: This was a retrospective analysis of HR data from two clinical trials evaluating the efficacy of controlled-onset, extended-release (COER)-verapamil. The effects of COER-verapamil were compared with placebo, nifedipine gastrointestinal therapeutic system (GITS), amlodipine, and the combination of amlodipine and atenolol. RESULTS: In patients with angina (n = 498), the change from baseline in HR following 4 weeks of treatment was -6.7 +/- 10.5 beats/min in the COER-verapamil group, -10.8 +/- 10.8 beats/min in the amlodipine/atenolol group, + 2.5 +/- 9.1 beats/ min in the amlodipine monotherapy group, and -1.3 +/- 10.5 beats/min in the placebo group (p<0.001). Data were stratified based on whether patients experienced asymptomatic ischemia during baseline ambulatory electrocardiographic monitoring. The circadian HR pattern was morphologically similar in all groups; however, differences in the magnitude of HR response were evident. In the subset of patients with asymptomatic ischemia (n = 101), treatment with amlodipine monotherapy increased HR compared with placebo. In this same subset of patients, HR reductions were achieved with COER-verapamil and amlodipine/atenolol. In patients with hypertension (n = 557), the change in HR following 10 weeks of treatment was -3.3 beats/min for patients treated with COER-verapamil compared with + 2.0 beats/min for patients treated with nifedipine GITS (p < 0.0001, between-group differences). CONCLUSION: This analysis demonstrates that morphologically similar circadian patterns of HR occur in both hypertensive patients and those with angina. In addition, significant variation exists among antianginal and antihypertensive agents regarding HR effects.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH P_Chronotherapy_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Randomized_Controlled_Trials_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH 
****** 10891904
----K 5
----T Autoantibodies to glutamic acid decarboxylase in patients with therapy-resistant epilepsy.
----A BACKGROUND: Autoantibodies to glutamic acid decarboxylase (GAD-A) are present in type 1 diabetes and stiff man syndrome (SMS), and have also been reported in cerebellar ataxia. Epilepsy was present in 4 of 19 patients with SMS and GAD-A, implying that epilepsy sometimes is associated with anti-GAD autoimmunity. METHODS: The authors investigated the prevalence of GAD-A in patients with therapy-resistant localization-related epilepsy (n = 51) and generalized epilepsy (n = 49) by a radiobinding assay. The positive samples were confirmed by immunohistochemistry and immunoblotting of recombinant human GAD65. RESULTS: GAD-A were found in eight patients with localization-related epilepsy, whereas none of the patients with generalized epilepsy, other neurologic disorders (n = 38), or the control subjects (n = 48) had GAD-A. Two patients had high levels of GAD-A, similar to SMS, whereas six patients had significantly lower titers, characteristic of type 1 diabetes. The two patients with high levels of GAD-A had GAD-A both in serum and CSF by immunohistochemistry and immunoblotting. Both of them had longstanding therapy-resistant temporal lobe epilepsy but did not have diabetes. One had a history of autoimmune disease, whereas the other had serologic evidence of multiple autoantibodies without any clinical signs of autoimmune disease. CONCLUSIONS: GAD autoimmunity may be associated with refractory localization-related epilepsy.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Autoantibodies_MeSH S_blood_MeSH Autoantibodies_blood_MeSH S_immunology_MeSH Autoantibodies_immunology_MeSH M_Cerebellum_MeSH S_drug_effects_MeSH Cerebellum_drug_effects_MeSH S_immunology_MeSH Cerebellum_immunology_MeSH S_pathology_MeSH Cerebellum_pathology_MeSH M_Drug_Resistance_MeSH S_immunology_MeSH Drug_Resistance_immunology_MeSH M_Epilepsy_MeSH S_blood_MeSH Epilepsy_blood_MeSH S_drug_therapy_MeSH Epilepsy_drug_therapy_MeSH S_immunology_MeSH Epilepsy_immunology_MeSH S_pathology_MeSH Epilepsy_pathology_MeSH M_Female_MeSH M_Glutamate_Decarboxylase_MeSH S_blood_MeSH Glutamate_Decarboxylase_blood_MeSH S_immunology_MeSH Glutamate_Decarboxylase_immunology_MeSH M_Human_MeSH M_Immunohistochemistry_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Radioligand_Assay_MeSH 
****** 10896486
----K I
----T Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH P_Esophagoscopy_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Ligation_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Recurrence_MeSH 
****** 10895836
----K I
----T Therapeutic benefits of ACE inhibitors and other antihypertensive drugs in patients with type 2 diabetes.
----A OBJECTIVE: To assess whether ACE inhibitors are superior to alternative agents for the prevention of cardiovascular events in patients with hypertension and type 2 diabetes. RESEARCH DESIGN AND METHODS: This study is a review and meta-analysis of randomized controlled trials that included patients with type 2 diabetes and hypertension who were randomized to an ACE inhibitor or an alternative drug, were followed for > or =2 years, and had adjudicated cardiovascular events. RESULTS: A total of 4 trials were eligible. The Appropriate Blood Pressure Control in Diabetes (ABCD) trial (n = 470) compared enalapril with nisoldipine, the Captopril Prevention Project (CAPPP) (n = 572) compared captopril with diuretics or beta-blockers, the Fosinopril Versus Amlodipine Cardiovascular Events Trial (FACET) (n = 380) compared fosinopril with amlodipine, and the U.K. Prospective Diabetes Study (UKPDS) (n = 758) compared captopril with atenolol. The cumulative results of the first 3 trials showed a significant benefit of ACE inhibitors compared with alternative treatments on the outcomes of acute myocardial infarction (63% reduction, P < 0.001), cardiovascular events (51% reduction, P < 0.001), and all-cause mortality (62% reduction, P = 0.010). These findings were not observed in the UKPDS. The ACE inhibitors did not appear to be superior to other agents for the outcome of stroke in any of the trials. None of the findings were explained by differences in blood pressure control. CONCLUSIONS: Compared with the alternative agents tested, ACE inhibitors may provide a special advantage in addition to blood pressure control. The question of whether atenolol is equivalent to captopril remains open. Conclusive evidence on the comparative effects of antihypertensive treatments will come from large prospective randomized trials.
----P Journal_Article Meta-Analysis 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10898425
----K I
----T Use of metoprolol CR/XL to maintain sinus rhythm after conversion from persistent atrial fibrillation: a randomized, double-blind, placebo-controlled study.
----A OBJECTIVES: The primary objective of the present study was to assess the efficacy of metoprolol CR/XL to reduce the risk of relapse after cardioversion of persistent atrial fibrillation to sinus rhythm. BACKGROUND: Indirect data from studies with d,l sotalol provide evidence that the beta-blocking effects of the compound are important in maintaining sinus rhythm after cardioversion of atrial fibrillation. METHODS: After successful conversion to sinus rhythm, 394 patients with a history of persistent atrial fibrillation were randomly assigned to treatment with metoprolol CR/XL or placebo. The two treatment groups were similar with respect to all pretreatment characteristics. Patients were seen on an outpatient basis for recording of resting electrocardiogram (ECG) after one week, one, three and six months of follow-up or whenever they felt that they had a relapse into atrial fibrillation or experienced an adverse event. RESULTS: In the metoprolol CR/XL group, 96 patients (48.7%) had a relapse into atrial fibrillation compared with 118 patients (59.9%) in the placebo group (p = 0.005). Heart rate in patients after a relapse into atrial fibrillation was significantly lower in the metoprolol group (98 +/- 23 beats/min) than in the placebo group (107 +/- 27 beats/min). The rate of adverse events reported was similar in both groups when the difference in follow-up time was taken into account. CONCLUSIONS: The results of this double-blind, placebo-controlled study in patients after cardioversion of persistent atrial fibrillation showed that metoprolol CR/XL was effective in preventing relapse into atrial fibrillation or flutter.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atrial_Fibrillation_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH P_Electric_Countershock_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__beta-1_antagonists_&_inhibitors_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10742707
----K E
----T Celiprolol augments the effect of physical exercise on insulin sensitivity and serum lipid levels in chronic heart failure.
----A PURPOSE: Impaired insulin sensitivity has been linked with chronic heart failure (CHF). Exercise has a beneficial effect on insulin sensitivity in healthy subjects. It is used also as an adjunctive therapy in patients with CHF. We studied the effect of randomized treatment with celiprolol, a vasodilating beta(1)-adrenoceptor antagonist, 200 mg once daily (n=20) or placebo (n=11) on serum lipid levels and insulin sensitivity in patients with CHF. In addition, all subjects participated in a 6-month exercise training protocol. Thirteen subjects in the celiprolol and eight subjects in the control group were on additional beta(1)-adrenoceptor antagonist as part of their tailored CHF therapy. Insulin sensitivity was determined using the hyperinsulinemic euglycemic clamp test (diabetic subjects excluded, n=11 for the celiprolol group and n=8 for the placebo group). RESULTS: Insulin sensitivity index (ISI) increased by 33% (P<0.05) in the celiprolol group and by 17% (NS) in the control group. The mean increase in the whole group was 20% [from 68.2+/-11.5 to 81.7+/-10.7 ml/min/kg (mU/l), P<0.05]. No change was found in the total cholesterol level. HDL cholesterol levels increased by 12% (from 0.98+/-0.05 to 1.10+/-0.05 mmol/l, P<0. 005), and HDL/total cholesterol and HDL/LDL cholesterol ratios by 15% and 16%, respectively (P<0.005). The increase in serum fasting HDL cholesterol level was greater in the celiprolol-treated group (P<0.05). At baseline ISI correlated with maximal oxygen uptake (r=0. 65, P<0.0001) and body mass index (r=-0.55, P<0.001). The change in ISI correlated weakly with the improvement in muscle exercise capacity (r=0.53, P<0.05). CONCLUSIONS: Insulin sensitivity and serum lipid levels may be favorably affected by exercise training in subjects with mild-to-moderate CHF. Celiprolol, a vasodilating beta1- selective adrenoceptor antagonist, potentiates this effect.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH P_Insulin_Resistance_MeSH S_physiology_MeSH Insulin_Resistance_physiology_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 10742710
----K E
----T Update of ELITE-II, BEST, CHAMP, and IMPRESS clinical trials in heart failure.
----A The ELITE-II, BEST and CHAMP Trials were reported for the first time at the American Heart Association in November 1999. These trials provide valuable new information to guide clinical practice in the management of heart failure and of myocardial infarction, although none mandate a major change from current clinical practice. The IMPRESS trial of the vasopeptidase inhibitor, omapatrilat, indicated a promising new treatment for the management of heart failure.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Exercise_Tolerance_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Pyridines_MeSH S_therapeutic_use_MeSH Pyridines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Thiazepines_MeSH S_therapeutic_use_MeSH Thiazepines_therapeutic_use_MeSH 
****** 10856731
----K E
----T MIC trial: metoprolol in patients with mild to moderate heart failure: effects on ventricular function and cardiopulmonary exercise testing.
----A Beta-blocker therapy results in a functional benefit in patients with heart failure (CHF) due to idiopathic dilated cardiomyopathy (DCM). This study assessed if similar effects were observed in patients with ischemic heart disease (CAD), NYHA II-III after 6 months of therapy with metoprolol. Methods and results: Fifty-two patients with CHF secondary to DCM (26 patients) and CAD (26 patients) and a left ventricular ejection fraction (EF)<40% were enrolled in the placebo-controlled study. The study medication was titrated over 6 weeks, the mean final dosage was 135 mg/day. Three patients died due to cardiogenic shock, two received placebo and one metoprolol. Eight patients did not complete the study due to non-compliance. Metoprolol significantly reduced heart rate at rest and after submaximal and maximal exercise. Vo(2)-max and Vo(2)-AT as well as the 6-min walk test improved significantly after metoprolol treatment. There was a significant increase in EF at rest (27.3-35. 2%), submaximal (28.5-37.7%) and maximal exercise (28.7-40.9%) in the metoprolol-treated patients. No differences were found between patients with CAD and DCM. We also observed reduced left ventricular volumes. Conclusion: The additional therapy with metoprolol improved cardiac function and the cardiopulmonary exercise capacity in patients with CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiac_Volume_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Prospective_Studies_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10856736
----K E
----T Clinical trials update: OPTIME-CHF, PRAISE-2, ALL-HAT.
----A This is a summary of reports of presentation made at the American College of Cardiology 49th Scientific Sessions, Anaheim, 12-15 March 2000. Studies with a particular interest for heart failure physicians have been reviewed. OPTIME-CHF: Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure. OPTIME-CHF was a randomised-controlled trial comparing a 48-h infusion of Milrinone or standard therapy in 951 patients recruited over a 2-year period. Patients were excluded if the investigator believed their clinical condition mandated inotropic therapy. Patients were randomised within 48 h of admission for an acute exacerbation of chronic heart failure to receive Milrinone or placebo infision for 48 h. Of the patients 43% were diabetics, 70% were receiving an angiotensin converting enzyme inhibitor, 25% were already on a beta-Blocker, and 34% had atrial fibrillation. There was no significant difference between the two groups in length of hospital stay during the index admission, subsequent readmissions and days in hospital over the following 60 days. Subjective clinical assessment scores were also no different. There was an average admission rate over the next year of one per patient in both groups. However, there was a significant increase in the incidence of sustained hypotension in the Milrinone group, which accounted for all of the increased adverse event rates for the active therapy. The 60-day mortality was 10% in both groups. This and previous trials of the oral formulation of Milrinone have now clearly demonstrated a lack of benefit with Milrinone in either during acute exacerbations of or in stable severe chronic heart failure [Packer M, Carver JR, Rodeheffer RJ et al. Effect of oral Milrinone on mortality in severe chronic heart failure. N Engl J Med 1991;325:1468-1475.]. Medium sized studies of Milrinone in patients with milder severities of heart failure also suggested an adverse impact on prognosis in the presence or absence of digoxin [DiBianco R, Shabetai R, Kostuk W, Moran J, Schlant RC, Wright R. A comparison of oral Milrinone, digoxin, and their combination in the treatment of patients with chronic heart failure. N Engl J Med 1989;320:677-683.]. Whether Milrinone even has a role for the management of a haemodyamic crisis requiring inotropic therapy must also be questioned.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Milrinone_MeSH S_therapeutic_use_MeSH Milrinone_therapeutic_use_MeSH M_Pyridines_MeSH S_therapeutic_use_MeSH Pyridines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiazepines_MeSH S_therapeutic_use_MeSH Thiazepines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10908094
----K I
----T The impact of beta-blockade on mortality rates in patients with congestive heart failure.
----A The beneficial effects of beta-adrenergic blockade on mortality rates in patients after a myocardial infarction have been clear for decades. The efficacy data are now just as apparent for patients with heart failure. Although there are many subgroups of patients in whom the mortality effects of beta-blockers are not proven, knowledge about these specific populations continues to increase. Nevertheless, more information is needed so that we can properly tailor our therapy for individual patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Meta-Analysis_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10908095
----K I
----T The role of beta-blockers in preventing sudden death in heart failure.
----A Sudden death accounts for one third to one half of the deaths in patients with heart failure. Recent studies using beta-adrenergic blockers in patients with reduced systolic function and heart failure symptoms have shown significant reductions in overall mortality rates. This article discusses the role of beta-blockers in preventing sudden death in these patients. Six large beta-blocker trials in patients with heart failure have been published to date, with a combined relative risk reduction for sudden death of 38% (confidence interval [CI] 0.53-0.23; P < .001). Although dependent on a nonmechanistic definition of sudden death, the clinical trials of beta-blockers to date have shown that they significantly reduce the risk of sudden death in patients with heart failure. Future studies are required to define the role of other heart failure therapies in the context of this new standard of care.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Patient_Selection_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Tachycardia__Ventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Ventricular_Fibrillation_MeSH S_prevention_&_control_MeSH Ventricular_Fibrillation_prevention_&_control_MeSH 
****** 10908097
----K E
----T Clinical use of beta-blockers in patients with heart failure.
----A Recognition of the role of the sympathetic nervous system in chronic heart failure has resulted in dramatic changes in the way heart failure is viewed, providing strong evidence for the therapeutic role for beta-adrenergic blocking agents. This treatment strategy does not provide short-term hemodynamic improvement and may even worsen symptoms initially. However, beta-blockers can be administered with good or even excellent tolerability by slowly withdrawing adrenergic support to the failing heart. Results of clinical trials have shown that long-term treatment with beta-blockers improves ventricular function and reduces mortality rates in patients with mild-to-moderate heart failure. Although the improvement in ventricular function is a beta-blocker class effect, there are distinct differences in antiadrenergic activity and tolerability among the first-, second-, and third-generation agents. These differences--as well as practical strategies for dose titration and the management of decompensation--are the focus of this article.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Meta-Analysis_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 10903600
----K E
----T A comparative study of the elective treatment of variceal hemorrhage with beta-blockers, transendoscopic sclerotherapy, and surgery: a prospective, controlled, and randomized trial during 10 years.
----A OBJECTIVE: To compare three options for the elective treatment of portal hypertension during a 10-year period. METHODS: Patients included in the trial were 18 to 76 years old, had a history of bleeding portal hypertension, and had undergone no prior treatment. Treatment options were beta-blockers (propranolol), sclerotherapy, and portal blood flow-preserving procedures (selective shunts and the Sugiura-Futagawa operation). RESULTS: A total of 119 patients were included: 40 in the pharmacology group, 46 in the sclerotherapy group,and 33 in the surgical group. The three groups showed no differences in terms of age, Child-Pugh classification, and cause of liver disease. The rebleeding rate was significantly lower in the surgical group than in the other two groups. The rebleeding rate was only 5% in the Child A surgical group, compared with 71% and 68% for the sclerotherapy and pharmacotherapy groups, respectively. Survival was better for the low-risk patients (Child A) in the three groups, but when the three options were compared, no significant difference was found. CONCLUSIONS: Portal blood flow-preserving procedures offer the lowest rebleeding rate in low-risk patients undergoing elective surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Endoscopy_MeSH M_Female_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_therapy_MeSH Hemorrhage_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH P_Sclerotherapy_MeSH S_methods_MeSH Sclerotherapy_methods_MeSH M_Time_Factors_MeSH M_Varicose_Veins_MeSH S_etiology_MeSH Varicose_Veins_etiology_MeSH S_therapy_MeSH Varicose_Veins_therapy_MeSH 
****** 10977478
----K E
----T The economic burden of congestive heart failure in a managed care population.
----A OBJECTIVE: To examine the economic burden of and treatment patterns for congestive heart failure (CHF) in a managed care population. STUDY DESIGN: Retrospective review of medical and pharmacy claims. PATIENTS AND METHODS: We reviewed integrated medical and pharmacy claims data from 6 independent-practice-association model health maintenance organizations to identify patients diagnosed with CHF. Of the approximately 1.4 million people enrolled in these managed care plans during the study period (January through December 1994), a total of 2777 patients (mean age, 56.9 years) met the study criteria, which included diagnostic codes for CHF and claims eligibility of at least 1 year. We reviewed the charges incurred by patients diagnosed with CHF for the 6 months after the initial CHF medical claim. We also examined the treatment received by each of these patients. RESULTS: During the study period, 378 of the 2777 patients with CHF (14%) were admitted to the hospital at a cost of almost $3 million (an average of $7863 per hospitalized patient). Seventy-eight percent of the study population received prescription drugs, at an average per-patient cost of $942. The most commonly prescribed drug class was angiotensin-converting enzyme inhibitors, prescribed for 38% of patients. Calcium channel blockers were prescribed for 33% of patients, but beta-blockers were prescribed for only 18% of patients. Hospitalization accounted for 54% of the total cost for CHF treatment, with prescription drugs accounting for 38%. CONCLUSION: Congestive heart failure represents a significant financial burden within a non-elderly managed care population. Improved management of the condition is needed to reduce the morbidity and mortality, as well as the costs of treatment, associated with CHF. Considerable data indicate that drugs such as beta-blockers and angiotensin-converting enzyme inhibitors can significantly decrease the morbidity and mortality of CHF. Further investigation is needed into whether increased use of prescription pharmaceuticals may reduce hospitalization rates and overall costs for CHF in this setting.
----P Journal_Article 
----M M_Aged_MeSH M_Cardiovascular_Agents_MeSH S_classification_MeSH Cardiovascular_Agents_classification_MeSH S_economics_MeSH Cardiovascular_Agents_economics_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH P_Cost_of_Illness_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Human_MeSH M_Insurance_Claim_Review_MeSH M_Male_MeSH M_Managed_Care_Programs_MeSH S_organization_&_administration_MeSH Managed_Care_Programs_organization_&_administration_MeSH M_Middle_Aged_MeSH M_Prescriptions__Drug_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10904510
----K E
----T Effect of treating isolated systolic hypertension on the risk of developing various types and subtypes of stroke: the Systolic Hypertension in the Elderly Program (SHEP).
----A CONTEXT: The Systolic Hypertension in the Elderly Program (SHEP) demonstrated that treating isolated systolic hypertension in older patients decreased incidence of total stroke, but whether all types of stroke were reduced was not evaluated. OBJECTIVE: To investigate antihypertensive drug treatment effects on incidence of stroke by type and subtype, timing of strokes, case-fatality rates, stroke residual effects, and relationship of attained systolic blood pressure to stroke incidence. DESIGN: The SHEP study, a randomized, double-blind, placebo-controlled trial began March 1, 1985, and had an average follow-up of 4.5 years. SETTING AND PARTICIPANTS: A total of 4736 men and women aged 60 years or older with isolated systolic hypertension at 16 clinical centers in the United States. INTERVENTIONS: Patients were randomly assigned to receive treatment with 12.5 mg/d of chlorthalidone (step 1); either 25 mg/d of atenolol or 0.05 mg/d of reserpine (step 2) could be added (n = 2365); or placebo (n = 2371). MAIN OUTCOME MEASURES: Occurrence, type and subtype, and timing of first strokes and stroke fatalities; and change in stroke incidence for participants (whether in active treatment or placebo groups) reaching study-specific systolic blood pressure goal (decrease of at least 20 mm Hg from baseline to below 160 mm Hg) compared with participants not reaching goal. RESULTS: A total of 85 and 132 participants in the active treatment and placebo groups, respectively, had ischemic strokes (adjusted relative risk [RR], 0.63; 95% confidence interval [CI], 0.48-0.82); 9 and 19 had hemorrhagic strokes (adjusted RR, 0.46; 95% CI, 0.21-1.02); and 9 and 8 had strokes of unknown type (adjusted RR, 1.05; 95% CI, 0.40-2. 73), respectively. Four subtypes of ischemic stroke were observed in active treatment and placebo group participants, respectively, as follows: for lacunar, n = 23 and n = 43 (adjusted RR, 0.53; 95% CI, 0.32-0.88); for embolic, n = 9 and n = 16 (adjusted RR, 0.56; 95% CI, 0.25-1.27); for atherosclerotic, n = 13 and n = 13 (adjusted RR, 0. 99; 95% CI, 0.46-2.15); and for unknown subtype, n = 40 and n = 60 (adjusted RR, 0.64; 95% CI, 0.43-0.96). Treatment effect was observed within 1 year for hemorrhagic strokes but was not seen until the second year for ischemic strokes. Stroke incidence significantly decreased in participants attaining study-specific systolic blood pressure goals. CONCLUSIONS: In this study, antihypertensive drug treatment reduced the incidence of both hemorrhagic and ischemic (including lacunar) strokes. Reduction in stroke incidence occurred when specific systolic blood pressure goals were attained. JAMA. 2000;284:465-471
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Brain_Ischemia_MeSH S_epidemiology_MeSH Brain_Ischemia_epidemiology_MeSH S_etiology_MeSH Brain_Ischemia_etiology_MeSH S_prevention_&_control_MeSH Brain_Ischemia_prevention_&_control_MeSH M_Cerebral_Hemorrhage_MeSH S_epidemiology_MeSH Cerebral_Hemorrhage_epidemiology_MeSH S_etiology_MeSH Cerebral_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Cerebral_Hemorrhage_prevention_&_control_MeSH M_Cerebrovascular_Accident_MeSH S_classification_MeSH Cerebrovascular_Accident_classification_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Reserpine_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH 
****** 10912742
----K E
----T The use of antihypertensive therapy in Spain (1986-1994).
----A We aimed to analyze the trends in antihypertensive therapy in Spain during the period 1986 to 1994, as well as the change in the pattern of different drugs, in relation to different national/international recommendations for hypertension treatment. Antihypertensive consumption was studied using the defined daily dose (DDD) and the DHD (DDD/1000 inhabitants/day) of each drug, as defined by the Drug Utilization Research Group of the European Office of the World Health Organization. The anatomical classification of hypotensive drugs has been made according to EPhMRA (European Pharmaceutical Market Association) guidelines. A significant increase of 117.4% (41.39/90 DHD) in antihypertensive drug consumption was observed in the period 1986 to 1994. In 1986 diuretics were the most consumed (30.27 DHD), followed by calcium antagonists (5.37), beta-blockers (3.93), and the angiotensin-converting enzyme (ACE) inhibitor (1.37). In 1994 ACE inhibitors, calcium antagonists, and beta-blockers increased significantly (P < .0001), whereas diuretics were still the most commonly prescribed. Nifedipine and captopril were the most used among calcium antagonists and ACE inhibitors. National and international recommendations had no effect on prescription patterns. Antihypertensive therapy of all types is increasing in Spain. Diuretics remain the most popular, beta-blockers stay stable, whereas the newer types are rising rapidly. National and international recommendations had no effect on prescription patterns.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Drug_Utilization_MeSH S_trends_MeSH Drug_Utilization_trends_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Prescriptions__Drug_MeSH S_statistics_&_numerical_data_MeSH Prescriptions__Drug_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH M_Spain_MeSH 
****** 10912975
----K E
----T Prevention of preeclampsia: a randomized trial of atenolol in hyperdynamic patients before onset of hypertension.
----A OBJECTIVE: To determine if assessment of maternal hemodynamics could predict women at risk for the development of preeclampsia, if treatment directed at hemodynamic abnormalities before the onset of hypertension could prevent preeclampsia, and if mothers could be treated in a way that protects fetal growth. METHODS: A double-blinded, randomized controlled trial was conducted. Subjects were considered to be at risk for preeclampsia if their cardiac output was greater than 7.4 L/min before 24 weeks' gestation. Nulliparous and diabetic subjects at risk were treated with 100 mg of atenolol or placebo. Cardiac output was measured by Doppler technique. Inulin and para-aminohippurate clearances were performed. RESULTS: Treatment with atenolol reduced the incidence of preeclampsia from 5 of 28 (18%) to 1 of 28 (3.8%), (P = .04). Nulliparous women determined to be at risk for preeclampsia were similar to diabetic women at risk. Each was significantly heavier and had inulin and para-aminohippurate clearances greater than the control group. Treatment with atenolol was associated with infants weighing 440 g less than infants in the nulliparous placebo group, (P = .02). No effect on birth weight was seen in the diabetic patients. Mothers of the smallest infants who were treated with atenolol could be identified by unexpectedly large reductions in cardiac output. CONCLUSION: Measurement of cardiac output in the second trimester identified women at risk for preeclampsia. Treatment with atenolol decreased the incidence of preeclampsia. Nulliparous and diabetic women at risk for preeclampsia were similar with regard to maternal hemodynamics, maternal weight, and renal function. Treatment with atenolol was associated with reduced infant birth weight.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Birth_Weight_MeSH S_drug_effects_MeSH Birth_Weight_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant__Newborn_MeSH M_Pre-Eclampsia_MeSH S_prevention_&_control_MeSH Pre-Eclampsia_prevention_&_control_MeSH M_Pregnancy_MeSH M_Pregnancy_in_Diabetics_MeSH S_drug_therapy_MeSH Pregnancy_in_Diabetics_drug_therapy_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10917072
----K 3
----T Proper use of antiarrhythmic therapy for reduction of mortality after myocardial infarction.
----A In this review, we summarise Vaughan Williams' classification of antiarrhythmic agents and the trials that have explored their efficacy in reducing mortality after myocardial infarction (MI). After analysing the data, it is clear that there is no role for class I antiarrhythmic agents as prophylaxis after MI since their use has been associated with increased mortality. Class II agents, i.e. beta-blockers, have demonstrated a reduction in mortality in combined and individual trials which extended for up to 6 years after the initial event. The class III drug, d,l-sotalol has been shown to have possible benefit, whereas its isomer without any beta-blocking properties, dexsotalol, has been shown to increase the incidence of arrhythmias. Amiodarone appears to reduce the incidence of deaths due to arrhythmia and sudden deaths without changing overall mortality. As a group, the calcium antagonists, class IV agents, have not been shown to reduce mortality and, in the case of nifedipine, may even increase it. Verapamil has been shown to be beneficial in one large study and may have a role in those patients in whom the use of beta-blockers is contraindicated. At this time, we recommend early implementation of beta-blockers for all patients without contraindications after MI. Further studies evaluating implantable defibrillators as primary and secondary prevention have provided significant risk reductions in certain high risk patient subsets. Future efforts will need to focus on more accurate risk stratification of post-MI patients and the role of both defibrillators and, possibly, amiodarone in improving survival.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Defibrillators__Implantable_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Risk_MeSH 
****** 10919124
----K 1
----T [Factors associated with changes in microalbuminuria during antihypertensive treatment]
----A BACKGROUND: The objective of the present study was to analyze the factors related with changes of microalbuminuria during antihypertensive treatment in patients with essential hypertension. METHODS: One hundred and six patients (57 men, mean age 40.8 [SD 6.6] years) never treated with antihypertensive treatment were included. At the beginning and after one year, blood pressure biochemical profile and urinary albumin excretion (UAE) were measured. After the initial evaluation, 53 patients received angiotensin converting enzyme inhibitors (ACEi) and 53 beta-blockers (BB). Hydrochlorothiazide was added to achieve the blood pressure target < 140/90 mmHg. RESULTS: The average of UAE was 32.1 (43.1) mg/24 h, and 41 (39%) patients had microalbuminuretics. After 12 months of treatment, a significative fall of systolic BP (-20.6 [8.03] mmHg, p < 0.001), and diastolic BP (-14.18 [10.34] mmHg, p < 0.001) were observed, whereas baseline glucose increases (3.08 [11.07] mg/dl, p = 0.006). The changes of UAE were only related with the baseline UAE values. Neither, age, sex, baseline diastolic BP and changes in diastolic BP were significantly related with the changes in UAE. In spite of similar mean BP reduction (medial BP 17.4 [10.9] vs 14.8 [10.4] mmHg), UAE only was reduced in patients treated with ACEi (LogUAE: 0.203 [0.872] mg/24 h; p < 0.04). In addition, in patients treated with BB a significative increase in baseline glucose (4.4 [12.3] mg/dl; p = 0.013) and uric acid (1.18 [4.18]; p = 0.031) were observed. CONCLUSIONS: In patients with essential hypertension, changes in microalbuminuria depends of the initial UAE values and the kind of antihypertensive treatment. ACEi produced higher UAE reduction and lower derangement of the glucose metabolism than BB.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Albuminuria_MeSH S_complications_MeSH Albuminuria_complications_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Male_MeSH 
****** 10923574
----K E
----T Durability of improvement achieved in a clinical trial. Is compliance an issue?
----A BACKGROUND: The effects seen in clinical trials may not translate to actual practice situations. We examined the persistence of blood pressure effects 31 months after a clinical trial of treatment with hypotensive agents. METHODS: Nineteen previously untreated middle-aged men with hypertension had their office and ambulatory blood pressure recorded after 4 weeks of placebo treatment, 4 weeks of active treatment in a clinical trial, and 31 months of treatment in clinical practice. All recording was done by the same physician (IE). RESULTS: Mean 24-hour blood pressure was 138/92 mm Hg after 4 weeks of placebo treatment, 128/85 mm Hg after 4 weeks of active treatment in the clinical trial, and 136/87 mm Hg after a mean of 31 months of treatment in clinical practice. The corresponding blood pressure values > or =140/90 mm Hg during the daytime were 47%, 24%, and 39%, and office blood pressures were 155/101, 145/93, and 150/91 mm Hg. Individual comparison revealed that 6 of the 19 patients had higher mean 24-hour blood pressure after several months of treatment in clinical practice than after 4 weeks of active treatment in the clinical trial. CONCLUSIONS: In our study, the significantly reduced blood pressure in the clinical trial did not persist when followed up in clinical practice. At follow-up, one third of the patients had blood pressure values similar to those before active treatment. The reason for this is unclear, but inconsistent compliance may play a part in the lack of durability of the improvements. Our results indicate that effects seen in short-term clinical trials may not translate to long-term benefits in clinical practice.
----P Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH P_Blood_Pressure_MeSH P_Clinical_Trials_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_In_Vitro_MeSH M_Middle_Aged_MeSH P_Patient_Compliance_MeSH M_Pilot_Projects_MeSH M_Sweden_MeSH 
****** 10918548
----K E
----T Practice vs ambulatory blood pressure measurement under treatment with ramipril (PLUR Study): a randomised, prospective long-term study to evaluate the benefits of ABPM in patients on antihypertensive treatment.
----A The usefulness of ambulatory blood pressure monitoring (ABPM) vs casual blood pressure measurement in the physicians practice (PM) for the routine management of patients with hypertension concerning total mortality and morbidity has been compared in a prospective, randomised, open multicentre study with a 5-year follow-up. The study was performed in general practitioners offices in Germany from 1991 to 1997. A total of 1298 patients with essential hypertension were included. Cardio- and cerebrovascular events, total mortality/morbidity and drug-saving effects in hypertensives treated according to two different methods of blood pressure measurement were the primary and secondary endpoints of the study. A total of 239 patients from group 1 (ABPM, n = 651), and 208 from group 2 (PM, n = 647) prematurely discontinued the study. The reason for discontinuation in 55 of these patients (20 from group 1 and 35 from group 2) was that they reached the main endpoint (total mortality/morbidity and cardio- and cerebrovascular events) of the study. The difference was statistically significant (P = 0.037) in favour of group 1. Cardio- and cerebrovascular events also occurred in a lower number of patients (n = 14) in group 1, as compared to group 2 (n = 24). The difference however was not significant (P = 0. 097). A difference in a direct drug-saving effect could not be observed between the two groups but 22% of the initially screened patients were detected with the ABPM to have white coat hypertension and thus these patients did not receive antihypertensive treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH 
****** 10920067
----K I
----T Differential effects of beta-blockers in patients with heart failure: A prospective, randomized, double-blind comparison of the long-term effects of metoprolol versus carvedilol.
----A BACKGROUND: Both metoprolol and carvedilol produce hemodynamic and clinical benefits in patients with chronic heart failure; carvedilol exerts greater antiadrenergic effects than metoprolol, but it is unknown whether this pharmacological difference results in hemodynamic and clinical differences between the 2 drugs. METHODS AND RESULTS: We randomized 150 patients with heart failure (left ventricular ejection fraction </=0.35) to double-blind treatment with either metoprolol or carvedilol. When compared with metoprolol (124+/-55 mg/d), patients treated with carvedilol (49+/-18 mg/d) showed larger increases in left ventricular ejection fraction at rest (+10.9+/-11.0 versus +7.2+/-7.7 U, P=0.038) and in left ventricular stroke volume and stroke work during exercise (both P<0. 05) after 13 to 15 months of treatment. In addition, carvedilol produced greater decreases in mean pulmonary artery pressure and pulmonary wedge pressure, both at rest and during exercise, than metoprolol (all P<0.05). In contrast, the metoprolol group showed greater increases in maximal exercise capacity than the carvedilol group (P=0.035), but the 2 drugs improved symptoms, submaximal exercise tolerance, and quality of life to a similar degree. After a mean of 23+/-11 months of follow-up, 21 patients in the metoprolol group and 17 patients in the carvedilol group died or underwent urgent transplantation. CONCLUSIONS: The present study demonstrates that during long-term therapy, carvedilol improves cardiac performance to a greater extent than metoprolol when administered to patients with heart failure in the doses shown to be effective in clinical trials. These differences were likely related to a greater antiadrenergic activity of carvedilol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10927824
----K 1
----T [Differences between young and elderly patients in a protocol for the diagnosis and follow-up of arterial hypertension]  .
----A OBJECTIVE: To determine possible differences between the control of hypertension in elderly patients and in young patients. DESIGN: Retrospective observation study of the differences between initial and final systolic and diastolic blood pressure, of their relationship to inclusion in medical treatment, and of the control obtained with different kinds of, and changes in, treatment, of drug association, periodic check-ups, vascular disease and risk factors. SETTING: The urban Azpilagana Health District in Pamplona. PATIENTS: 389 hypertense patients were studied retrospectively: 196 of 70 or over and 193 between 45 and 60. MAIN RESULTS: More older patients were treated medically (91.8% vs 84.5%, p = 0.024), and received combined two-drug treatment (30.1% vs 19.7%, p < 0.001), although the young people received more than two hypertension drugs more often (11.4% vs 2.5%, p < 0.001). Final control (< 140/90) was achieved more often among young people (39.9% vs 26.5%, p = 0.005). In the older patients group initial higher diastolic pressure was related to final pressure control. More older patients had periodic check-ups at the health centre (73.3% vs 63.7%, p < 0.001), but this practice only improved relative control (< or = 140/90) in young people (p = 0.001). Older patients used more diuretics (p < 0.001) and less beta-blockers (p < 0.001), with no differences for other hypertension drugs. CONCLUSIONS: There are differences based on age in treatment and control of hypertension patients. Older patients with diastolic hypertension are controlled more easily. Altogether and in both groups analysed, the percentage of people with normal pressure after treatment was higher than in other studies.
----P Journal_Article 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Sex_Distribution_MeSH M_Vascular_Diseases_MeSH S_physiopathology_MeSH Vascular_Diseases_physiopathology_MeSH 
****** 10924295
----K 5
----T Management of patients with myocardial infarction and hypertension.
----A This is the first systematic survey of cardiology manpower in Europe. Hitherto, there has been no published information on the number of cardiologists in the different European nations and whether it was growing or stable. Important differences in the number of cardiologists and trainees are observed, with the highest figures in Greece, Italy and France (more than 80/10(6)inhabitants) and the lowest in the Scandinavian nations, Austria, Germany and the U.K. (35 or less/10(6)inhabitants). This is partly due to different roles and the activities of the cardiologists in these countries as well as their capacity to undertake various cardiological procedures. Some comparisons with the U.S.A. and projections for the year 2000 are also made.
----P Journal_Article Review Review__Tutorial 
----M M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Coronary_Care_Units_MeSH S_methods_MeSH Coronary_Care_Units_methods_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 10924316
----K E
----T Efficacy of carvedilol on complex ventricular arrhythmias in dilated cardiomyopathy: double-blind, randomized, placebo-controlled study.
----A AIMS: The aim of the present study was to investigate whether the addition of carvedilol to conventional therapy in dilated cardiomyopathy patients is associated with further benefits in the treatment of complex non-sustained ventricular arrhythmias (Lown class III, IV or V). METHODS AND RESULTS: We recruited 168 patients with ischaemic or idiopathic dilated cardiomyopathy, with complex ventricular arrhythmias. Patients able to tolerate low doses of carvedilol were randomized to treatment with carvedilol or placebo for 6 months. Carvedilol treatment improved ventricular function and reduced the incidence of arrhythmic episodes. Notably, by the end of the first month of treatment, the antiarrhythmic efficacy of the drug was significantly greater in patients with ischaemic than in those with idiopathic dilated cardiomyopathy, an effect that could probably be attributed to the anti-ischaemic properties of carvedilol. After 3 months, at a time when ejection fraction was significantly improved in all treated patients, the antiarrhythmic efficacy of carvedilol was similar in the two study groups. CONCLUSIONS: Carvedilol antiarrhythmic efficacy was paralleled by the improvement in ejection fraction, independent of the aetiology of heart failure. The possibility of adding to an already 'optimized' conventional therapy a drug able to reduce the incidence of complex non-sustained ventricular arrhythmias is a therapeutic option that should be considered in the treatment of these patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Tachycardia__Ventricular_MeSH S_complications_MeSH Tachycardia__Ventricular_complications_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH S_ultrasonography_MeSH Tachycardia__Ventricular_ultrasonography_MeSH 
****** 10933570
----K E
----T Fibrinolytic/hemostatic variables in arterial hypertension: response to treatment with irbesartan or atenolol.
----A Essential hypertension is often accompanied by abnormalities of the coagulation/fibrinolytic system, predisposing to a procoagulant state. The aim of the present study was to compare the effects of atenolol (beta1-blocker agent) and irbesartan (angiotensin II type 1 receptor antagonist) on plasma levels of hemostatic/fibrinolytic and endothelial function markers in a cohort of previously untreated hypertensives. Fifty-four patients were randomly assigned to atenolol 25 to 150 mg (26 patients) or irbesartan 75 to 300 mg (28 patients). The plasma levels of plasminogen activator inhibitor-1 antigen, thrombomodulin, tissue factor pathway inhibitor antigen, fibrinogen, and factor XII were determined before and after 6 months of therapy. Age, gender distribution, body mass index, lipid profile, and baseline values of the measured markers were similar in both groups. Baseline values for systolic and diastolic blood pressure, as well as the reduction after treatment, were not significantly different between the two groups. Treatment with irbesartan was associated with a significant decrease in the levels of all the parameters. Similar findings were observed in the atenolol group, except for factor XII and tissue factor pathway inhibitor levels, which were not significantly decreased in this group. The reduction, however, of fibrinogen, plasminogen activator inhibitor-1, and thrombomodulin was significantly greater in the irbesartan than in the atenolol group. In conclusion, the results indicated that, despite an equally controlled blood pressure, 6-month therapy with irbesartan was associated with a more favorable modification of hemostatic/fibrinolytic status than atenolol.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Coagulation_MeSH S_drug_effects_MeSH Blood_Coagulation_drug_effects_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Fibrinolysis_MeSH S_drug_effects_MeSH Fibrinolysis_drug_effects_MeSH M_Hemostasis_MeSH S_drug_effects_MeSH Hemostasis_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 10935777
----K E
----T The value of repeated echocardiographic evaluation in patients with idiopathic dilated cardiomyopathy during treatment with metoprolol or captopril.
----A Serial echocardiographic investigations were carried out on patients with idiopathic dilated cardiomyopathy, to evaluate treatment effects on left ventricular (LV) performance during therapy with either metoprolol or captopril. Thirty-two patients (23 males and 9 females) with mild to moderate symptoms of heart failure (NYHA II-III) and a mean age of 49 years were included in the investigation. The patients were investigated with Doppler echocardiography before treatment, after 3 and 6 months of treatment (either metoprolol or captopril) and 1 month after withdrawal of treatment. Intra- and inter-investigator reproducibility was acceptable, with a coefficient of variation of less than 5% for LV dimensions. A reduction in LV dimensions was seen in both treatment groups. In the metoprolol group there was also an increase in LV stroke volume and fractional shortening. The non-invasive data were in accordance with invasive measurements of stroke volume and LV filling pressure. In patients with idiopathic dilated cardiomyopathy and mild to moderate symptoms of heart failure, echocardiography seemed to be sufficiently reproducible to be used for determination of treatment effects in a longitudinal heart failure study. Both metoprolol and captopril were well tolerated and had favourable effects on LV performance.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH P_Echocardiography__Doppler_MeSH S_drug_effects_MeSH Echocardiography__Doppler_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Reproducibility_of_Results_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 10934984
----K 5
----T Choosing a first-line drug in the management of elevated blood pressure: what is the evidence? 2: Beta-blockers.
----A Elevated blood pressure is associated with an increased risk of cardiovascular illness and death. Efforts to reduce that risk have led to recommendations for a wide array of nondrug and drug therapies. Choosing the optimal first-line drug for hypertensive patients should address a hierarchy of treatment goals: decrease in morbidity and mortality associated with hypertension, decrease in blood pressure, good tolerance, dosing convenience and low cost. This article examines the evidence for beta-blockers as a class of first-line antihypertensive drugs in light of these treatment goals. The evidence indicates that beta-blockers are probably not as effective in reducing morbidity and mortality as low-dose thiazide diuretics and that there may be significant differences in effectiveness among various beta-blockers.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Decision_Making_MeSH M_Diuretics__Thiazide_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_economics_MeSH Diuretics__Thiazide_economics_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Incidence_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 10937930
----K E
----T The carvedilol hibernation reversible ischaemia trial; marker of success (CHRISTMAS). The CHRISTMAS Study Steering Committee and Investigators.
----A BACKGROUND: Carvedilol improves left ventricular (LV) function when heart failure is due to LV systolic dysfunction, but the magnitude of the response is heterogeneous among patients with coronary disease, possibly reflecting the presence or volume of hibernating myocardium. AIMS: The primary objective of the study is to determine whether the presence of hibernating myocardium predicts the magnitude of improvement in LV ejection fraction in response to carvedilol among patients with heart failure and LV systolic dysfunction due to coronary disease. METHODS: The study is a prospective, randomised, parallel-group, double-blind, multi-centre study comparing carvedilol and placebo over a period of approximately 6 months in the above patient population. The primary end-point is the comparison of the mean change, from baseline to the final visit, in radionuclide-determined LV ejection fraction among patients on placebo with those on carvedilol stratified according to the presence of hibernating myocardium. Hibernating status will be determined by a combination of echocardiographic and myocardial perfusion (technetium-99m sestamibi) imaging. RESULTS: 255 patients have undergone screening tests of which 207 have been randomised so far. The study intends to randomise 400 patients and the first report of results is expected in 2000. CONCLUSIONS: As far as we are aware this is the first randomised controlled trial to investigate the effects of treatment in patients stratified according to the presence of hibernating myocardium. The study will provide insights into the prevalence of myocardial hibernation, its natural history, and its influence on prognosis as well as the interaction between the presence of hibernating myocardium and the effects of treatment with carvedilol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Stunning_MeSH S_complications_MeSH Myocardial_Stunning_complications_MeSH S_diagnosis_MeSH Myocardial_Stunning_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Stunning_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Stunning_physiopathology_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_prevention_&_control_MeSH Ventricular_Dysfunction__Left_prevention_&_control_MeSH 
****** 10937931
----K E
----T Update of REACH-1 and MERIT-HF clinical trials in heart failure. Cardio.net Editorial Team.
----A BACKGROUND: This article reviews the design and results of REACH-1 (Research on Endothelin Antagonism in Chronic Heart Failure) and MERIT (Metoprolol controlled and Extended release, Randomised Intervention Trial in congestive Heart Failure), two recently reported clinical trials that investigated, respectively, the role of a non-selective endothelin antagonist (bosentan) and of a beta-selective blocker for the treatment of heart failure. RESULTS: The REACH-1 trial demonstrated that initiation of bosentan therapy is associated with an increased risk of worsening heart failure. However, long-term therapy with bosentan may have improved symptoms and favourably altered the progression of heart failure. The MERIT-HF clinical trial indicated that beta-blockade using metoprolol confers a significant beneficial effect on total mortality in patients with stable chronic heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelins_MeSH S_antagonists_&_inhibitors_MeSH Endothelins_antagonists_&_inhibitors_MeSH M_Europe_MeSH S_epidemiology_MeSH Europe_epidemiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Sulfonamides_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 10937953
----K E
----T Amlodipine reduces myocardial ischaemia during exercise without compromising left ventricular function in patients with silent ischaemia: a randomised, double-blind, placebo-controlled study.
----A BACKGROUND: Left ventricular systolic function is reduced during episodes of silent ischaemia in patients with coronary artery disease (CAD). In most normal subjects left ventricular ejection fraction (LVEF) increases at least 5% during exercise whereas LVEF often remains unchanged or decreases in patients with CAD. The anti-ischaemic effect of calcium antagonists is well documented including a capability to reduce exercise-induced electrocardiographic ST-depressions, whereas the effect of these drugs on LV volume changes during exercise in patients with silent ischaemia is unknown. AIM: The aim of this study was to evaluate the effect of amlodipine on rest and exercise LVEF in patients with silent ischaemia. METHODS: Twenty-one patients completed a double-blind placebo-controlled cross-over study. Conventional exercise test and radionuclide cardiographies during exercise were used for determining haemodynamic parameters. RESULTS: Exercise-induced electrocardiographic ST-depressions were reduced in 83% of the patients having ST-deviations during placebo even though 10 patients were already treated with a beta-blocker. Amlodipine did not affect left ventricular systolic function compared to placebo, neither at rest nor during exercise. CONCLUSION: The results indicated that amlodipine is a safe anti-ischaemic drug in patients with silent ischaemia concerning cardiac function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radionuclide_imaging_MeSH Coronary_Disease_radionuclide_imaging_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10937984
----K E
----T Beta-blocker therapy in advanced heart failure: clinical characteristics and long-term outcomes.
----A AIMS: To evaluate the clinical characteristics and long-term outcomes of advanced heart failure patients (NYHA Class IIIb-IV) receiving beta-blocker therapy vs. those patients not receiving beta-blockers at randomization in the FIRST trial, a randomized, double-blind, placebo-controlled trial of epoprostenol vs. usual care in advanced heart failure. METHODS AND RESULTS: The patient population consisted of 471 patients enrolled in FIRST with Class IIIb-IV heart failure, left ventricular ejection fraction (LVEF) of <30%, advanced hemodynamic abnormalities, and standard pharmacologic treatment of ACE-inhibitor, diuretics, and/or digoxin. The study cohort consisted of 448 patients not receiving beta-blockers and 23 patients receiving beta-blockers at randomization for the FIRST trial. Patients in the beta-blocker group had decreased rates of any clinical event (P = 0.03), worsening heart failure (P = 0.001), and death or worsening heart failure (P = 0.0008) than patients not receiving beta-blockers. After adjusting for prognostically important variables, the favorable effect of beta-blockers on worsening heart failure (P = 0.02) and death or worsening heart failure (P = 0.02) persisted. CONCLUSION: Patients with advanced heart failure who receive beta-blocker therapy have a lower rate of hospitalization and are less likely to experience worsening heart failure or death at 6 months than patients who are not treated with beta-blockers. These observational data contribute to the growing body of data demonstrating a favorable effect of beta-blockers on clinical outcomes in heart failure.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Epoprostenol_MeSH S_therapeutic_use_MeSH Epoprostenol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10937988
----K I
----T Update of recent clinical trials in heart failure and myocardial infarction.
----A BACKGROUND: There are currently many on-going clinical trials assessing therapies for the treatment of patients with heart failure. AIMS: The purpose of this series of papers is to present concise summaries of current randomised trials in the field of heart failure and myocardial infarction (MI). METHODS: Data from large double-blind, placebo-controlled trials, which are on-going or have only recently been published, are given in a format allowing easy comparison. Where appropriate, data from smaller studies are included. RESULTS: Major studies which are examined in this issue include CIBIS II, MERIT-HF, RESOLVD, SPICE, VEST, MACH-1, ATLAS, RALES, CIDS and CASH. These trials assess the efficacy and safety of beta-blocker, angiotensin-II-receptor blocker, positive inotropic agent, calcium antagonist, angiotensin-converting enzyme (ACE) inhibitor, aldosterone receptor blocker, and antiarrhythmic interventions in the treatment of heart failure. CONCLUSIONS: The presentation of data from these on-going trials should allow an up-to-date assessment, by physicians, of the most appropriate and effective treatment for patients with heart failure. It is evident that some therapies may play no further role in the treatment of heart failure, due to the increased risk of mortality associated with their administration, whilst others may convey significant benefits.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH 
****** 10938490
----K E
----T Experience of commencing Carvedilol in elderly patients with heart failure in a routine outpatient clinic.
----A Carvedilol has been shown to be beneficial for patients with heart failure, but it is not clear how it should be initiated in routine clinical practice, particularly in the elderly. This study is a retrospective review of 19 patients of age 80+/-4 years with heart failure, who had Carvedilol treatment initiated in a routine outpatient clinic. No patient experienced a worsening of their heart failure or required admission to hospital. There was a mean reduction in heart rate of 11 beats/min. Carvedilol was tolerated by 68% of the patients. Thus, Carvedilol can be safely initiated in a routine outpatient clinic in appropriately selected elderly patients.
----P Journal_Article 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH P_Ambulatory_Care_Facilities_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Feasibility_Studies_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Outpatients_MeSH M_Prescriptions__Drug_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH 
****** 10938494
----K E
----T Screening, endpoint classification, and safety monitoring in the Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF).
----A The MERIT-HF study was designed to investigate the effect of once-daily dosing of metoprolol succinate CR/XL added to standard therapy in patients with chronic heart failure. A screening programme, aiming at identifying eligible patients for the study was used by 231 out of 313 sites, resulting in 8912 screened patients. These patients were older, more often women, had marginally higher ejection fraction and were more often in NYHA class IV compared to the finally randomised patients. There was a positive correlation between the number of screened and randomised patients and due to the high inclusion rate the number of randomised patients was increased from 3200 to 3991 patients. The clinical events were defined by a manual and were based on identical classifications made independently by two members of an Independent Endpoint Committee. Data from the case report form and the classifications made by the Endpoint Committee were in accordance for hospitalisation due to worsening heart failure on 722 occasions. On 207 occasions the data from the case report forms and the classification made by the committee differed regarding this clinical event. The Independent Safety Committee monitored safety aspects of the study by using asymmetric group sequential procedures. The study was stopped early on recommendation from the Independent Safety Committee, when the second pre-specified interim analysis (50% of total number of expected deaths) showed that the criterion for stopping due to benefit had been met and exceeded. In conclusion, a screening programme facilitated patient recruitment and showed the characteristics of the background population, the event classification was improved by using an independent endpoint committee, and the safety monitoring allowed an early closure of the study due to mortality benefit, without jeopardising the final analyses of the results.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Monitoring_MeSH M_Female_MeSH P_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Patient_Selection_MeSH M_Safety_MeSH M_Survival_Rate_MeSH 
****** 10938495
----K I
----T Design and methodology of the CAPRICORN trial - a randomised double blind placebo controlled study of the impact of carvedilol on morbidity and mortality in patients with left ventricular dysfunction after myocardial infarction.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Human_MeSH M_Incidence_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Practice_Guidelines_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH M_Research_Design_MeSH M_Safety_MeSH M_Survival_Rate_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 10938496
----K 5
----T Are beta-blockers effective in patients who develop heart failure soon after myocardial infarction? A meta-regression analysis of randomised trials.
----A BACKGROUND: The great majority of post-infarction studies of beta-blockers were conducted in an era when these agents were widely held to be contra-indicated for the management of heart failure. We now know that beta-blockers are highly effective for the management of patients with chronic stable heart failure. However, there remains uncertainty about their role in the setting of post-infarction heart failure and ventricular dysfunction. AIM: the primary objective in this paper, was to investigate the extent to which heart failure or evidence of major cardiac dysfunction influenced outcome in previous trials of beta-blockers in heart failure after myocardial infarction. METHODS: We assessed the extent to which the inclusion of patients with heart failure or major cardiac dysfunction influenced outcome in randomised trials of long-term use of beta-blockade after myocardial infarction. The primary analysis was to assess the extent to which the proportion of patients included in each trial with heart failure influenced the relative odds of all-cause mortality in the trials. All randomised trials without crossover with treatment lasting more than one month and with 50 or more patients were considered. All those that provided information on the proportion of patients with heart failure or major cardiac dysfunction in the original or subsequent articles were included in the analysis. RESULTS: Overall treatment with a beta-blocker was associated with a 22.6% reduction in the odds of death (95% C1 11-32.3%). There were very few data on the effects of beta-blockers after myocardial infarction in patients with documented left ventricular systolic dysfunction. In the analysis that included heart failure as a factor, treatment with a beta-blocker was associated with a non-significant interaction with the presence of heart failure. However, because the group including heart failure patients were at higher risk, the absolute benefit of treatment with beta-blockers appeared greater in this group. CONCLUSIONS: This analysis suggests that the relative benefit of beta-blockers on mortality after a myocardial infarction is similar in the presence or absence of heart failure but that the absolute benefit may be greater in the former. However, as current clinical practice has changed radically from the time when the majority of these trials were conducted, further trial evidence would be desirable.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Odds_Ratio_MeSH P_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10942742
----K I
----T Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest : the Cardiac Arrest Study Hamburg (CASH).
----A BACKGROUND: We conducted a prospective, multicenter, randomized comparison of implantable cardioverter-defibrillator (ICD) versus antiarrhythmic drug therapy in survivors of cardiac arrest secondary to documented ventricular arrhythmias. METHODS AND RESULTS: From 1987, eligible patients were randomized to an ICD, amiodarone, propafenone, or metoprolol (ICD versus antiarrhythmic agents randomization ratio 1:3). Assignment to propafenone was discontinued in March 1992, after an interim analysis conducted in 58 patients showed a 61% higher all-cause mortality rate than in 61 ICD patients during a follow-up of 11.3 months. The study continued to recruit 288 patients in the remaining 3 study groups; of these, 99 were assigned to ICDs, 92 to amiodarone, and 97 to metoprolol. The primary end point was all-cause mortality. The study was terminated in March 1998, when all patients had concluded a minimum 2-year follow-up. Over a mean follow-up of 57+/-34 months, the crude death rates were 36.4% (95% CI 26.9% to 46.6%) in the ICD and 44.4% (95% CI 37.2% to 51.8%) in the amiodarone/metoprolol arm. Overall survival was higher, though not significantly, in patients assigned to ICD than in those assigned to drug therapy (1-sided P=0.081, hazard ratio 0.766, [97.5% CI upper bound 1.112]). In ICD patients, the percent reductions in all-cause mortality were 41.9%, 39.3%, 28. 4%, 27.7%, 22.8%, 11.4%, 9.1%, 10.6%, and 24.7% at years 1 to 9 of follow-up. CONCLUSIONS: During long-term follow-up of cardiac arrest survivors, therapy with an ICD is associated with a 23% (nonsignificant) reduction of all-cause mortality rates when compared with treatment with amiodarone/metoprolol. The benefit of ICD therapy is more evident during the first 5 years after the index event.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amiodarone_MeSH S_adverse_effects_MeSH Amiodarone_adverse_effects_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH P_Defibrillators__Implantable_MeSH S_adverse_effects_MeSH Defibrillators__Implantable_adverse_effects_MeSH M_Female_MeSH M_Heart_Arrest_MeSH S_drug_therapy_MeSH Heart_Arrest_drug_therapy_MeSH S_therapy_MeSH Heart_Arrest_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH P_Resuscitation_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10942632
----K E
----T A nine-month, placebo-controlled study of the effects of growth hormone treatment on lipoproteins and LDL size in abdominally obese men.
----A Abdominal/visceral obesity is associated with blunted growth hormone (GH) secretion and an unfavourable lipoprotein pattern. In this study, the effect of GH treatment on LDL size and on serum lipoprotein concentrations was determined in abdominally obese men. Thirty men, aged 48-66 years, with a body mass index (BMI) of 25-35 kg/m(2)and a waist:hip ratio of >0.95, received treatment with GH (9. 5 microg/kg/day) or placebo for 9 months.Serum concentrations of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) and apolipoprotein B (apoB) were reduced (P<0.05, P<0.05 and P<0.001 vs placebo, respectively). Serum lipoprotein(a) [Lp(a)] concentration increased (P<0.05 vs. placebo). Mean low density lipoprotein (LDL) particle diameter was marginally increased by active treatment as compared with placebo (P =0.08). No changes were observed in the serum concentrations of high density lipoprotein-cholesterol (HDL-C), apolipoprotein A-I (apoA-I) and apolipoprotein E (apoE).In conclusion, 9 months of GH treatment in abdominally obese men beneficially reduced serum concentrations of TC, LDL-C and apoB, and marginally increased mean LDL diameter, while serum Lp(a) increased. The ultimate effect of GH therapy on the cardiovascular risk remains, however, to be determined.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Abdomen_MeSH M_Aged_MeSH M_Apolipoproteins_B_MeSH S_blood_MeSH Apolipoproteins_B_blood_MeSH M_Apolipoproteins_E_MeSH S_blood_MeSH Apolipoproteins_E_blood_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Human_Growth_Hormone_MeSH S_adverse_effects_MeSH Human_Growth_Hormone_adverse_effects_MeSH S_therapeutic_use_MeSH Human_Growth_Hormone_therapeutic_use_MeSH M_Lipoprotein(a)_MeSH S_blood_MeSH Lipoprotein(a)_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_MeSH S_blood_MeSH Lipoproteins__LDL_blood_MeSH S_drug_effects_MeSH Lipoproteins__LDL_drug_effects_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_blood_MeSH Obesity_blood_MeSH S_drug_therapy_MeSH Obesity_drug_therapy_MeSH M_Placebos_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10950398
----K I
----T Lowering of blood pressure and predictors of response in patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint.
----A The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel-group study comparing the effects of losartan with those of atenolol on the reduction of cardiovascular complications in patients (n = 9,194) with essential hypertension and with electrocardiographically (ECG) documented left ventricular hypertrophy (LVH). Baseline blood pressure was 174.4/97.8 mm Hg (mean), age 66.9 years, body mass index 28.0 kg/m2; 54.1% were women and 12.5% had diabetes mellitus. This population will be treated until at least 1,040 have a primary endpoint. After five scheduled visits and 12 months of follow-up, blood pressure decreased by 23.9/12.8 mm Hg to 150.5/85.1 mm Hg (target < 140/90 mm Hg). The mandatory titration level of < or = 160/95 mm Hg was reached by 72.1% of the patients. At the 12-month visit, 22.7% of all patients were taking blinded study drug alone, 44.3% were taking blinded drug plus hydrochlorothiazide (HCTZ), and 17.7% were taking blinded drugs plus HCTZ and additional drugs. Controlling for all other variables, patients in the US received more medication and had 2.4 times the odds of achieving blood pressure control than patients in the rest of the study (P < .001). Previously untreated patients (n = 2,530) had a larger initial decrease in blood pressure compared with those previously treated. Diabetics (n = 1,148) needed more medication than nondiabetics to gain blood pressure control. Only 13.9% of the patients had discontinued blinded study drug and 1.4% missed the revisit at 12 months. These data demonstrate both the successful lowering of blood pressure during 12 months of follow-up in a large cohort of patients with hypertension and LVH on ECG, but also emphasize the need for two or more drugs to control high blood pressure in most of these patients. Being previously treated and having diabetes were associated with less blood pressure response, whereas living in the US indicated better blood pressure control. It has been possible to keep most of these patients with complicated hypertension taking blinded study drug for 12 months.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10946034
----K E
----T Low-density lipoprotein particle size, triglycerides, and high-density lipoprotein cholesterol as risk factors for coronary heart disease in older Japanese-American men.
----A Decreased low-density lipoprotein (LDL) particle size is associated with coronary heart disease (CHD) risk among middle-aged Caucasian populations, and has been consistently correlated with increased plasma levels of triglyceride and decreased levels of high-density lipoprotein (HDL) cholesterol. This study examines whether these risk factors predict CHD among older Japanese-American men. With use of the Honolulu Heart Program Lipoprotein Exam 3 (1980 to 1982) as baseline, and 12-year follow-up for CHD events, a nested, case-control study was designed. One hundred forty-five incident CHD cases were identified and matched to 2 controls each. LDL particle diameter (size) was determined by gradient gel electrophoresis. A 10-angstrom (A) decrease in LDL size at baseline was associated with increased risk of incident CHD (relative risk 1.28, 95% confidence interval 1.01 to 1.63). After adjustment for baseline risk factors, the LDL size association was no longer statistically significant (relative risk 1.13, 95% confidence interval 0.86 to 1.49). When principal components analysis was used to define a composite variable for LDL size, triglycerides, and HDL cholesterol, this component predicted CHD independent of smoking, alcohol consumption, physical activity, body mass index, hypertension, diabetes, and beta-blocker use (p <0.01). Therefore, this prospective analysis of data from older, Japanese-American men demonstrated that decreased LDL size is a univariate predictor of incident CHD, and that a composite risk factor of LDL size, triglyceride, and HDL cholesterol was a risk factor for CHD independent of other risk factors.
----P Journal_Article 
----M M_Aged_MeSH M_Asian_Americans_MeSH M_Case-Control_Studies_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_ethnology_MeSH Coronary_Disease_ethnology_MeSH M_Electrophoresis__Gel__Pulsed-Field_MeSH M_Hawaii_MeSH M_Human_MeSH M_Japan_MeSH S_ethnology_MeSH Japan_ethnology_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_MeSH S_blood_MeSH Lipoproteins__LDL_blood_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Particle_Size_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 10952492
----K E
----T Infarct size and recurrence of ventricular arrhythmias after defibrillator implantation.
----A Infarct size as determined by perfusion imaging is an independent predictor of mortality after implantable cardioverter defibrillator (ICD) implantation in patients with coronary artery disease (CAD) and life-threatening ventricular arrhythmias (VA). However, its value as a predictor of VA recurrence and hospitalisation after ICD implantation is unknown. Therefore, the objective of this study was to evaluate whether infarct size as determined by perfusion imaging can help to identify patients who are at high risk for recurrence of VA and hospitalisation after ICD implantation. We studied 56 patients with CAD and life-threatening VA. Before ICD implantation, all patients underwent a uniform study protocol including a thallium-201 stress-redistribution perfusion study. A defect score as a measurement of infarct size was calculated using a 17-segment 5-point scoring system. Study endpoints during follow-up were documented episodes of appropriate anti-tachycardia pacing and/or shocks for VA and cardiac hospitalisation for electrical storm (defined as three or more appropriate ICD interventions within 24 h), heart failure or angina. After a mean follow-up of 470+/-308 days, 22 patients (39%) had recurrences of VA. In univariate analysis, predictors for recurrence were: (a) ventricular tachycardia (VT) as the initial presenting arrhythmia (86% vs 59% for patients without ICD therapy, P=0.04), (b) treatment with beta-blockers (36% vs 68%, P=0.03) and (c) a defect score (DS) > or = 20 (64% vs 32%, P=0.03). In multivariate analysis, VT as the presenting arrhythmia (chi2=5.51, P=0.02) and a DS > or = 20 (chi2=4.22, P=0.04) remained independent predictors. Cardiac hospitalisation was more frequent in patients with a DS > or = 20 (44% vs 13% for patients with DS < 20, P=0.015) and this was particularly due to more frequent hospitalisations for electrical storm (24% vs 3% for patients with DS < 20, P=0.037). The extent of scarring determined by perfusion imaging can separate patients with CAD into high- and low-risk groups for recurrence of VA and cardiac hospitalisation after ICD implantation.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_radionuclide_imaging_MeSH Coronary_Disease_radionuclide_imaging_MeSH P_Defibrillators__Implantable_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_radionuclide_imaging_MeSH Myocardial_Infarction_radionuclide_imaging_MeSH M_Predictive_Value_of_Tests_MeSH M_Recurrence_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Ventricular_MeSH S_epidemiology_MeSH Tachycardia__Ventricular_epidemiology_MeSH M_Thallium_Radioisotopes_MeSH S_diagnostic_use_MeSH Thallium_Radioisotopes_diagnostic_use_MeSH M_Time_Factors_MeSH M_Tomography__Emission-Computed__Single-Photon_MeSH M_Ventricular_Fibrillation_MeSH S_epidemiology_MeSH Ventricular_Fibrillation_epidemiology_MeSH 
****** 10951826
----K 1
----T Effects of carvedilol in heart failure due to dilated cardiomyopathy. Results of a double-blind randomized placebo-controlled study (CARIBE study).
----A OBJECTIVE: To assess the effects of carvedilol in patients with idiopathic dilated cardiomyopathy. METHODS: In a double-blind randomized placebo-controlled study, 30 patients (7 women) with functional class II and III heart failure were assessed. Their ages ranged from 28 to 66 years (mean of 43 +/- 9 years), and their left ventricular ejection fraction varied from 8% to 35%. Carvedilol was added to the usual therapy of 20 patients; placebo was added to the usual therapy of 10 patients. The initial dose of carvedilol was 12.5 mg, which was increased weekly until it reached 75 mg/day, according to the patient's tolerance. Clinical assessment, electrocardiogram, echocardiogram, and radionuclide ventriculography were performed in the pretreatment phase, being repeated after 2 and 6 months of medication use. RESULTS: A reduction in heart rate (p = 0.016) as well as an increase in left ventricular shortening fraction (p = 0.02) and in left ventricular ejection fraction (p = 0.017) occurred in the group using carvedilol as compared with that using placebo. CONCLUSION: Carvedilol added to the usual therapy for heart failure resulted in better heart function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_etiology_MeSH Cardiac_Output__Low_etiology_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH 
****** 10951880
----K E
----T [The stress ergometry test in diabetics and non-diabetics]
----A OBJECTIVE: Evaluate risk factors of ischaemic heart disease (IHD) and the importance of burdening on a bicycle ergometer (BE) in the diagnosis of IHD in diabetic and non-diabetic subjects. CHARACTERISTIC OF GROUP: The authors evaluated in a retrospective study all 308 patients subjected to BE during the period 11/98-1/99 in Konstantinovy Lazne. Characteristics of diabetic vs. non-diabetic subjects: number (97 vs. 211), men (70.1 vs. 70.14%) mean age (59.76 vs. 58.01), height (1.71 vs. 1.71 m), body weight (85.91 vs. 81.40 kg), BMI (29.36 vs. 27.68 g/m2), total cholesterol (5.73 vs. 5.51 mmol/l,) triacylglycerols (2.63 vs. 2.08 mmol/l), fasting blood sugar level (7.31 vs. 4.88 mmol/l), hypertension (24.74 vs. 37.44%), hyperuricaemia (40.21 vs. 27.01%), IHD (93.81 vs. 93.84%), ischaemia of the lower extremities (6.19 vs. 13.74%), cerebrovascular episodes (7.22 vs. 5.21%), smokers 10.31 vs. 5.21%), ex-smokers (47.42 vs. 57.82%), non-smokers (42.27 vs. 36.97%). The diabetic patients were treated in 31.96% with PAD, in 5.15% with insulin and in 62.89% by diet only. EVALUATION: BE was used to assess and set the load tolerance, i.e. with regard to the current medication. The conclusion of BE is from the aspect of IHD either positive (ECG signs of coronary insufficiency), negative (without signs of coronary insufficiency at the level of 85% aerobic capacity according to Astrand) or impossible to evaluate (without signs of coronary insufficiency, while not attaining this level of load). Positive ergometric examinations were divided into symptomatic ones (i.e. with stenocardias during BE) and asymptomatic (silent ischaemia). In diabetic vs. non-diabetic subjects there were 0% vs. 6.16% symptomatically positive BE, 27.84% vs. 11.37% positive BE with silent ischaemia, 17.53% vs. 20.85% negative BE and 54.64% vs. 61.61% BE which could not be evaluated. The watt training tolerance was 51.55 vs. 57.26 W. CONCLUSIONS: In diabetics (31.49% of the group) there was a significantly higher body weight, BMI, TG. As to risk factors of IHD and manifestations of atherosclerosis there were among diabetics more patients with a history of a cerebrovascular episode, more smokers and conversely fewer hypertonic subjects and fewer with ischaemia of the lower extremities than in non-diabetic subjects. During BE in diabetics there were more silent ischaemias than in non-diabetics. None of the diabetics with a positive BE suffered from symptomatic ischaemia. The high percentage of BE which cannot be evaluated in both groups is due to the concurrent administration of drugs, in particular beta-blockers and the protocol of the examination (an increasing loading test after 4 min. a 25 W) which is suitable for setting the training load and not for assessment of coronary insufficiency (for this purpose the protocol after 2 min. a 50 W is more suitable). In the conclusion the authors evaluate the importance and informative value of different diagnostic examinations for detection of IHD or its severity in diabetic and non-diabetic subjects.
----P Journal_Article 
----M M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_English_Abstract_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Sensitivity_and_Specificity_MeSH 
****** 10954004
----K E
----T Dihydropyridine calcium antagonists and renal function in hypertensive kidney transplant recipients.
----A OBJECTIVE: To investigate whether calcium antagonists are nephroprotective in hypertensive cyclosporine-treated renal allograft recipients. METHODS: We studied 50 hypertensive and 17 normotensive renal transplants (eight females, nine males; 14-54 years, mean age 38.8 +/- 3.5 years). Hypertensive patients were randomized to be treated with (+Ca; 11 females, 13 males; 20-65 years, mean age 43.1 +/- 3 years) or without (-Ca; 15 females, 11 males; 25-60 years, mean age 41.3 +/- 2.5 years) a calcium antagonist (nitrendipine or nifedipine). Additional antihypertensives were given stepwise according to a standardized protocol: beta1-adrenoceptor blocker, diuretic alpha1-adrenoceptor blocker or vasodilator. Data were analysed at 0, 1, 2 and 3 years on an intention-to-treat basis. RESULTS: Hypertensive patients had a higher body mass index at 0/3 years (23.7 +/- 0.6/25.1 +/- 0.6 kg/m2) than normotensive patients (22.2 +/- 0.6/22.1 +/- 0.7 kg/m2). During the study, blood pressure in normotensive transplants was always slightly, but not significantly, lower than that of transplants with treated hypertension. There was no difference between the groups (+Ca) and (-Ca). Cr51-ethylenediaminetetracetic acid (EDTA) clearance (0/2 years) was 58 +/- 4/57 +/- 6 ml/min in normotensives, 52 +/- 4/47 +/- 4 ml/min in hypertensives (+Ca) and 47 +/- 4/49 +/- 6 ml/min in hypertensives (-Ca). Proteinuria (0/3 years) was 0.16 +/- 0.04/0.15 +/- 0.02 g/24 h in normotensive, 0.26 +/- 0.08/0.23 +/- 0.05 g/24 h in hypertensives (+Ca) and 0.26 +/- 0.07/0.22 +/- 0.05 g/24 h in hypertensives (-Ca). CONCLUSIONS: Post-transplant hypertension is associated with higher body mass index and poor renal function. No difference in the course of Cr51-EDTA clearance, serum creatinine, proteinuria or blood pressure was observed between groups treated with or without calcium antagonists. Calcium antagonists and conventional antihypertensive treatment have the same nephroprotective effect in hypertensive renal transplants, when treatment is started 3 months after transplantation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Body_Mass_Index_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cyclosporine_MeSH S_blood_MeSH Cyclosporine_blood_MeSH M_Dihydropyridines_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Renal_physiopathology_MeSH M_Immunosuppressive_Agents_MeSH S_blood_MeSH Immunosuppressive_Agents_blood_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Kidney_Function_Tests_MeSH M_Kidney_Transplantation_MeSH S_physiology_MeSH Kidney_Transplantation_physiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_metabolism_MeSH Proteinuria_metabolism_MeSH 
****** 10954006
----K E
----T Left ventricular wall stresses and wall stress-mass-heart rate products in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint reduction in hypertension.
----A OBJECTIVE: Left ventricular (LV) hypertrophy on echocardiogram (ECG) strongly predicts coronary heart disease events, but the mechanisms linking increased LV mass to ischemic vascular events is uncertain. DESIGN: Variables related to myocardial oxygen demand were compared among normotensive adults and patients with mild and more severe hypertension, and among groups of moderately hypertensive patients with target organ damage in relation to gender, LV geometry and LV systolic function. SETTING: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) trial, in which hypertensive patients with ECG LV hypertrophy (Cornell voltage-duration product, > 2440 mm x ms and/or SV1 + RV(5-6) > 38 mm) were randomized to > or = 4 years double-blinded treatment with losartan or atenolol. PATIENTS/PARTICIPANTS: A total of 964 LIFE participants enrolled in an echocardiographic substudy, and groups of 282 employed hypertensive and 366 apparently normal adults. INTERVENTIONS: None. MAIN OUTCOME MEASURES: ECG LV parameters contributing to myocardial oxygen demand (wall stresses, LV mass, heart rate and wall stress-mass-heart rate products). RESULTS: In both women and men, stepwise increases from reference subjects to employed hypertensives to LIFE patients were observed for LV wall stresses, mass and stress-mass-heart rate products. LIFE men patients had slightly higher wall stresses and significantly higher triple products than women. Wall stresses were increased in patients with normal LV geometry, eccentric or concentric hypertrophy; triple products were about three and two times normal with eccentric and concentric hypertrophy, with smaller increases in other geometric groups. Patients with decreased LV fractional shortening had two times normal end-systolic stresses and three or four times normal triple products; smaller increases in stresses and triple products occurred with decreased LV midwall function. CONCLUSIONS: Hypertensive patients with ECG LV hypertrophy have increased LV wall stresses and stress-mass-heart rate products, suggesting a contribution of high myocardial oxygen demand to increased risk in such patients. Particularly high stresses and triple products were associated with echocardiographic LV hypertrophy, and subnormal LV chamber and midwall function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Europe_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Oxygen_Consumption_MeSH S_physiology_MeSH Oxygen_Consumption_physiology_MeSH M_Sex_Characteristics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH M_Ventricular_Function__Left_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 10954008
----K E
----T Serum uric acid, diuretic treatment and risk of cardiovascular events in the Systolic Hypertension in the Elderly Program (SHEP).
----A OBJECTIVE: To assess longitudinally the association of serum uric acid and its change due to diuretic treatment with cardiovascular events in hypertensive patients. DESIGN: Cohort study in a randomized trial. SETTING: Cohort of hypertensive patients. PARTICIPANTS: A total of 4327 men and women, aged > or = 60 years, with isolated systolic hypertension, randomized to placebo or chlorthalidone, with the addition of atenolol or reserpine if needed, were observed for 5 years. MAIN OUTCOME MEASURES: Major cardiovascular events, coronary events, stroke and all-cause mortality. RESULTS: Cardiovascular event rates for quartiles of baseline serum uric acid were: I, 32.7 per 1000 person-years; II, 34.5 per 1000 person-years; III, 38.1 per 1000 person-years; and IV, 41.4 per 1000 person-years (P for trend = 0.02). The adjusted hazard ratio (HR), of cardiovascular events for the highest quartile of serum uric acid versus the lowest quartile was 1.32 (95% CI, 1.03-1.69). The benefit of active treatment was not affected by baseline serum uric acid. After randomization, an increase of serum uric acid < 0.06 mmol/l (median change) in the active treatment group was associated with a HR of 0.58 (0.37-0.92) for coronary events compared with those with a serum uric acid increase > or = 0.06 mmol/l. This difference was not explained by blood pressure effects. Those with a serum uric acid increase > or = 0.06 mmol/l in the active treatment group had a similar risk of coronary events as the placebo group. CONCLUSIONS: Serum uric acid independently predicts cardiovascular events in older persons with isolated systolic hypertension. Monitoring serum uric acid change during diuretic treatment may help to identify patients who will most benefit from treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biological_Markers_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Reserpine_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Uric_Acid_MeSH S_blood_MeSH Uric_Acid_blood_MeSH 
****** 10955372
----K E
----T Effect of atenolol and celiprolol on acetylcholine-induced coronary vasomotion in coronary artery disease.
----A Earlier studies have reported on the potentiated muscarinic vasoconstriction of intracoronary acetylcholine after metoprolol application in patients with coronary artery disease. The present study investigated the effect of celiprolol, atenolol, and placebo on acetylcholine-induced vasomotion in patients with coronary artery disease. Furthermore, direct effects on coronary vasomotion and on hemodynamics were evaluated. Acetylcholine (intracoronary concentrations of 6.3x10(-7), 2.0x10(-6), and 6.3x10(-6) M) was given before and after double-blind celiprolol (0.30 mg/kg IV), atenolol (0.15 mg/kg IV), or placebo in 3x12 patients. Vasomotion was investigated by quantitative coronary angiography in proximal and distal segments of epicardial coronary arteries, and by the determination of the coronary resistance index based on Doppler-flow measurements. The investigated drugs had no direct affect on the diameter of the epicardial coronary arteries. However, celiprolol, in contrast to atenolol, significantly reduced systemic vascular resistance (change after atenolol: from 1,855+/-308 to 2,161+/-550 dyne s cm(-5); celiprolol: 1,691+/-435 to 1,411+/-343 dyne s cm(-5); and placebo: 1,722+/-215 to 1,710+/-213 dyne s cm(-5), p<0.001) and the coronary resistance index (change after atenolol: 2.52+/-3.58 to 2.86+/-4.24; celiprolol: 2.70+/-1.55 to 2.49+/-2.26; and placebo: 1.97+/-1.35 to 1.92+/-1.25, p<0.01). Celiprolol, atenolol, and placebo did not have different effects on acetylcholine-induced coronary vasomotion of epicardial conductance vessels (diminution of proximal lumen diameter before/after atenolol: 0.42+/-0.39/0.44+/-0.39 mm; celiprolol: 0.32+/-0.26/0.30+/-0.24 mm; and placebo: 0.36+/-0.29/0.43+/-0.40 mm) and of coronary resistance vessels (reduction of coronary resistance index before/after atenolol: 1.95 +/-4.74/ 1.92+/-3.74; celiprolol: 0.98+/-0.73/1.41+/-1.50; and placebo: 1.16+/-1.29/1.16+/-1.04). In contrast to atenolol, celiprolol possesses vasodilative properties in systemic and coronary resistance vessels. There was no direct effect on the diameter of conductance vessels. Acetylcholine-induced coronary vasomotion both in conductance and resistance vessels was not influenced by the beta blockers that were studied. This suggests that atenolol and celiprolol do not influence endothelium-dependent, nitric oxide related vasomotion.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Coronary_Vessels_MeSH S_drug_effects_MeSH Coronary_Vessels_drug_effects_MeSH S_physiopathology_MeSH Coronary_Vessels_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 10952803
----K E
----T Drug treatment for bleeding oesophageal varices.
----A At the time of diagnosis of cirrhosis, varices are present in about 60% of decompensated and 30% of compensated patients. The risk factors for the first episode of variceal bleeding in cirrhotic patients are the severity of liver dysfunction, a large size of the varices and the presence of endoscopic red colour signs, but only a third of patients who suffer variceal haemorrhage demonstrate the above risk factors. The only treatment that does not require sophisticated equipment or the skills of a specialist, and is immediately available, is vasoactive drug therapy. Hence, drug therapy should be considered to be the initial treatment of choice and can be administered while the patient is transferred to hospital, as has been done in one recent study. Moreover, drug therapy is no longer considered to be only a 'stop-gap' therapy until definitive endoscopic therapy is performed. Several recent trials have reported an efficacy similar to that of emergency sclerotherapy in the control of variceal bleeding. Furthermore, recent evidence suggests that those patients with high variceal or portal pressure are likely to continue to bleed or re-bleed early, implying that prolonged therapy lowering the portal pressure over several days may be the optimal treatment. Pharmacological treatment with beta-blockers is safe, effective and the standard long-term treatment for the prevention of recurrence of variceal bleeding. The combination of beta-blockers with isosorbide-5-mononitrate needs further testing in randomized controlled trials. The use of haemodynamic targets for the reduction of the HVPG response needs further study, and surrogate markers of the pressure response need evaluation. Ligation has recently been compared with beta-blockers for primary prophylaxis, but there is as yet no good evidence to recommend banding for primary prophylaxis if beta-blockers can be given.
----P Journal_Article Review Review__Academic 
----M M_Acute_Disease_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH M_Hemostatics_MeSH S_therapeutic_use_MeSH Hemostatics_therapeutic_use_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Vasoconstrictor_Agents_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 10961964
----K E
----T Elevated C-reactive protein levels and impaired endothelial vasoreactivity in patients with coronary artery disease.
----A BACKGROUND: Elevated C-reactive protein (CRP) serum levels, an exquisitely sensitive objective marker of inflammation, relate to long-term prognosis in patients with coronary artery disease and in apparently healthy men. Because abnormalities of endothelial regulation of vascular function may contribute to the occurrence of coronary events, we tested the hypothesis that elevated CRP levels are associated with an abnormal systemic endothelial vascular reactivity. METHODS AND RESULTS: Endothelium-dependent (10 to 50 microg/min acetylcholine) and endothelium-independent (2 to 8 microg/min sodium nitroprusside) forearm blood flow responses were measured with venous occlusion plethysmography in 60 male patients with angiographically documented coronary artery disease. Forearm blood flow responses to acetylcholine were inversely correlated with CRP serum levels (r=-0.46, P:=0.001). With multivariate analysis that included the classic risk factors for coronary artery disease, elevated CRP serum level remained a statistically significant independent predictor of a blunted endothelial vasodilator capacity. Most important, normalization of elevated CRP levels over time was associated with a normalization of endothelium-mediated forearm blood flow responses after 3 months. CONCLUSIONS: Thus, elevated CRP serum levels indicative of a systemic inflammatory response are associated with a blunted systemic endothelial vasodilator function. The identification of elevated CRP levels as a transient independent risk factor for endothelial dysfunction might provide an important clue to link a systemic marker of inflammation to atherosclerotic disease progression.
----P Clinical_Trial Journal_Article 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Brachial_Artery_MeSH M_C-Reactive_Protein_MeSH S_analysis_MeSH C-Reactive_Protein_analysis_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Endothelium__Vascular_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Follow-Up_Studies_MeSH M_Forearm_MeSH M_Human_MeSH M_Inflammation_MeSH S_blood_MeSH Inflammation_blood_MeSH M_Infusions__Intra-Arterial_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Nitroprusside_MeSH S_pharmacology_MeSH Nitroprusside_pharmacology_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Risk_Factors_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10972367
----K I
----T Randomised trial of effects of calcium antagonists compared with diuretics and beta-blockers on cardiovascular morbidity and mortality in hypertension: the Nordic Diltiazem (NORDIL) study.
----A BACKGROUND: Calcium antagonists are a first-line treatment for hypertension. The effectiveness of diltiazem, a non-dihydropyridine calcium antagonist, in reducing cardiovascular morbidity or mortality is unclear. We compared the effects of diltiazem with that of diuretics, beta-blockers, or both on cardiovascular morbidity and mortality in hypertensive patients. METHODS: In a prospective, randomised, open, blinded endpoint study, we enrolled 10,881 patients, aged 50-74 years, at health centres in Norway and Sweden, who had diastolic blood pressure of 100 mm Hg or more. We randomly assigned patients diltiazem, or diuretics, beta-blockers, or both. The combined primary endpoint was fatal and non-fatal stroke, myocardial infarction, and other cardiovascular death. Analysis was done by intention to treat. FINDINGS: Systolic and diastolic blood pressure were lowered effectively in the diltiazem and diuretic and beta-blocker groups (reduction 20.3/18.7 vs 23.3/18.7 mm Hg; difference in systolic reduction p<0.001). A primary endpoint occurred in 403 patients in the diltiazem group and in 400 in the diuretic and beta-blocker group (16.6 vs 16.2 events per 1000 patient-years; relative risk 1.00 [95% CI 0.87-1.15], p=0.97). Fatal and non-fatal stroke occurred in 159 patients in the diltiazem group and in 196 in the diuretic and beta-blocker group (6.4 vs 7.9 events per 1000 patient-years; 0.80 [0.65-0.99], p=0.04) and fatal and non-fatal myocardial infarction in 183 and 157 patients (7.4 vs 6.3 events per 1000 patient-years; 1.16 [0.94-1.44], p=0.17). INTERPRETATION: Diltiazem was as effective as treatment based on diuretics, beta-blockers, or both in preventing the combined primary endpoint of all stroke, myocardial infarction, and other cardiovascular death.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Accident_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Life_Tables_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10972368
----K E
----T Morbidity and mortality in patients randomised to double-blind treatment with a long-acting calcium-channel blocker or diuretic in the International Nifedipine GITS study: Intervention as a Goal in Hypertension Treatment (INSIGHT).
----A BACKGROUND: The efficacy of antihypertensive drugs newer than diuretics and beta-blockers has not been established. We compared the effects of the calcium-channel blocker nifedipine once daily with the diuretic combination co-amilozide on cardiovascular mortality and morbidity in high-risk patients with hypertension. METHODS: We did a prospective, randomised, double-blind trial in Europe and Israel in 6321 patients aged 55-80 years with hypertension (blood pressure > or = 150/95 mm Hg, or > or = 160 mm Hg systolic). Patients had at least one additional cardiovascular risk factor. We randomly assigned patients nifedipine 30 mg in a long-acting gastrointestinal-transport-system (GITS) formulation (n=3157), or co-amilozide (hydrochlorothiazide 25 mg [corrected] plus amiloride 2.5 mg; n=3164). Dose titration was by dose doubling, and addition of atenolol 25-50 mg or enalapril 5-10 mg. The primary outcome was cardiovascular death, myocardial infarction, heart failure, or stroke. Analysis was done by intention to treat. FINDINGS: Primary outcomes occurred in 200 (6.3%) patients in the nifedipine group and in 182 (5.8%) in the co-amilozide group (18.2 vs 16.5 events per 1000 patient-years; relative risk 1.10 [95% CI 0.91-1.34], p=0.35). Overall mean blood pressure fell from 173/99 mm Hg (SD 14/8) to 138/82 mm Hg (12/7). There was an 8% excess of withdrawals from the nifedipine group because of peripheral oedema (725 vs 518, p<0.0001), but serious adverse events were more frequent in the co-amilozide group (880 vs 796, p=0.02). Deaths were mainly non-vascular (nifedipine 176 vs co-amilozide 172; p=0.81). 80% of the primary events occurred in patients receiving randomised treatment (157 nifedipine, 147 co-amilozide, difference 0.33% [-0.7 to 1.4]). INTERPRETATION: Nifedipine once daily and co-amilozide were equally effective in preventing overall cardiovascular or cerebrovascular complications. The choice of drug can be decided by tolerability and blood-pressure response rather than long-term safety or efficacy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amiloride_MeSH S_administration_&_dosage_MeSH Amiloride_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Chemistry__Pharmaceutical_MeSH M_Delayed-Action_Preparations_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Life_Tables_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10972606
----K E
----T Total intravenous anesthesia with a propofol-ketamine combination during coronary artery surgery.
----A OBJECTIVE: To evaluate the cardiovascular effects of a propofol-ketamine combination in patients undergoing coronary artery surgery. DESIGN: Prospective, randomized study. SETTING: Tertiary care teaching hospital, single center. PARTICIPANTS: Seventy-eight adult patients. INTERVENTIONS: Patients were randomly allocated to receive propofol-ketamine for induction and maintenance of anesthesia (n = 36) or fentanyl-enflurane (controls, n = 42). MEASUREMENTS AND MAIN RESULTS: Hemodynamics and other variables were recorded during and after surgery and for 24 hours in the intensive care unit. Before cardiopulmonary bypass (CPB), there was similar incidence of treatment for hypotension (42% of patients in both groups), tachycardia (propofol-ketamine, 6%; controls, 5%), and myocardial ischemia (propofol-ketamine, 3%; controls, 12%). In the propofol-ketamine group, there was a decreased requirement for inotropic agents after CPB (22% of patients) compared with controls (49% of patients; p = 0.02). There was a reduced incidence of myocardial infarctions (creatine kinase myocardial band >133 U/L) in the propofol-ketamine group compared with the control group (0% v 14%; p = 0.02; Fisher's exact test). Patients in the propofol-ketamine group were more likely to have their tracheas extubated within 8 hours of arrival in the intensive care unit compared with controls (33% v 7%; p = 0.01; Cochran-Mantel-Haenzel test). CONCLUSIONS: The propofol-ketamine combination was associated with a similar incidence of pre-CPB hypotension and ischemia, a decreased need for inotropes after CPB, an earlier time to tracheal extubation, and a reduced incidence of myocardial infarctions compared with controls.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M P_Anesthesia__Intravenous_MeSH P_Anesthetics__Combined_MeSH S_pharmacology_MeSH Anesthetics__Combined_pharmacology_MeSH M_Anesthetics__Dissociative_MeSH S_pharmacology_MeSH Anesthetics__Dissociative_pharmacology_MeSH M_Anesthetics__Inhalation_MeSH S_pharmacology_MeSH Anesthetics__Inhalation_pharmacology_MeSH P_Anesthetics__Intravenous_MeSH S_pharmacology_MeSH Anesthetics__Intravenous_pharmacology_MeSH P_Coronary_Artery_Bypass_MeSH M_Enflurane_MeSH S_pharmacology_MeSH Enflurane_pharmacology_MeSH M_Female_MeSH M_Fentanyl_MeSH S_pharmacology_MeSH Fentanyl_pharmacology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH P_Ketamine_MeSH S_pharmacology_MeSH Ketamine_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxygen_MeSH S_blood_MeSH Oxygen_blood_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH P_Propofol_MeSH S_pharmacology_MeSH Propofol_pharmacology_MeSH M_Prospective_Studies_MeSH 
****** 10979055
----K I
----T High blood pressure and diabetes mellitus: are all antihypertensive drugs created equal?
----A OBJECTIVE: To analyze the available data to assess the benefits of antihypertensive therapy in hypertensive patients with diabetes mellitus. METHODS: A MEDLINE search of English-language articles published until June 1999 was undertaken with the use of the terms diabetes mellitus, hypertension or blood pressure, and therapy. Pertinent articles cited in the identified reports were also reviewed. Included were only prospective randomized studies of more than 12 months' duration that evaluated the effect of drug treatment on morbidity and mortality in diabetic hypertensive patients. We estimated the risk associated with combination of diabetes mellitus and hypertension and the effect of treatment on morbidity and mortality. RESULTS: The coexistence of diabetes mellitus doubled the risk of cardiovascular events, cardiovascular mortality, and total mortality in hypertensive patients (approximate relative risk of 1.73-2.77 for cardiovascular events, 2.25-3.66 for cardiovascular mortality, and 1.73-2.18 for total mortality). Intensive blood pressure control to levels lower than 130/85 mm Hg was beneficial in diabetic hypertensive patients. All 4 drug classes-diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, and calcium antagonists-were effective in reducing cardiovascular events in diabetic hypertensive patients. In elderly diabetic patients with isolated systolic hypertension, calcium antagonists reduced the rate of cardiac end points by 63%, stroke by 73%, and total mortality by 55%. In more than 60% of diabetic hypertensive patients, combination therapy was required to control blood pressure. CONCLUSIONS: Intensive control of blood pressure reduced cardiovascular morbidity and mortality in diabetic patients regardless of whether low-dose diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists were used as a first-line treatment. A combination of more than 1 drug is frequently required to control blood pressure and may be more beneficial than monotherapy.
----P Journal_Article Review Review__Academic 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_mortality_MeSH Diabetic_Angiopathies_mortality_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10978803
----K E
----T Part 7: the era of reperfusion. Section 2: acute stroke. European Resuscitation Council.
----A 
----P Consensus_Development_Conference Guideline Journal_Article Practice_Guideline Review 
----M M_Acute_Disease_MeSH M_Algorithms_MeSH M_Cerebrovascular_Accident_MeSH S_therapy_MeSH Cerebrovascular_Accident_therapy_MeSH M_Emergencies_MeSH M_Human_MeSH M_Reperfusion_MeSH S_methods_MeSH Reperfusion_methods_MeSH S_standards_MeSH Reperfusion_standards_MeSH 
****** 10980854
----K E
----T Beta-blockers and amiodarone for the primary prevention of sudden cardiac death.
----A Sudden cardiac death remains a major public health care problem, generally occurring in patients with ventricular dysfunction. Beta-blockers, already of proven benefit for patients after myocardial infarction, have recently been shown to improve functional status and mortality outcomes in patients with heart failure. Amiodarone, a potent antiarrhythmic drug, was recently studied in a number of randomized clinical trials involving patients with heart failure and patients after myocardial infarction. Routine use of amiodarone cannot be recommended in these patient groups, but serious adverse outcomes were not observed. When antiarrhythmic drug therapy is required, amiodarone is the drug of choice for patients with structural heart disease.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Analysis_MeSH M_Ventricular_Fibrillation_MeSH S_complications_MeSH Ventricular_Fibrillation_complications_MeSH S_drug_therapy_MeSH Ventricular_Fibrillation_drug_therapy_MeSH 
****** 10980877
----K E
----T Beta-blockers and spironolactone in heart failure.
----A Neurohormonal antagonism is now recognized as an essential treatment modality for heart failure. As a prime example, the benefits of blocking the renin-angiotensin system with angiotensin converting enzyme inhibitors are clearly established for all four New York Heart Association classes. In this clinical trials review, we discuss two other therapies with neurohormonal targets: beta-blockers and the sympathetic nervous system, and the aldosterone antagonist spironolactone.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10983362
----K 1
----T [A comparative efficiency of amitriptyline, fluoxetine and maprotiline in prevention of migraine in attack-free period]
----A To reduce frequency and severity of the attacks, migraine was treated preventively between the attacks. The most effective drugs were beta-blockers and antidepressants. In a single-blind study we estimated comparative efficiency of amitriptiline (inhibitor of noradrenaline and serotonin reuptake and 5-HT2-receptor antagonist) 12.5-25 mg/daily, fluoxetine (a selective serotonin reuptake inhibitor) 10-20 mg/daily, and maprotiline (a selective noradrenaline reuptake inhibitor) 10-25 mg/daily. The duration of the therapy of migraine between the attacks was 12 weeks. Each group included 20 patients. 46 patients completed the whole course of therapy: 14 patients received amitriptyline, 16 patients--fluoxetine, and 16 patients--maprotiline. Positive results of the treatment (a reduction of the frequency of the migraine attacks during a treatment by 50% as compared with the baseline period) were observed in 71% of the patients treated with amitriptyline, in 56% of the patients treated with fluoxetine, and in 38% of the patients treated with maprotiline. All the drugs were able to reduce both intensity and duration of a headache. Index of the Quality of Life in the patients with migraine was increased in the groups treated with either amitriptyline or fluoxetine, but not in a group treated with maprotiline. The results obtained agree with the notion about high efficiency of antidepressants given between migraine attacks. Amitriptyline and fluoxetine were more efficient in preventive therapy than maprotiline. These findings suggested indirectly, that the efficiency of antidepressants in treatment of migraine is explained by inhibition of serotonin reuptake and by 5-HT2-receptor antagonism, while influence on the inhibition of noradrenaline reuptake was not so significant.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Acute_Disease_MeSH M_Adrenergic_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Adrenergic_Uptake_Inhibitors_therapeutic_use_MeSH M_Adult_MeSH M_Amitriptyline_MeSH S_therapeutic_use_MeSH Amitriptyline_therapeutic_use_MeSH M_Analgesics__Non-Narcotic_MeSH S_therapeutic_use_MeSH Analgesics__Non-Narcotic_therapeutic_use_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_therapeutic_use_MeSH Fluoxetine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Maprotiline_MeSH S_therapeutic_use_MeSH Maprotiline_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 10981082
----K E
----T Centrally acting antihypertensive drugs: re-emergence of sympathetic inhibition in the treatment of hypertension.
----A Central regulation of the sympathetic nervous system plays an important role in the maintenance of blood pressure. In a subset of patients with essential hypertension, sympathetic activation may contribute to the development and maintenance of hypertension. Unlike the first generation of centrally active antihypertensive drugs, the second generation may be superior because of its selectivity to I1-imidazoline receptor and selective binding to the vasomotor center. Lack of a2 effects differentiates moxonidine from clonidine with respect to monoxidine"s superior side-effect profile (little or no sedation or dry mouth). Clinical trials show that moxonidine is as effective as angiotensin-converting enzyme inhibitors (eg, enalapril and captopril), b-blockers (e.g., atenolol), calcium-channel blockers (e.g., long-acting nifedipine), and diuretics (eg, hydrochlorothiazide) in lowering blood pressure and that it has superior tolerability. Thus, central modulation of the sympathetic nervous system has re-emerged as an exciting target for blood pressure reduction. Given the multiple adverse effects of sympathetic stimulation in various disease processes, including congestive heart failure, moxonidine may be the next therapeutic option for the management of hypertension and the prevention of target organ dysfunction.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Imidazoles_MeSH S_pharmacology_MeSH Imidazoles_pharmacology_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Treatment_Outcome_MeSH 
****** 10981092
----K I
----T Three recently published trials in hypertension.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_physiopathology_MeSH Diabetes_Mellitus_physiopathology_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Randomized_Controlled_Trials_MeSH 
****** 10981178
----K E
----T Coronary heart disease prevention As the primary goal in contemporary trials in the treatment of hypertension.
----A The prevention of coronary heart disease remains one of the greatest challenges for antihypertensive therapy. Previous trials have identified a shortfall in the protection of hypertensive patients against coronary heart disease compared with that predicted from observational studies. The present question is whether newer classes of drugs or drug combinations (calcium channel blockers, angiotensin converting enzyme inhibitors) can redress the shortfall compared with older agents (diuretics, beta-blockers). However, to answer this question only two trials (Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial [ALLHAT] and Anglo Scandinavian Cardiac Outcomes Trial [ASCOT]) are of sufficient size to be adequately powered to address this issue. ALLHAT and ASCOT have completed randomization of patients and will report on morbidity and mortality within 3 to 4 years.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10987351
----K E
----T Usefulness of beta blocker therapy in patients with Takayasu arteritis and moderate or severe aortic regurgitation.
----A The objective of the present study was to evaluate the benefit of beta-blocker therapy for patients with Takayasu arteritis complicated by moderate or severe aortic regurgitation. Clinical and echocardiographic evaluation was performed in 20 Japanese women in a follow-up period of 7.0 +/- 2.0 years. The patients were divided into 2 groups: Group A (n=10) patients who did not receive beta-blockers, and Group B (n=10) patients treated with long-term (5.1 +/- 1.6 years) therapeutic doses of beta-blockers. Left ventricular wall thickness increased significantly in all Takayasu patients who did not receive beta-blockers. Consequently, a remarkable increment in left ventricular mass took place (232 +/- 59 to 361 +/- 79 g; p < 0.005). In the same group, progressive worsening of the symptoms, with no reduction in the percent fractional shortening, was observed in 2 patients, while reduction of this last index was present in 1 asymptomatic patient. On the other hand, among the patients who were treated with beta-blockers, left ventricular mass still increased in 6 cases, while it clearly decreased in the other 4 cases (290 +/- 171 to 284 +/- 61 g; NS). The increment in wall thickness or left ventricular mass observed among patients with beta-blocker therapy was clearly less than the one registered among those who had not received beta-blockers. Furthermore, no worsening of the symptoms and/or left ventricular performance was observed during the follow-up period for patients receiving beta-blockers. We conclude that beta-blocker therapy can slow and even reverse the progression of left ventricular hypertrophy in patients with Takayasu arteritis complicated by moderate or severe aortic regurgitation. The mechanism still needs to be elucidated. We believe an effective reduction in the excessive afterload imposed on the left ventricle to be most likely responsible, but cardiac beta-receptor up-regulation might also be involved. Deterioration of the clinical status and/or impairment of left ventricular function were not associated with beta-blocker therapy in our patients. Therefore, these agents can be used safely alone or in addition to standard anti-hypertensive therapy when attempting to reduce excessive afterload, in spite of the presence of severe aortic regurgitation.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aortic_Valve_Insufficiency_MeSH S_etiology_MeSH Aortic_Valve_Insufficiency_etiology_MeSH S_ultrasonography_MeSH Aortic_Valve_Insufficiency_ultrasonography_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Takayasu's_Arteritis_MeSH S_complications_MeSH Takayasu's_Arteritis_complications_MeSH S_drug_therapy_MeSH Takayasu's_Arteritis_drug_therapy_MeSH 
****** 10987353
----K E
----T Predictors of short-term outcome in Chinese patients with ambulatory heart failure for heart transplantation with ejection fraction <25%.
----A Heart transplantation (HT) provides longer survival than that of the natural history in patients with dilated cardiomyopathy (DCM). However, the optimal timing for cardiac transplantation and predictors of mortality in patients with end-stage cardiomyopathy (ESCM) has been poorly defined. The primary purpose of this study focused on the natural history of ambulatory patients with ESCM for HT assessment. Secondly, we tried to determine prognostic factors of individuals with the poorest short-term outcome and the optimal timing for HT in patients with ESCM. Finally, clinical treatment with angiotensin converting-enzyme inhibitors (ACEIs), carvedilol and amiodarone in the prevention of mortality caused by ESCM, were retrospectively evaluated. The short-term outcomes of 119 referral patients with ESCM for four years were observed. The patients had New York Heart Association class III to IV dyspnea at initial assessment for HT. Left ventricular ejection fraction (LVEF) was 17 +/- 6% and cardiac index (CI) was 2.0 +/- 0.6l/min/m2. After optimization of medical treatment, the patients were divided into two major groups according to CI equal to or less than 2.0l/min/m2 and more than 2.0l/min/m2. HTs were accepted in 88 patients and the patients were divided into two groups: medical treatment (group 1, 56 patients) or HT (group 3, 32 patients); HT was not accepted in the other 31 patients (group 2). We studied the probability of the survival curve and prognostic variables of the groups with medical treatment in the follow-up of 12 +/- 9 months. During follow-up, 49 patients were alive without HT. The remaining 38 patients died; 27 patients were in group 1 and 11 patients were in group 2. Eight deaths in group 2 were sudden. The actuarial survival rate among the non-HT population was 73%, 68%, 63 %, and 56 % at 3, 6, 9 and 12 months, respectively. The actuarial survival rate among group 1 was 70 %, 59 %, 55 %, and 52 % at 3, 6, 9 and 12 months, respectively. The actuarial survival rate among group 2 was 87 %, 85 %, 77 %, and 65 % at 3, 6, 9 and 12 months, respectively. A comparison, excluding patients with HT, was performed with those who had survived < 1 year and > or 1 year after assessment, and those who had died. Two parameters were independent predictors of prognosis on univariate and multivariate analysis: total pulmonary vascular resistance (TPR) > or = 14 Wood units (W) and CI < 1.65 l/min/m2 at 6 and 12 months after assessment. Treatment with amiodarone for ventricular tachycardia (VT) showed no convincing role in the prevention of sudden death in our patients. Also, treatment with ACEIs or carvedilol for heart failure was unconvincing to improve the short-term outcome in this study. Our results suggest in properly selected patients that HT should be considered within six months among patients with severe heart failure. Hemodynamic parameters associated with right cardiac function are important determinants of mortality caused by progressive heart failure. Predictors such as CI and TPR may be considered as important markers of mortality in prediction of short-term outcome in patients with ESCM, as other predictors reported in the literature.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiomyopathy__Congestive_MeSH S_mortality_MeSH Cardiomyopathy__Congestive_mortality_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_surgery_MeSH Cardiomyopathy__Congestive_surgery_MeSH M_Child_MeSH M_China_MeSH S_epidemiology_MeSH China_epidemiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Transplantation_MeSH S_mortality_MeSH Heart_Transplantation_mortality_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH P_Stroke_Volume_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 10989729
----K 1
----T [Local pulse pressure and regression of arterial wall hypertrophy during antihypertensive treatment. CELIMENE study. The Celiprolol Intima-Media Enalapril Efficacy study]
----A BACKGROUND: Local Pulse Pressure (PP) is an independent determinant of carotid artery wall thickness, stronger than mean BP. The present study was designed to assess whether a beta-adrenoceptor antagonist or an ACE inhibitor-based treatment was able to reduce carotid artery wall hypertrophy through the reduction in carotid PP rather than by lowering mean BP, and whether the influence of local PP reduction could also be detected at the site of a muscular artery, the radial artery. METHODS AND RESULTS: Ninety-eight essential hypertensive patients were randomised to 9 months of double-blind treatment with either celiprolol or enalapril. Arterial parameters were determined with high resolution echotracking systems. PP was measured locally with PP applanation tonometry, and independently of mean BP. After 9 month's treatment, mean BP, carotid PP and intima-media thickness (IMT) decreased significantly, with no difference between the tow groups. The reduction in carotid pression pulsee, but not in mean BP, was a major independent determinant of the reduction in carotid IMT. Radial artery IMT and PP decreased significantly with both treatments. However, the reduction in radial artery IMT was not related to the changes in radial artery PP. CONCLUSION: The regression of carotid artery wall hypertrophy during long-term antihypertensive treatment was dependent on the reduction in local PP rather than on the lowering of mean BP. The effect of PP lowering on IMT reduction was observed at the site of an elastic artery but not at the site of a muscular artery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carotid_Arteries_MeSH S_drug_effects_MeSH Carotid_Arteries_drug_effects_MeSH S_pathology_MeSH Carotid_Arteries_pathology_MeSH S_ultrasonography_MeSH Carotid_Arteries_ultrasonography_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy_MeSH M_Male_MeSH M_Pulse_MeSH M_Radial_Artery_MeSH S_drug_effects_MeSH Radial_Artery_drug_effects_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tunica_Intima_MeSH S_drug_effects_MeSH Tunica_Intima_drug_effects_MeSH M_Tunica_Media_MeSH S_drug_effects_MeSH Tunica_Media_drug_effects_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 10993002
----K 1
----T [Economic significance of heart failure. An overview of costs and economics of therapy]
----A The economic burden of congestive heart failure is significant. Approximately 1 to 2% of total health care expenditure is attributed to the diagnosis, treatment and prevention of congestive heart failure. A great share of this expenditure is related to the costs of long-term complications and productivity losses. In order to manage these costs, providers and policymakers increasingly have to focus on economically attractive interventions. Pharmacoeconomic analyses aid the systematic selection of cost-effective drug therapy in congestive heart failure in an era of increasing cost-containment.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Costs_and_Cost_Analysis_MeSH M_Economics__Pharmaceutical_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Health_Expenditures_MeSH M_Heart_Failure__Congestive_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 10993003
----K 1
----T [The symptomatic patient with pathologic coronary angiogram. "evidence-based" or "best-evidence medicine" in the interventional cardiology]
----A Ischemic heart disease is the most frequent cause of death in industrialized countries. This is a result of persistent risk factors and aging of the population. Medical progress with application of conservative, surgical or interventional strategies indeed reduced the morbidity and mortality of arteriosclerotic diseases, but markedly increased the medical care costs. The result is a discussion about the optimal use of the different therapeutic measures under consideration of the evidence based medicine. This article reviews several recently published clinical trials and discusses, which patient with symptomatic coronary artery disease should undergo a conservative strategy, percutaneous or surgical revascularization.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_English_Abstract_MeSH P_Evidence-Based_Medicine_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Meta-Analysis_MeSH M_Middle_Aged_MeSH M_Myocardial_Revascularization_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Stents_MeSH M_Time_Factors_MeSH 
****** 10997755
----K E
----T The COHERE Registry: hype or hope?
----A 
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Trials_MeSH S_standards_MeSH Clinical_Trials_standards_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Registries_MeSH M_Research_Design_MeSH 
****** 10995404
----K E
----T Randomised comparison of the effects of nicardipine and esmolol on coronary artery wall stress: implications for the risk of plaque rupture.
----A OBJECTIVE: To determine whether the beta blocker esmolol reduces coronary artery wall stress more than the short acting dihydropyridine calcium antagonist nicardipine. DESIGN: Randomised double blind placebo controlled trial. SETTING: Tertiary cardiology centre. PATIENTS: Patients with coronary artery disease. INTERVENTIONS: 20 patients were randomised double blind to an infusion of nicardipine (n = 10) or esmolol (n = 10) titrated to reduce systolic blood pressure by 20 mm Hg. MAIN OUTCOME MEASURES: Peak systolic wall circumferential stress. RESULTS: Esmolol reduced peak coronary stress by a mean of 0.17 x 10(6) dyn/cm(2) (95% confidence interval (CI) 0.14 to 0.21 x 10(6) dyn/cm(2)) compared with a reduction of 0.07 x 10(6) dyn/cm(2) (95% CI 0.05 to 0.10 x 10(6) dyn/cm(2)) after nicardipine. Peak systolic radius was reduced by 0.04 mm (95% CI 0.03 to 0.06 mm) after esmolol compared with an increase of 0.08 mm (95% CI 0.05 to 0.10 mm) after nicardipine. Heart rate increased by 11.5 beats/min (95% CI 6.9 to 16.2 beats/min) after nicardipine and decreased by 5.3 beats/min (95% CI 1.9 to 8.6 beats/min) after esmolol. CONCLUSIONS: Intravenous esmolol is more effective than nicardipine at reducing circumferential coronary artery wall stress.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Coronary_Vessels_MeSH S_drug_effects_MeSH Coronary_Vessels_drug_effects_MeSH S_ultrasonography_MeSH Coronary_Vessels_ultrasonography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nicardipine_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stress__Mechanical_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultrasonography__Interventional_MeSH 
****** 11004045
----K E
----T A comparative study between a calcium channel blocker (Nicardipine) and a combined alpha-beta-blocker (Labetalol) for the control of emergence hypertension during craniotomy for tumor surgery.
----A We compared the efficacy of the combination of enalaprilat/labetalol with that of enalaprilat/nicardipine to prevent emergence postcraniotomy hypertension. A prospective, randomized open labeled clinical trial was designed to compare the incidence of breakthrough hypertension (systolic blood pressure [SBP] > 140 mm Hg) and adverse effects (hypotension, tachycardia, and bradycardia) between the two drug combinations. Secondarily, the effects of the drugs on SBP, mean blood pressure, and diastolic blood pressure were evaluated over the course of the study. Forty-two patients received enalaprilat 1.25 mg IV at dural closure followed by either multidose nicardipine 2 mg IV or labetalol 5 mg IV to maintain the SBP below 140 mm Hg. SBP was similarly controlled in both groups. There was a marginally smaller incidence of failures and adverse effects with labetalol. Blood pressure profiles were similar for both groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH P_Anesthesia_Recovery_Period_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Bradycardia_MeSH S_chemically_induced_MeSH Bradycardia_chemically_induced_MeSH M_Brain_Neoplasms_MeSH S_surgery_MeSH Brain_Neoplasms_surgery_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH P_Craniotomy_MeSH M_Enalaprilat_MeSH S_therapeutic_use_MeSH Enalaprilat_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Incidence_MeSH M_Labetalol_MeSH S_adverse_effects_MeSH Labetalol_adverse_effects_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nicardipine_MeSH S_adverse_effects_MeSH Nicardipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Tachycardia_MeSH S_chemically_induced_MeSH Tachycardia_chemically_induced_MeSH M_Treatment_Outcome_MeSH 
****** 11041675
----K E
----T Effect of angiotensin-converting enzyme inhibition compared with conventional therapy on cardiovascular morbidity and mortality in hypertension: the Captopril Prevention Project (CAPP) randomized trial. The Captopril Prevention Project (CAPP) Study Group.
----A A number of investigations have recently been published on the role of microsatellite instability (MSI) in the process of colorectal carcinogenesis. The data concerning colorectal adenomas are difficult to compare (due to differences in the tumor collection, selection and number of analyzed loci, definition of high and low instability and histological types), and this review therefore examines the significance of the results of these publications. We then discuss the extent to which MSI and its effects on the integrity of the genome are early or late events in the malignant transformation, and which clinicopathological features are presented by MSI-positive adenomas. Finally, we consider the clinical importance of microsatellite status for the diagnosis of hereditary nonpolyposis colorectal cancer and the possibility of preventing adenomas and carcinomas by nonsteroidal anti-inflammatory drugs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Meta-Analysis_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 11009288
----K E
----T Comparison of quinapril versus atenolol: effects on blood pressure and cardiac mass after renal transplantation.
----A Based on epidemiologic facts on elevated cardiovascular mortality in renal allograft recipients, an echocardiographic 2-year follow-up in hypertensive renal allograft recipients was conducted. This study provides evidence that, in contrast to atenolol, quinapril, independent of blood pressure reduction, reduces left ventricular hypertrophy and improves left ventricular diastolic function in this population.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Heart_Ventricles_MeSH S_anatomy_&_histology_MeSH Heart_Ventricles_anatomy_&_histology_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiology_MeSH Heart_Ventricles_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Isoquinolines_MeSH S_pharmacology_MeSH Isoquinolines_pharmacology_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Kidney_Transplantation_MeSH S_physiology_MeSH Kidney_Transplantation_physiology_MeSH M_Middle_Aged_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 11014332
----K E
----T Current status of safety and efficacy of calcium channel blockers in cardiovascular diseases: a critical analysis based on 100 studies.
----A Recently, serious concerns have been expressed about the long-term safety of the calcium channel blockers (CCBs) as a group. Safety and efficacy are, however, ultimately linked to each other; therefore both must be evaluated especially in the therapy of angina and hypertension, the main clinical indications for CCBs. The structural, functional, and pharmacokinetic heterogeneity of CCBs means that the efficacy and dangers of one subclass, such as the short-acting dihydropyridines (DHPs), in one situation, such as unstable angina, do not necessarily apply in other clinical situations. One hundred studies are reviewed according to their methods of data collection: case series, case control, cohort, randomized controlled trials (RCTs), and meta-analyses. Large, well-designed RCTs and the meta-analyses based on these trials remain the gold standard. Observational studies, though potentially less reliable sources of information because of selection bias, may nevertheless produce hypotheses that must then be tested in RCTs. Regarding safety, both observational studies and RCTs suggest that adverse effects of CCBs may be linked to short-acting agents, specifically short-acting nifedipine. Two good studies favor the safety of verapamil, even in short-acting form. Incomplete but increasing overall evidence favors the safety of longer-acting DHPs. Heart failure remains a class contraindication to the use of all CCBs, with some exceptions. Regarding efficacy, there are positive results of RCTs with CCBs in 2 specific clinical situations, namely, verapamil in postinfarct protection in the absence of pre-existing heart failure, and 2 outcome studies on hypertension with longer acting DHPs. These results cannot automatically be applied to other clinical situations and to other CCBs. For example, there is no evidence for the safety or efficacy of DHPs used without beta blockers in postinfarct patients. In diabetic hypertensives, 2 relatively large RCTs show that the blood pressure can be reduced by DHP-based therapy in diabetics, with a reduction in hard end points. To achieve current blood pressure goals, combination therapy is almost always necessary, and in diabetics there is strong evidence that 1 essential component should be an angiotensin converting enzyme inhibitor. The future aim with CCBs must be to obtain a large database gathered from RCTs, which will give the same certainty about efficacy and safety that already holds for use of the diuretics in hypertension, beta-blockers in postmyocardial infarction patients, and the angiotensin converting enzyme inhibitors in heart failure.
----P Journal_Article Review Review__Academic 
----M M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH M_Chronic_Disease_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 11022900
----K E
----T Prospective studies of diagnosis and intervention: the Dutch experience.
----A This prospective multicenter study included 1,205 patients, who were referred for difficult-to-treat hypertension or analysis of possible secondary hypertension. After a standardized selection protocol based on sharply defined drug-resistant hypertension or renal function impairment during angiotensin-converting enzyme inhibition, patients underwent renal scintigraphy and a captopril-renin challenge test. A set of clinical characteristics was also recorded. Sensitivity and specificity of renal scintigraphy for diagnosing renal artery stenosis were 0.72 and 0.90 and of the captopril-renin test 0.77 to 0.91 and 0.69 to 0.75 depending on the criterion used. The clinical characteristics were used to construct a clinical prediction rule for renal artery stenosis, which had a sensitivity of 0.68 and a specificity of 0.87 at a cut-off level of 30% predicted probability. However, with the prediction rule a sensitivity of 0.90 could be reached by performing arteriography only in patients with a predicted probability of stenosis of > or =10%, resulting in a considerable reduction of the number of arteriograms to be made. A diagnostic strategy is advocated starting with drug-resistant hypertension and continuing to renal arteriography only in patients with increased probability of stenosis. Patients with atherosclerotic renal artery stenosis were then randomized to balloon angioplasty (n = 56) versus antihypertensive medication (n = 50). Three months after randomization 22 patients from the medication group underwent balloon angioplasty in second instance. In an intention-to-treat analysis, no difference in blood pressure was found between the groups after 3 months, nor after 12 months of follow-up, although there was a small medication-sparing effect of balloon angioplasty. The lack of a beneficial effect of balloon angioplasty compared with medication could not be attributed to the high stenosis recurrence rate after angioplasty, nor to the fact that the inclusion criterion was set at a stenosis level of > or =50% so that patients with relatively mild stenosis were also included. Renal function after angioplasty was slightly better in the angioplasty group than in the medication group, and improvement of the renal scintigram occurred more often after angioplasty. Apart from the treatment of patients with specific characteristics, the presented therapeutic approach starts with extending the antihypertensive drug therapy to control blood pressure. Only if blood pressure cannot be controlled or if renal function deteriorates, balloon angioplasty (with stent placement) is indicated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Algorithms_MeSH M_Angiography_MeSH M_Angioplasty__Balloon_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_diagnostic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_diagnostic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Captopril_MeSH S_diagnostic_use_MeSH Captopril_diagnostic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Netherlands_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Radioisotope_Renography_MeSH M_Recurrence_MeSH M_Renal_Artery_Obstruction_MeSH S_complications_MeSH Renal_Artery_Obstruction_complications_MeSH S_diagnosis_MeSH Renal_Artery_Obstruction_diagnosis_MeSH S_therapy_MeSH Renal_Artery_Obstruction_therapy_MeSH M_Sensitivity_and_Specificity_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11025624
----K I
----T A double blind controlled study of propranolol and cyproheptadine in migraine prophylaxis.
----A Role of propranolol and cyproheptadine in the prophylaxis of migraine was studied in a controlled double blind trial. Two hundred fifty-nine patients were divided into four groups. Each group was either given a placebo, cyproheptadine, propranolol or a combination of the latter two drugs. The patients were followed for a period of three months. Significant relief in frequency, duration and severity from migranous attacks was seen in all drug treated groups over placebo. Significant correlation in response was seen in frequency, duration and severity in all the groups which received drugs. Statistically more significant relief was seen in cyproheptadine and propranolol treated group as compared to individual drug treated groups. In cyproheptadine and propranolol treated groups, the dropout rate was lower and associated symptoms were better relieved than in other groups. The study shows efficacy of combination of cyproheptadine and propranolol in migraine prophylaxis.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Cyproheptadine_MeSH S_administration_&_dosage_MeSH Cyproheptadine_administration_&_dosage_MeSH S_adverse_effects_MeSH Cyproheptadine_adverse_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Serotonin_Antagonists_MeSH S_administration_&_dosage_MeSH Serotonin_Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Antagonists_adverse_effects_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 11023935
----K E
----T Effects of antihypertensive therapy on glucose and insulin metabolism and on left ventricular mass: A randomized, double-blind, controlled study of 21 obese hypertensives.
----A BACKGROUND: Glucose and insulin levels are associated with left ventricular mass (LVM) in insulin-resistant individuals. Antihypertensive drugs have different effects on glucose and insulin metabolism (GIM) and on LVM. To evaluate whether the effects of antihypertensive therapy on LVM are associated with its effects on GIM, we compared the effects of atenolol and perindopril on these parameters in a group of insulin-resistant, obese hypertensives. METHODS AND RESULTS: A total of 21 obese, nondiabetic hypertensives who were aged 55+/-12 years, had a body mass index of 32.8+/-5.0 kg/m(2), were free of coronary or valvular heart disease, and had normal LV function were randomized to treatment with atenolol (n=11) or perindopril (n=10). Echocardiographic LVM corrected for height (LVM/height) and GIM (3-hour intravenous glucose tolerance test) were measured after 4 to 6 weeks of washout and 6 months of treatment. Baseline characteristics were similar in both groups. Atenolol and perindopril effectively reduced blood pressure (from 149+/-13/98+/-4 to 127+/-8/82+/-6 mm Hg and from 148+/-9/98+/-4 to 129+/-9/82+/-6 mm Hg, respectively, for the atenolol and perindopril groups; P:=0.002). Atenolol significantly worsened GIM parameters, fasting glucose levels (5.3+/-0.9 to 6.0+/-1.5 mmol/L; P:=0.003), fasting insulin levels (121+/-121 to 189+/-228 pmol/L; P:=0.03), and most other relevant metabolic measures (P:<0.05 for all). Perindopril did not affect GIM. Atenolol did not affect LVM/height (119+/-12 to 120+/-17 g/m; P:=0.8), whereas perindopril significantly reduced LVM/height (120+/-13 to 111+/-19 g/m; P:=0.04). CONCLUSIONS: In obese, hypertensive individuals, adequate and similar blood pressure control was achieved with perindopril and atenolol. However, perindopril but not atenolol was associated with a more favorable GIM profile and led to a significant regression of LVM.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_MeSH S_metabolism_MeSH Glucose_metabolism_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_metabolism_MeSH Heart_Ventricles_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Insulin_MeSH S_metabolism_MeSH Insulin_metabolism_MeSH M_Insulin_Resistance_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH S_metabolism_MeSH Obesity_metabolism_MeSH M_Perindopril_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10980208
----K E
----T Usefulness of impaired chronotropic response to exercise as a predictor of mortality, independent of the severity of coronary artery disease.
----A Chronotropic incompetence, or an attenuated heart rate response to exercise, has been shown to be associated with an adverse outcome. It is not known whether chronotropic incompetence predicts all-cause mortality independent of angiographic severity of coronary artery disease (CAD). Study subjects included consecutive patients who underwent first-time, symptom-limited exercise treadmill testing and coronary angiography within 90 days; no patient was taking beta blockers or had a history of heart failure, valve disease, or prior revascularization. Chronotropic response was measured in 2 ways: (1) failure to reach 85% of the age-predicted maximum heart rate, and (2) a low chronotropic index, a measure of exercise heart rate response that accounts for effects of age, physical fitness, and resting heart rate. Angiographic severity of CAD was assessed using the Duke Prognostic Weight Score, with a score > or = 42 considered to be indicative of severe CAD. Among 384 eligible patients, failure to reach 85% of the age-predicted maximum heart rate occurred in 61 (16%) and a low chronotropic index was noted in 133 (35%). Severe CAD was present in 63 (16%). During 6 years of follow-up there were 56 deaths. Mortality was predicted by failure to reach target heart rate (RR 1.85, 95% confidence interval [CI] 1.01 to 3.39, chi-square = 4, p = 0.05), by severe CAD (RR 2.21, 95% CI 1.24 to 3.95, chi-square = 8, p = 0.007), and, most strongly, by a low chronotropic index (RR 2.72, 95% CI 1.60 to 4.61, chi-square = 15, p = 0.0002). In a multivariable model, low chronotropic index remained predictive of death (adjusted RR 2.22, 95% CI 1.29 to 3.82, p = 0.004), whereas severe CAD no longer predicted death (adjusted RR 1.27, 95% CI 0.70 to 2.31, p > 0.4). Thus, chronotropic incompetence is a strong and independent predictor of death, even after accounting for the angiographic severity of CAD.
----P Journal_Article 
----M M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Electrocardiography_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_physiology_MeSH Myocardial_Contraction_physiology_MeSH M_Ohio_MeSH S_epidemiology_MeSH Ohio_epidemiology_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Survival_Rate_MeSH 
****** 11039742
----K 5
----T Comparison of the clinical success rates and quality of life effects of brimonidine tartrate 0.2% and betaxolol 0.25% suspension in patients with open-angle glaucoma and ocular hypertension. Brimonidine Outcomes Study Group II.
----A PURPOSE: To compare the clinical effectiveness and the impact on quality of life of twice-daily brimonidine 0.2% with those of twice-daily betaxolol 0.25% in patients with glaucoma or ocular hypertension. METHODS: A prospective, double-masked, randomized, comparative, multicenter, 4-month "real-life" clinical trial involving 188 patients. Medications were instilled twice daily. Efficacy was determined through measurement of intraocular pressure; safety and tolerability were measured using reports of adverse events, a quality of life survey (Glaucoma Disability Index), heart rate, and blood pressure. Patients with an inadequate response in intraocular pressure after 1 month or those who experienced significant adverse events in the first month were switched to the alternative study arm and remained taking the alternative medication for a total of 4 months or left the study. The main outcome measure was clinical success, as determined by evaluation of the efficacy, safety, and tolerability of drug treatment, and was achieved when the investigator recommended that the patient continue the treatment after completion of the study. RESULTS: As initial therapy, clinical success was achieved in 74% of patients treated with brimonidine, as compared with 57% of patients treated with betaxolol (P = 0.027). The overall mean decrease in intraocular pressure from baseline was 5.9 mm Hg with brimonidine and 3.8 mm Hg with betaxolol. Both treatments were well tolerated, and there were no significant between-group differences in the incidence of adverse events or in the quality of life summary scores. CONCLUSIONS: Twice-daily brimonidine 0.2% and betaxolol 0.25% suspension were safe and effective as first-line therapy for glaucoma and ocular hypertension. In this study, brimonidine showed clinical effectiveness superior to that of betaxolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH P_Quality_of_Life_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Suspensions_MeSH M_Treatment_Outcome_MeSH 
****** 11045900
----K 5
----T Orphan G-protein coupled receptors: novel drug targets for the pharmaceutical industry.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Drug_Industry_MeSH M_GTP-Binding_Proteins_MeSH S_chemistry_MeSH GTP-Binding_Proteins_chemistry_MeSH S_drug_effects_MeSH GTP-Binding_Proteins_drug_effects_MeSH S_genetics_MeSH GTP-Binding_Proteins_genetics_MeSH M_Human_MeSH M_Receptors__Cell_Surface_MeSH S_chemistry_MeSH Receptors__Cell_Surface_chemistry_MeSH S_drug_effects_MeSH Receptors__Cell_Surface_drug_effects_MeSH S_genetics_MeSH Receptors__Cell_Surface_genetics_MeSH M_Research_MeSH 
****** 11045137
----K 1
----T [Addition of beta blockers in chronic heart failure]
----A Chronic heart failure is an increasing cause of hospital admission in the Netherlands and Belgium. Despite numerous medical treatment modalities, the mortality remains high. Recent placebo-controlled randomized studies suggest that the addition of beta-blockers in stabilized, optimally pretreated patients with chronic heart failure using angiotensin converting enzyme (ACE) inhibitors, diuretics and digitalis, is accompanied by an additional absolute decrease in mortality by about 5% and a relative decrease in mortality by about 35%. Also the number hospitalization frequency decreases. Initially, the beneficial effects of beta-blockers on symptoms are only minor or absent. During the initiation period some clinical deterioration may occur which has to be treated accordingly; these patients are, however, difficult to identify. Initiation has to be done using low doses and should be restricted to stabilized, optimally treated patients. Doses should only be increased every 2 to 4 weeks until target doses are reached. These findings must not be extrapolated automatically to all cases of heart failure, since patients in the trials may differ considerably from those encountered in general practice.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Cardiovascular_Agents_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11055467
----K I
----T Results of the STOP-Hypertension-2 trial.
----A The second Swedish Trial in Old patients with Hypertension (STOP-Hypertension-2) was conducted to compare the effects of "newer" antihypertensive therapies (angiotensin converting enzyme [ACE] inhibitors and calcium antagonists) and established therapies (beta-blockers and diuretics) on cardiovascular mortality and morbidity in elderly hypertensive patients. A total of 6614 patients were randomized to receive conventional treatment, ACE inhibitors or calcium antagonists, and followed for a mean of 5 years. The primary endpoint was a combination of fatal stroke, fatal myocardial infarction and other fatal cardiovascular disease; secondary endpoints were a combination of fatal or non-fatal stroke or myocardial infarction, and other cardiovascular mortality. The three treatments produced similar reductions in supine systolic blood pressure. There were no significant differences in the risk of cardiovascular events between patients receiving conventional therapy and those receiving newer therapies. All three treatments were well tolerated. The STOP-Hypertension-2 results thus add to the extensive literature showing the benefits of blood pressure reduction in elderly hypertensive patients. Moreover, they are consistent with current management guidelines which emphasise the importance of the achieved blood pressure reduction in the prevention of cardiovascular events.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 11055468
----K E
----T The outcome of STOP-Hypertension-2 in relation to the 1999 WHO/ISH hypertension guidelines.
----A The 1999 hypertension management guidelines issued by the World Health Organization and the International Society of Hypertension emphasize the importance of blood pressure reduction in the prevention of cardiovascular events. Furthermore, they conclude that the benefits of treatment are due to blood pressure lowering per se, rather than to any specific antihypertensive therapy. The results of the second Swedish Trial in Old Patients with Hypertension (STOP-Hypertension-2) are consistent with these recommendations, since in this trial angiotensin converting enzyme (ACE) inhibitors and calcium antagonists reduced blood pressure to the same extent as conventional therapy with beta-blockers and diuretics in elderly hypertensive patients, and the three treatments produced similar reductions in the risk of cardiovascular events. Furthermore, a first subgroup analysis of cardiovascular mortality showed that the three treatments seemed equally effective in diabetic patients. The STOP-Hypertension-2 data, therefore, are fully consistent with the 1999 hypertension management guidelines, and underline the advantages offered by both older and newer antihypertensive therapies.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Guidelines_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_World_Health_Organization_MeSH 
****** 11057841
----K 5
----T Optimizing beta-blocker use after myocardial infarction.
----A Although beta-adrenergic blockers can significantly reduce mortality after a myocardial infarction, these agents are prescribed to only a minority of patients. Underutilization of beta blockers may be attributed, in part, to fear of adverse effects, especially in the elderly and in patients with concomitant disorders such as diabetes or heart failure. However, studies have shown that such patients are precisely the ones who derive the greatest benefit from beta blockade. Advancing age or the presence of potentially complicating disease states is usually not a justification for withholding beta-blocker therapy. With use of cardioselective agents and through careful dosing and monitoring, the benefits of beta blockers after myocardial infarction far outweigh the potential risks in most patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Drug_Utilization_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH M_Lung_Diseases_MeSH S_complications_MeSH Lung_Diseases_complications_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Patient_Education_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Teaching_Materials_MeSH M_United_States_MeSH 
****** 11054621
----K E
----T Carvedilol improves endothelium-dependent dilatation in patients with coronary artery disease.
----A OBJECTIVE: Flow-mediated, endothelium-dependent dilatation (FMD) of the coronary and peripheral circulation is impaired by increased oxidative stress in patients with coronary artery disease (CAD). Carvedilol is a novel beta-blocker that also shows an antioxidant effect in vitro. However, the effect of carvedilol on endothelial dysfunction associated with established coronary atherosclerosis has not been examined in the clinical setting. METHODS: We studied 29 patients with CAD, including 17 with recent myocardial infarction and 12 with stable effort angina pectoris. Nineteen patients received carvedilol (10 with infarction and 9 with angina), and 10 were treated with placebo (7 with infarction and 3 with angina). We also studied 13 age- and sex-matched control subjects. Brachial FMD during reactive hyperemia and nitroglycerin-induced, endothelium-independent dilatation were assessed by high-resolution ultrasound. RESULTS: FMD was smaller in patients with CAD compared with controls, although nitroglycerin-induced dilatation was similar. Carvedilol significantly improved FMD after long-term treatment (5. 1% +/- 0.4% at baseline to 7.8% +/- 0.3% after 4 months; P <.01) but not after short-term treatment (5.1% +/- 0.4% at baseline to 5.0% +/- 0.7% after 2 hours). Placebo therapy had no effect on endothelial dysfunction. Neither carvedilol nor placebo had an effect on nitroglycerin-induced dilatation after short- and long-term treatment. Long-term carvedilol therapy also significantly decreased the plasma level of thiobarbituric acid-reactive substances compared with placebo (carvedilol, 5.8 +/- 0.4 nmol/mL to 4.6 +/- 0.3 nmol/mL, P <.01; placebo, 5.9 +/- 0.4 nmol/mL to 5.8 +/- 0.4 nmol/mL, P = not significant). CONCLUSION: These findings suggest that the improvement of endothelial function by carvedilol may be caused by its antioxidant activity.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antioxidants_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11054501
----K E
----T Hemostatic abnormalities in patients with congestive heart failure: diagnostic significance and clinical challenge.
----A Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. However, this disease continues to cause one of the highest morbidities and mortalities in the Western world. The pathophysiology of heart failure is complex and much of our understanding revolves strictly around the neurohormonal mechanisms involved. Various pharmacologic interventions have significantly improved morbidity and include ACE inhibitors, beta-blockers, diuretics, and inotropic agents. Yet, no consensus has been reached regarding the use of anticoagulants or antiplatelet agents. It has been suggested that CHF is associated with altered hemostasis, but whether this prothrombotic state contributes to the pathogenesis and progression of the disease is unknown. The purpose of this review article is to discuss our current knowledge of platelet activation, thrombin generation, fibrinolysis, and endothelial dysfunction in CHF patients, and the potential role of anticoagulants and/or antiplatelet agents in preventing these hemostatic abnormalities.
----P Journal_Article Review Review__Tutorial 
----M M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Biological_Markers_MeSH M_Clinical_Trials_MeSH M_Endothelins_MeSH S_blood_MeSH Endothelins_blood_MeSH S_physiology_MeSH Endothelins_physiology_MeSH M_Fibrinolysis_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH P_Hemostasis_MeSH M_Human_MeSH M_Platelet_Activation_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Thrombin_MeSH S_physiology_MeSH Thrombin_physiology_MeSH M_Thromboembolism_MeSH S_prevention_&_control_MeSH Thromboembolism_prevention_&_control_MeSH M_Warfarin_MeSH S_therapeutic_use_MeSH Warfarin_therapeutic_use_MeSH 
****** 11056773
----K E
----T Prophylactic esmolol infusion for the control of cardiovascular responses to extubation after intracranial surgery.
----A INTRODUCTION: Emergence from general anaesthesia and extubation are often accompanied by significant surges in heart rate and blood pressure. To document these changes and the efficacy of low-dose beta-blocker infusions in ameliorating these rises, we undertook a descriptive dose-ranging study comparing the use of esmolol to placebo in patients emerging from neuro-anaesthesia. MATERIALS AND METHODS: Thirty-six patients undergoing intracranial surgery were randomised to receive saline, esmolol 100 micrograms/kg/min or 200 micrograms/kg/min infusions. The number of patients developing severe hypertension or tachycardia in each group was compared using Fisher's exact test. RESULTS: Systolic blood pressure (SBP) and heart rate (HR) increased in all 3 groups during emergence and peaked at extubation. The proportion of patients with severe tachycardia or hypertension was reduced from 92% in the placebo group to 40% (P = 0.02) and 8% (P = 0.001) in the low and intermediate dose esmolol groups, respectively. Results were better in the intermediate dose group but the difference was not statistically significant. Two patients from the esmolol infusion groups required supplemental medication for bradycardia. CONCLUSION: Severe hypertension or tachycardia occurs in 92% of patients during extubation following neuro-anaesthesia and warrants the consideration of routine prophylaxis. Prophylactic esmolol infusion for the control of haemodynamic disturbances during extubation is feasible and safe. A modest level of obtundation is evident at 100 micrograms/kg/min but a rate of 200 micrograms/kg/min may prove to be more effective.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Brain_Diseases_MeSH S_surgery_MeSH Brain_Diseases_surgery_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Monitoring_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Infusions__Intravenous_MeSH M_Injections__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Tachycardia_MeSH S_drug_therapy_MeSH Tachycardia_drug_therapy_MeSH S_etiology_MeSH Tachycardia_etiology_MeSH S_physiopathology_MeSH Tachycardia_physiopathology_MeSH M_Ventilator_Weaning_MeSH S_adverse_effects_MeSH Ventilator_Weaning_adverse_effects_MeSH S_instrumentation_MeSH Ventilator_Weaning_instrumentation_MeSH 
****** 11059637
----K E
----T Exploring new treatment strategies in heart failure.
----A Heart failure remains a major and increasing cause of mortality and morbidity, even when the best available treatments are used. One of its key causes is neuroendocrine activation via the sympathetic nervous system and the renin-angiotensin system (RAS). Neuroendocrine blockers of the sympathetic nervous system (beta-blockers) and of the RAS (angiotensin-converting enzyme [ACE] inhibitors and angiotensin II type 1 [AT1] receptor blockers) therefore have an important potential therapeutic role in heart failure. The promising results from clinical trials with beta-blockers suggest that these drugs will become an established part of the future management of patients with mild to moderate symptomatic heart failure. Blockade of the RAS with ACE inhibitors has also been shown to be effective in reducing the risk of morbidity and mortality in patients with heart failure. Blockade of the AT1-receptor, with agents such as candesartan, produces more specific and, theoretically, more complete blockade of the major negative cardiovascular effects of angiotensin II than is possible using ACE inhibitors, whilst maintaining placebo-like tolerability. Furthermore, AT1-receptor blockade leads to increased stimulation of the angiotensin II type 2 (AT2) receptor, which, according to experimental data, may have favourable cardiovascular effects. Following encouraging results from two pilot studies, a major new international study programme - CHARM (Candesartan in Heart failure - Assessment of Reduction in Mortality and morbidity) - has been initiated to define the clinical benefits of candesartan cilexetil in a wide variety of patients with symptomatic heart failure. CHARM is the first study to accept all relevant heart failure patients who may benefit from RAS blockade, irrespective of their left ventricular function or tolerance of ACE inhibitors. The 6500 patients to be recruited will be divided among three integrated outcome studies. Two of these studies will examine the effect of candesartan cilexetil versus placebo in patients with an ejection fraction of 40% or less who are tolerant or intolerant of ACE inhibitors. The third study arm will examine the benefits of candesartan cilexetil in a previously seldom studied group: those with symptomatic heart failure, but with preserved left-ventricular systolic function. Recruitment of patients into the study has started.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 11059968
----K E
----T Gender-related differences in modulation of heart rate in patients with congestive heart failure.
----A INTRODUCTION: The prognosis of women with congestive heart failure (CHF) is better than that for men, but the mechanisms underlying the female survival advantage are not well understood. CHF is characterized by profound abnormalities in cardiac autonomic control that contribute to progressive circulatory failure and influence survival. METHODS AND RESULTS: Time- and frequency-domain heart rate variability (HRV) indexes were obtained from 24-hour Holter recordings and compared to assess the role of gender in 131 men and 68 women with CHF (mean age 60 +/- 13.6 years, range 21 to 87; New York Heart Association Functional Class III [66%] and IV [34%]). Gender-related differences in HRV were observed only in the subset of patients with nonischemic heart failure (55 men and 39 women). Among the time-domain indexes, the SD of the RR intervals (76 +/- 5.3 msec vs 55.3 +/- 3.2 msec, P < 0.0001) and indexes denoting parasympathetic modulation, the percentage of RR intervals with >50 msec variation (4.0% +/- 1.0% vs 6.5% +/- 1.3%, P = 0.02), and the square root of mean squared differences of successive RR intervals (19.1 +/- 3.3 vs 28.4 +/- 3.8, P = 0.004) were higher in women. Among the frequency-domain indexes, the total power (7.5 +/- 0.13 ln-msec2 vs 8.3 +/- 0.14 ln-msec2, P = 0.0002), the ultralow-frequency power (7.2 +/- 0.11 ln-msec2 vs 8.0 +/- 0.14 In-msec2, P < 0.0001), the low-frequency power (3.8 +/- 0.25 ln-msec2 vs 4.8 +/- 0.28 ln-msec2, P = 0.006), and the high-frequency power (3.8 +/- 0.24 ln-msec2, vs 4.6 +/- 0.26 ln-msec2, P = 0.003) were greater in women than in men. CONCLUSION: Women with nonischemic CHF have an attenuated sympathetic activation and parasympathetic withdrawal compared with men. Gender-based differences in autonomic responses in the setting of CHF may be related to the female survival advantage.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Autonomic_Nervous_System_MeSH S_physiology_MeSH Autonomic_Nervous_System_physiology_MeSH M_Female_MeSH P_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sex_Characteristics_MeSH 
****** 11058925
----K 1
----T Response of blood pressure to maximum exercise in hypertensive patients under different therapeutic programs.
----A OBJECTIVE: To evaluate the behavior of blood pressure during exercise in patients with hypertension controlled by frontline antihypertension drugs. METHODS: From 979ergometric tests we retrospectively selected 49 hypertensive patients (19 males). The age was 53+/-12 years old and normal range rest arterial pressure (< or = 140/90 mmHg) all on pharmacological monotherapy. There were 12 on beta blockers; 14 on calcium antagonists, 13 on diuretics and 10 on angiotensin converting enzyme inhibitor. Abnormal exercise behavior of blood pressure was diagnosed if anyone of the following criteria was detected: peak systolic pressure above 220 mmHg, raising of systolic pressure > or = 10 mmHg/MET; or increase of diastolic pressure greater than 15 mmHg. RESULTS: Physiologic response of arterial blood pressure occurred in 50% of patients on beta blockers, the best one (p<0.05), in 36% and 31% on calcium antagonists and on diuretics, respectively, and in 20% on angiotensin converting enzyme inhibitor, the later the least one (p<0.05). CONCLUSION: Beta-blockers were more effective than calcium antagonists, diuretics and angiotensin-converting enzyme inhibitors in controlling blood pressure during exercise, and angiotensin converting enzyme inhibitors the least effective drugs.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH 
****** 11061055
----K E
----T Monotherapy with amlodipine or atenolol versus their combination in stable angina pectoris.
----A BACKGROUND: The basic cause of angina pectoris is imbalance between the metabolic needs of the myocardium and the capacity of the coronary circulation to deliver sufficient oxygenated blood to satisfy these needs. HYPOTHESIS: The study was undertaken to evaluate whether the effect of combined amlodipine and atenolol therapy on patients with stable angina pectoris and with ST-depression during exercise testing and 48-h ambulatory electrocardiographic monitoring is superior to that of either agent given alone. METHODS: Patients with stable angina pectoris and ST depression during exercise and ambulatory monitoring were randomized to receive amlodipine (n = 116) or atenolol (n = 116), or both (n = 119). All patients were also treated with short- and long-acting nitrates. The design was a double-blind, randomized, triple-arm parallel group study with 10 weeks of administration of the test medication. RESULTS: In terms of time to onset of ST depression > 1 mm, time to onset of angina, total exercise time, maximum achieved workload, and peak intensity of angina, amlodipine and atenolol alone were as effective as their combination. During ambulatory monitoring, atenolol was more effective than amlodipine regarding total time and number of ST-depression episodes, and as effective as the combined drugs. CONCLUSION: For individual patients with stable angina pectoris, combination of a beta blocker with a calcium antagonist is not necessarily more effective than either drug given alone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography__Ambulatory_statistics_&_numerical_data_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH 
****** 11060685
----K 5
----T beta-blockers in heart failure: recently completed and ongoing clinical trials.
----A beta-Blockers have emerged as an important therapy in patients with symptomatic left ventricular systolic dysfunction. Early studies demonstrated that beta-blocker therapy improved left ventricular function, reduced neurohumoral activity and reduced heart failure symptoms in these patients. While none of these small studies demonstrated a significant benefit in terms of overall survival, several meta-analyses suggested that beta-blocker therapy could, in fact, reduce mortality in patients with left ventricular systolic dysfunction and mild to moderate heart failure symptoms (New York Heart Association class II or III). Three large, recently completed, trials have confirmed the benefit of beta-blockade in these patients. This report reviews some of the initial clinical studies of beta-blockade in heart failure, examines the findings of the three large multicentre trials and other relevant research. Finally, ongoing trials designed to assess the relative efficacy of different beta-blockers and evaluate the utility of beta-blockade in specific subsets of patients with heart failure are discussed.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 11071026
----K 5
----T Efficacy and side effects of latanoprost monotherapy compared to adding dorzolamide to timolol in patients with glaucoma and ocular hypertension--a three-month randomised study. Spanish Latanoprost Study Group.
----A PURPOSE: To compare the efficacy and safety of latanoprost monotherapy or dorzolamide and timolol in glaucoma patients inadequately controlled on adrenergic beta-receptor antagonist therapy. METHODS: A total of 164 patients with primary open-angle glaucoma, capsular glaucoma or ocular hypertension were included in a three-month, open-label, randomised multicentre study. Patients with open-angle glaucoma were required to have IOP at least 22 mmHg and patients with ocular hypertension were required to have IOP at least 27 mmHg, on treatment with one or two ocular hypotensive drugs of which at least one had to be a beta-blocker. All patients were treated with timolol, 5 mg/ml twice daily, for a 2-4 week run-in period. They were then randomised to latanoprost, 50 microg/ml once daily, or timolol 5 mg/ml plus dorzolamide, 20 mg/ml twice daily. The difference in mean diurnal IOP change from baseline to month 3 was compared in the two groups. RESULTS: When patients were switched to latanoprost, mean diurnal IOP was reduced by 5.2 mmHg (23%) compared to 4.0 mmHg (17%) in the group in which dorzolamide was added to timolol. The difference of 1.2 mmHg was statistically significant (p = 0.005). The majority of adverse events during both treatments were judged as mild. CONCLUSIONS: The results suggest that a switch to latanoprost monotherapy is an alternative to combined treatment with timolol and dorzolamide in patients inadequately controlled on a topical adrenergic beta-receptor antagonist alone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_administration_&_dosage_MeSH Carbonic_Anhydrase_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11069435
----K 5
----T Drugs used in secondary prevention after myocardial infarction: case presentation.
----A 
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Clinical_Trials_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH 
****** 11070565
----K E
----T Combination therapy with beta-adrenergic blockade and amlodipine as second line treatment in essential hypertension.
----A In hypertension both beta-blockers and calcium antagonists are drugs with proved efficacy. Because only half the patients respond to a single drug, even at full dosage, a second hypotensive agent is frequently required to obtain adequate blood pressure control. The combination of a dihydropyridine calcium antagonist and a beta-blocker can be justified by their different mechanisms of action. A randomised double blind parallel group study versus placebo was performed, in order to assess the efficacy of atenolol combined with amlodipine in the treatment of stage I-II essential hypertension not controlled by atenolol alone. Twenty-four-hour arterial blood pressure monitoring showed that amlodipine added to atenolol produced a statistically significant reduction of blood pressure values compared with placebo in patients whose blood pressure was not controlled by atenolol alone. Blood pressure circadian rhythm was unchanged. The reduction of side-effects, obtained by adding a dihydropyridine derivate to a beta-blocker, confirms the effectiveness of this combination.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 11078300
----K E
----T Ten-year outcome after coronary angioplasty in patients with single-vessel coronary artery disease and comparison with the results of the Coronary Artery Surgery Study (CASS).
----A The 10-year results of randomized trials comparing percutaneous transluminal coronary angioplasty (PTCA) in patients with single-vessel coronary artery disease (CAD) with coronary artery bypass grafting (CABG) and medical treatment are not available yet. The aim of this evaluation was to compare our 10-year follow-up results after PTCA in patients with single-vessel CAD with the 10-year follow-up results after CABG and medical treatment in the Coronary Artery Surgery Study (CASS) trial. We evaluated the clinical outcome of 509 patients with single-vessel CAD 10 years after coronary angioplasty. The data were compared with the results of 214 patients with single-vessel CAD after CABG or medical treatment from the CASS trial. End points were defined as death and myocardial infarction. Statistical evaluation was performed by life-table analysis and 2-sided Fisher's exact test. The rate of survival was 86% 10 years after PTCA compared with 85% after CABG and 82% after medical treatment in patients from the CASS trial (p = NS). Survival free from myocardial infarction was 77% after coronary angioplasty, 70% after CABG, and 72% after medical treatment (p = NS). Thus, in patients with single-vessel CAD, infarct-free survival 10 years after coronary angioplasty compared favorably with the results after bypass surgery or medical treatment from the CASS trial.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_mortality_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_mortality_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH S_mortality_MeSH Coronary_Artery_Bypass_mortality_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Disease-Free_Survival_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Germany_MeSH S_epidemiology_MeSH Germany_epidemiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Questionnaires_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11079666
----K E
----T Nonselective beta-adrenergic blocking agent, carvedilol, improves arterial baroflex gain and heart rate variability in patients with stable chronic heart failure.
----A OBJECTIVES: The purpose of this study was to investigate in a case-controlled study whether carvedilol increased baroreflex sensitivity and heart rate variability (HRV). BACKGROUND: In chronic heart failure (CHF), beta-adrenergic blockade improves symptoms and ventricular function and may favorably affect prognosis. Although beta-blockade therapy is supposed to decrease myocardial adrenergic activity, data on restoration of autonomic balance to the heart and, particularly, on vagal reflexes are limited. METHODS: Nineteen consecutive patients with moderate, stable CHF (age 54 +/- 7 years, New York Heart Association [NYHA] class II to III, left ventricular ejection fraction [LVEF] 24 +/- 6%), treated with optimized conventional medical therapy, received carvedilol treatment. Controls with CHF were selected from our database on the basis of the following matching criteria: age +/- 3 years, same NYHA class, LVEF +/- 3%, pulmonary wedge pressure +/- 3 mm Hg, peak volume of oxygen +/- 3 ml/kg/min, same therapy. All patients underwent analysis of baroreflex sensitivity (phenylephrine method) and of HRV (24-h Holter recording) at baseline and after six months. RESULTS: Beta-blockade therapy was associated with a significant improvement in symptoms (NYHA class 2.1 +/- 0.4 vs. 1.8 +/- 0.5, p < 0.01), systolic and diastolic function (LVEF 23 +/- 7 vs. 28 +/- 9%, p < 0.01; pulmonary wedge pressure 17 +/- 8 vs. 14 +/- 7 mm Hg, p < 0.05) and mitral regurgitation area (7.0 +/- 5.1 vs. 3.6 +/- 3.0 cm2, p < 0.01). No significant differences were observed in either clinical or hemodynamic indexes in control patients. Phenylephrine method increased significantly after carvedilol (from 3.7 +/- 3.4 to 7.1 +/- 4.9 ms/mm Hg, p < 0.01) as well as RR interval (from 791 +/- 113 to 894 +/- 110 ms, p < 0.001), 24-h standard deviation of normal RR interval and root mean square of successive differences (from 56 +/- 17 to 80 +/- 28 ms and from 12 +/- 7 to 18 +/- 9 ms, all p < 0.05), while all parameters remained unmodified in controls. During a mean follow-up of 19 +/- 8 months a reduced number of cardiac events (death plus heart transplantation, 58% vs. 31%) occurred in those patients receiving beta-blockade. CONCLUSIONS: Besides the well-known effects on ventricular function, treatment with carvedilol in CHF restores both autonomic balance and the ability to increase reflex vagal activity. This protective mechanism may contribute to the beneficial effect of beta-blockade treatment on prognosis in CHF.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Chronic_Disease_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11081782
----K I
----T Comparison of antihypertensive treatments in preventing cardiovascular events in elderly diabetic patients: results from the Swedish Trial in Old Patients with Hypertension-2. STOP Hypertension-2 Study Group.
----A BACKGROUND: The benefits of treating hypertension in elderly diabetic patients, in terms of achieving reductions in cardiovascular morbidity and mortality, have been documented in several recent prospective trials. There has, however, been some controversy regarding the effect of different antihypertensive drugs on the frequency of myocardial infarction in this group of patients. DESIGN: STOP Hypertension-2 was a prospective, randomized, open trial with blinded endpoint evaluation. METHODS: We studied 6614 elderly patients aged 70-84 years; 719 of them had diabetes mellitus at the start of the study (mean age 75.8 years). Patients were randomly assigned to one of three treatment strategies: conventional antihypertensive drugs (diuretics or beta-blockers), calcium antagonists, or angiotensin converting enzyme (ACE) inhibitors. RESULTS: Reduction in blood pressure was similar in the three treatment groups of diabetics. The prevention of cardiovascular mortality was also similar; the frequency of this primary endpoint did not differ significantly between the three groups. There were, however, significantly fewer (P = 0.025) myocardial infarctions during ACE inhibitor treatment (n = 17) than during calcium antagonist treatment (n = 32; relative risk 0.51, 95% confidence interval 0.28-0.92); but a (non-significant) tendency to more strokes during ACE inhibitor treatment (n = 34 compared with n = 29; relative risk 1.16, 95% confidence interval 0.71-1.91). CONCLUSION: Treatment of hypertensive diabetic patients with conventional antihypertensive drugs (diuretics, beta-blockers, or both) seemed to be as effective as treatment with newer drugs such as calcium antagonists or ACE inhibitors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Sweden_MeSH 
****** 11076821
----K E
----T Sex differences in management and outcome after acute myocardial infarction in the 1990s: A prospective observational community-based study. Israeli Thrombolytic Survey Group.
----A BACKGROUND: Previous studies have suggested that women with acute myocardial infarction (AMI) are less aggressively managed than are men. The aim of this study was to assess sex differences in medical and invasive coronary procedures (angiography, PTCA, and CABG) in AMI patients admitted to cardiac care units (CCUs) in Israel in the mid 1990s and their association with early and 1-year prognosis. METHODS AND RESULTS: We studied 2867 consecutive AMI patients (2125 men, 74%) hospitalized in all 25 CCUs in Israel from 3 prospective nationwide surveys conducted in 1992, 1994, and 1996. Women were, on average, older than men (69 versus 61 years, P:<0.0001) and had a higher prevalence of hypertension, diabetes, Killip class >/=II on admission, and in-hospital complications. Women received aspirin and beta-blockers less often than did men, but these differences were not significant after age adjustment. The unadjusted rates of thrombolysis, angiography, and PTCA/CABG use were lower in women than in men but not after covariate adjustment: 42% versus 48% (adjusted odds ratio [OR] 0.92, 95% CI 0.77 to 1.11), 23% versus 31% (OR 0.88, 95% CI 0.70 to 1.09), and 15% versus 19% (OR 0.93, 95% CI 0.72 to 1.19), respectively. The 30-day mortality was higher in women than in men (17.6% versus 9.6%, respectively; OR 1.39, 95% CI 1.06 to 1.82), but the 30-day to 1-year mortality rate was not (9.1% versus 5.6%, respectively; hazard ratio 1.18, 95% CI 0.84 to 1.66). CONCLUSIONS: This prospective nationwide observational community-based study of consecutive AMI patients hospitalized in the CCUs in the mid 1990s indicates that women fare significantly worse than do men at 30 days but not thereafter at 1-year. The difference in 30-day outcome was not influenced by the use of different therapeutic modalities, including thrombolysis and invasive coronary procedures, but was rather due to the older age and greater comorbidity of women; these findings seem also to explain the less frequent use of invasive procedures in women.
----P Journal_Article 
----M M_Age_Distribution_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angiography_MeSH S_utilization_MeSH Angiography_utilization_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_utilization_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_utilization_MeSH M_Comorbidity_MeSH M_Coronary_Artery_Bypass_MeSH S_utilization_MeSH Coronary_Artery_Bypass_utilization_MeSH M_Diabetes_Mellitus_MeSH S_diagnosis_MeSH Diabetes_Mellitus_diagnosis_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH M_Female_MeSH M_Health_Surveys_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Israel_MeSH S_epidemiology_MeSH Israel_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Odds_Ratio_MeSH M_Outcome_Assessment_(Health_Care)_MeSH S_statistics_&_numerical_data_MeSH Outcome_Assessment_(Health_Care)_statistics_&_numerical_data_MeSH M_Prevalence_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Sex_Distribution_MeSH M_Sex_Factors_MeSH M_Thrombolytic_Therapy_MeSH S_utilization_MeSH Thrombolytic_Therapy_utilization_MeSH P_Women's_Health_MeSH 
****** 11082141
----K E
----T Baseline characteristics in relation to electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan intervention for endpoint reduction (LIFE) in hypertension study. The Life Study Investigators.
----A The Losartan Intervention For Endpoint (LIFE) reduction in hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of atenolol on the reduction of cardiovascular morbidity and mortality. A total of 9194 patients with hypertension and ECG left ventricular hypertrophy (LVH) by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria were enrolled in the study, with baseline clinical and ECG data available in 8785 patients (54% women; mean age, 67+/-7 years). ECG LVH by Cornell voltage-duration product criteria was present in 5791 patients (65.9%) and by Sokolow-Lyon voltage in 2025 patients (23.1%). Compared with patients without ECG LVH by Cornell voltage-duration product criteria, patients with ECG LVH by this method were older; more obese; more likely to be female, white, and to have never smoked; more likely to be diabetic and have angina; and had slightly higher systolic, diastolic, and pulse blood pressures. In contrast, patients with ECG LVH by Sokolow-Lyon criteria were slightly younger; less obese; more likely to be male, black, and current smokers; less likely to have diabetes; more likely to have angina and a history of cerebrovascular disease; and had higher systolic and pulse blood pressure but slightly lower diastolic blood pressure than patients without ECG LVH by this method. By use of multivariate logistic regression analyses, presence of ECG LVH by Cornell voltage-duration product criteria was predominantly associated with higher body mass index, increased age, and female gender, whereas presence of ECG LVH by Sokolow-Lyon voltage criteria was predominantly related to lower body mass index, male gender, and black race. Thus, hypertensive patients who meet Cornell product and Sokolow-Lyon voltage criteria are associated with different, but potentially equally adverse, risk factor profiles.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_diagnosis_MeSH Hypertrophy__Left_Ventricular_diagnosis_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11082143
----K E
----T Hypertension and its treatment in postmenopausal women: baseline data from the Women's Health Initiative.
----A Little is known about the patterns of treatment and adequacy of blood pressure control in older women. The Women's Health Initiative, a 40-center national study of risk factors and prevention of heart disease, breast and colorectal cancer, and osteoporosis in postmenopausal women, provides a unique opportunity to examine these issues in the largest, multiethnic, best-characterized such cohort. Baseline data from the initial 98 705 women, aged 50 to 79 years, enrolled were analyzed to relate prevalence, treatment, and control of hypertension to demographic, clinical, and risk-factor covariates, and logistic regression analyses were performed to estimate odds ratios after adjusting for multiple potential confounders. Overall, 37.8% of the women had hypertension, which is defined as systolic blood pressure >/=140 mm Hg and/or diastolic blood pressure >/=90 mm Hg or being on medication for high blood pressure; 64.3% were treated with drugs, and blood pressure was controlled in only 36.1% of the hypertensive women, with lower rates of control in the oldest group. After adjustment for multiple covariates, current hormone users had higher prevalence than did nonusers (odds ratio 1.25). Hypertensive women had more comorbid conditions than did nonhypertensive women, and women with comorbidities were more likely to be treated pharmacologically. Diuretics were used by 44.3% of hypertensives either as monotherapy or in combination with other drug classes. As monotherapy, calcium channel blockers were used in 16%, angiotensin-converting enzyme inhibitors in 14%, beta-blockers in 9%, and diuretics in 14% of the hypertensive women. Diuretics as monotherapy were associated with better blood pressure control than any of the other drug classes as monotherapy. In conclusion, hypertension in older women is not being treated aggressively enough because a large proportion, especially those most at risk for stroke and heart disease by virtue of age, does not have sufficient blood pressure control.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comorbidity_MeSH M_Estrogen_Replacement_Therapy_MeSH S_statistics_&_numerical_data_MeSH Estrogen_Replacement_Therapy_statistics_&_numerical_data_MeSH M_Ethnic_Groups_MeSH S_statistics_&_numerical_data_MeSH Ethnic_Groups_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH P_Postmenopause_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11085197
----K E
----T Role of growth hormone in chronic heart failure. Therapeutic implications.
----A Congestive heart failure is a multiple aetiology, high prevalence, poor prognosis cardiovascular disorder. Medical treatment of dilated cardiomyopathy is aimed at alleviating the symptoms of heart failure. Diuretics, ACE inhibitors and very recently, beta-blockers have been shown to have favourable effects on symptoms, exercise capacity and mortality. Growth hormone (GH) and insulin-like growth factor (IGF)-1 are involved in several physiological processes such as the control of muscle mass and function, body composition and regulation of nutrient metabolism. The roles of GH and IGF-1 as modulators of myocardial structure and function are well established. Receptors for both GH and IGF-1 are expressed by cardiac myocytes; therefore, GH may act directly on the heart or via the induction of local or systemic IGF-1, whereas IGF-1 may act by endocrine, paracrine or autocrine mechanisms. Patients with acromegaly have an increased propensity to develop ventricular hypertrophy and cardiovascular diseases and, in addition, an impaired cardiac efficiency is observed in patients with GH deficiency. Animal models of pressure and volume overload have demonstrated up-regulation of cardiac IGF-1 production and expression of GH and IGF-1 receptors, implying that the local regulation of these factors is influenced by haemodynamic changes. Moreover, experimental studies suggest that GH and IGF-1 have stimulatory effects on myocardial contractility, possibly mediated by changes in intracellular calcium handling. Heart failure is caused by ventricular dilatation with abnormal wall thickening, which leads to impaired cardiac performance; therefore, based on the evidence available for GH we would expect beneficial effects from the use of GH in these patients. Several papers highlight the positive influence of GH in the regulation of heart development and performance. In patients with GH deficiency, GH administration dramatically improves cardiac function. In small nonblind studies, both short and long term GH treatment have demonstrated beneficial effects in patients with heart failure secondary to ischaemic or idiophatic cardiomyopathy. Recently, two randomised, placebo-controlled studies, did not show significant GH-mediated improvement in cardiac performance in patients with dilated cardiomyopathy, despite significant increases in IGF-1. Acquired GH resistance, might be an important feature of severe heart failure and explain the different responses to GH therapy seen in different patients. Whether GH treatment will finally find a place, and with which modalities, in the treatment of heart failure remains to be established.
----P Journal_Article Review Review__Tutorial 
----M M_Acromegaly_MeSH S_etiology_MeSH Acromegaly_etiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH M_Human_MeSH P_Human_Growth_Hormone_MeSH S_deficiency_MeSH Human_Growth_Hormone_deficiency_MeSH S_metabolism_MeSH Human_Growth_Hormone_metabolism_MeSH S_physiology_MeSH Human_Growth_Hormone_physiology_MeSH S_secretion_MeSH Human_Growth_Hormone_secretion_MeSH S_therapeutic_use_MeSH Human_Growth_Hormone_therapeutic_use_MeSH M_Insulin-Like_Growth_Factor_I_MeSH S_biosynthesis_MeSH Insulin-Like_Growth_Factor_I_biosynthesis_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11085202
----K E
----T Nicorandil. An updated review of its use in ischaemic heart disease with emphasis on its cardioprotective effects.
----A Nicorandil is a drug with both nitrate-like and ATP-sensitive potassium-channel (K+ ATP) activating properties. By virtue of this dual mechanism of action, the drug acts as a balanced coronary and peripheral vasodilator and reduces both preload and afterload. The K+ ATP channel has been shown to be involved in the phenomenon of myocardial preconditioning, and studies in animal models of ischaemia-reperfusion-induced myocardial stunning or infarction indicate that nicorandil has cardio-protective effects. Studies in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) have shown that the administration of nicorandil reduces ST-segment elevation during ischaemia. Nicorandil significantly improved the results of exercise tolerance tests versus baseline in patients with stable effort angina pectoris in early noncomparative trials. The drug also improved the results of exercise tolerance tests relative to placebo in early randomised, double-blind, placebo-controlled trials. In randomised, double-blind comparative studies in patients with angina pectoris, nicorandil has demonstrated equivalent efficacy, as measured by exercise tolerance testing, to isosorbide di- and mononitrate, metoprolol, propranolol, atenolol, diltiazem, amlodipine and nifedipine. The effects of nicorandil on various aspects of myocardial recovery from ischaemic damage caused by acute myocardial infarction have been investigated in the short term. Regional left ventricular (LV) wall motion, a marker of myocardial function, was significantly improved in nicorandil recipients relative to control. The main adverse event associated with nicorandil as treatment for angina pectoris is headache. This can be minimised by commencing nicorandil at a low dose in patients prone to headache. There have been infrequent case reports of mouth ulcers in patients receiving nicorandil; causality has not been conclusively established, but product prescribing information indicates that an alternative treatment should be considered if persistent aphthous or severe mouth ulceration occurs. Thus, nicorandil remains a useful background therapy for patients with angina pectoris. The drug has also demonstrated potential cardioprotective effects when used as part of an intervention strategy directly after acute myocardial infarction in high-risk patients. Further large scale longer term studies of nicorandil in this latter indication are awaited with interest.
----P Journal_Article Review Review__Tutorial 
----M M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Animals_MeSH M_Clinical_Trials_MeSH M_Female_MeSH M_Half-Life_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Intestinal_Absorption_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nicorandil_MeSH S_adverse_effects_MeSH Nicorandil_adverse_effects_MeSH S_metabolism_MeSH Nicorandil_metabolism_MeSH S_pharmacokinetics_MeSH Nicorandil_pharmacokinetics_MeSH S_therapeutic_use_MeSH Nicorandil_therapeutic_use_MeSH M_Potassium_Channels_MeSH S_drug_effects_MeSH Potassium_Channels_drug_effects_MeSH M_Tissue_Distribution_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_metabolism_MeSH Vasodilator_Agents_metabolism_MeSH S_pharmacokinetics_MeSH Vasodilator_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11083735
----K E
----T Early changes in longitudinal performance predict future improvement in global left ventricular function during long term beta adrenergic blockade.
----A OBJECTIVE: Contraction of longitudinal and subendocardial myocardial muscle fibres is reflected in descent of the atrioventricular (AV) plane. The aim was therefore to determine whether beta blocker treatment with prolongation of diastole might result in improved function as reflected by AV plane movements in patients with chronic heart failure. DESIGN: Double blind, randomised, placebo controlled and open intervention study. SETTING: University hospital. PATIENTS: Patients with congestive heart failure: placebo controlled (n = 26) and an open protocol (n = 15). INTERVENTIONS: 12 months of metoprolol treatment. MAIN OUTCOME MEASURES: Short axis and long axis echocardiography, invasive haemodynamics, radionuclide angiography. RESULTS: Recovery of systolic and diastolic function during metoprolol treatment was reflected by early changes in mean (SD) AV plane amplitude, from 5.3 (2.0)% to 7.1 (3.2)% and 7.8 (3. 1)% (at 3 and 12 months, respectively; p < 0.05). In a multivariate analysis, only the change in AV plane amplitude by three months was independently associated with improvement in pulmonary capillary wedge pressure by six months (r = 0.80, p = 0.017). Change in AV plane amplitude by three months was also a better predictor of improvement in ejection fraction by 12 months (r = 0.78, p < 0.001) than changes in radionuclide ejection fraction by three months (r = 0.34, p = 0.049). CONCLUSIONS: Improvement in longitudinal contraction was closely associated with a decrease in left ventricular filling pressure during metoprolol treatment. This association was stronger than changes in short axis performance or radionuclide ejection fraction, emphasising the importance of AV plane motion for left ventricular filling and systolic performance in patients with heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympatholytics_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11083738
----K E
----T Baseline predictors of tolerability to carvedilol in patients with chronic heart failure.
----A OBJECTIVE: To determine baseline predictors of tolerance to the alpha/beta blocker carvedilol in everyday clinical practice. DESIGN: Retrospective analysis of tolerance to carvedilol in patients with chronic heart failure. Tolerance was defined as currently on carvedilol or on it at the time of death or heart transplantation. To meet the criteria for tolerance, carvedilol had to be prescribed at a stable dose for >/= 3 months. SETTING: Everyday clinical practice, comprising both hospital specialist practice and private practice. Tolerance was assessed in all patients prescribed carvedilol for chronic heart failure in those practices. PATIENTS: 808 consecutive patients in both hospital specialist (611 patients) and private practice (197 patients). MAIN OUTCOME MEASURES: Baseline predictors of tolerance assessed by proportional hazards analysis. Both univariate and multivariate analyses were performed. RESULTS: Within the entire cohort of 808 patients, 95 had stopped carvedilol, 606 were currently receiving the drug, 50 had died, and 44 had received a heart transplant. Overall, 88% of patients tolerated carvedilol (87% in the hospital specialist group, 92% in the private practitioner group). Factors that indicated impaired tolerance by univariate analysis were increased age in years (hazard ratio 1.01, 95% confidence interval (CI) 1.0 to 1.3), low diastolic blood pressure (hazard ratio 1.04, 95% CI 1.02 to 1.08), and raised plasma urea concentration (hazard ratio 1.04, 95% CI 1.02 to 1.05). New York Heart Association (NYHA) class was also a marker of tolerance (proportion not tolerated: 3% class I; 9% class II; 13% class III, 22% class IV). By multivariate analysis, no single baseline variable was an independent marker of inability to tolerate carvedilol. Tolerance was also assessed in relation to traditional precautions or relative contraindications to beta blockade. Tolerance in these subgroups was: chronic obstructive airways disease/asthma 85% (89 patients), diabetes 86% (127 patients), peripheral vascular disease 84% (58 patients), concomitant amiodarone treatment 83% (230 patients), and heart rate < 70 beats/min 84% (184 patients). CONCLUSIONS: beta Blocker treatment was well tolerated in everyday clinical practice, including non-hospital-based private practice. There was no single predictor of poor tolerance on multivariate analysis, although there was a clear association with NYHA class as well as age, diastolic blood pressure, and plasma urea on univariate analysis. Carvedilol was tolerated well among selected patients with traditional contraindications to beta blockade in this situation.
----P Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_contraindications_MeSH Carbazoles_contraindications_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Infant_MeSH M_Infant__Newborn_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_contraindications_MeSH Propanolamines_contraindications_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11086468
----K I
----T Beta blocker benefits patients with advanced heart failure.
----A 
----P Clinical_Trial Multicenter_Study News Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Survival_Analysis_MeSH 
****** 11089713
----K E
----T Failure of evidence-based medicine in the treatment of hypertension in older patients.
----A OBJECTIVE: Throughout the 1990s, the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure recommended initial antihypertensive therapy with a thiazide diuretic or a beta-blocker based on evidence from randomized, controlled trials, unless an indication existed for another drug class. The committee also recommended beta-blockers in hypertensive patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors in patients with congestive heart failure (CHF). Our objective was to determine whether prescribing practices for older hypertensive patients are consistent with evidence-based guidelines. METHODS: We examined prescription patterns from January 1, 1991 through December 31, 1995 for 23,748 patients 65 years or older with a new diagnosis of hypertension from the New Jersey Medicaid program and that state's Pharmacy Assistance for the Aged and Disabled program (PAAD). We linked drug use data with information on demographic variables and comorbid medical conditions. RESULTS: During the study period, calcium channel blockers were the most commonly prescribed initial therapy for hypertension (41%), followed by ACE inhibitors (24%), thiazide diuretics (17%), and beta-blockers (10%). Eliminating patients with diabetes mellitus, CHF, angina, or history of MI did not substantially affect these results. Overall, initial use of a thiazide declined from 22% in 1991 to 10% in 1995, while initial use of a calcium channel blocker increased from 28% to 43%, despite publication during these years of studies demonstrating a benefit of thiazides in older patients. Only 15% of older hypertensive patients with a history of MI received beta-blockers. CONCLUSIONS: Prescribing practices for older hypertensive patients are not consistent with evidence-based guidelines. Interventions are needed to encourage evidence-driven prescribing practices for the treatment of hypertension.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH P_Antihypertensive_Agents_MeSH P_Drug_Utilization_Review_MeSH P_Evidence-Based_Medicine_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Medicaid_MeSH M_New_Jersey_MeSH M_Outcome_Assessment_(Health_Care)_MeSH M_Physician's_Practice_Patterns_MeSH M_Support__Non-U_S__Gov't_MeSH M_United_States_MeSH 
****** 11092108
----K E
----T Bisoprolol alone and in combination with amlodipine or nifedipine in the treatment of chronic stable angina.
----A Beta-blockers and calcium antagonists are both effective monotherapy for stable angina. When symptoms persist, these two agents are commonly co-prescribed in the hope that this combination has added benefit compared with monotherapy alone. We investigated the additional efficacy of the calcium antagonists amlodipine and nifedipine when added to bisoprolol in patients with stable angina. Patients were randomised in a multicentre, single-blind study, with crossover of three treatments consisting of bisoprolol 10 mg once daily, bisoprolol plus nifedipine 20 mg twice daily, and bisoprolol plus amlodipine 5 mg once daily. Exercise tests were performed at the end of each four-week study period and the exercise time to onset of angina was assessed. A total of 198 patients from 17 centres were recruited of whom 147 were evaluable for efficacy. There were no statistically significant differences in exercise duration to onset of angina between any of the groups. The combination of bisoprolol plus nifedipine was least well tolerated. In summary, this study suggests there is little benefit in adding a calcium antagonist to bisoprolol in treating patients with stable angina.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH M_Analysis_of_Variance_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Chronic_Disease_MeSH M_Cross-Over_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Single-Blind_Method_MeSH 
****** 11093573
----K E
----T Is diltiazem as effective as diuretics and beta-blockers in preventing complications from hypertension?
----A 
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Norway_MeSH M_Randomized_Controlled_Trials_MeSH M_Sweden_MeSH M_Treatment_Outcome_MeSH 
****** 11095154
----K E
----T Cerebral complications of hypertension.
----A Ischaemic and degenerative brain diseases are a major health problem leading to a devastating loss of autonomy. Hypertension has been shown to carry an increased risk not only for cerebrovascular morbidity and mortality but also for cognitive impairment and dementia. Although diastolic blood pressure is considered an important risk factor, it is now clear that isolated systolic hypertension and elevated pulse pressure also play an important role in the development of brain complications. Therefore the treatment of these conditions must urgently become a widespread tool of prevention. All the randomised placebo-controlled trials completed for the last 30 years have shown a reduction in fatal and/or non-fatal strokes. In the most recent trials in isolated systolic hypertension in older patients, the benefit was even greater because of the higher risk in these populations. The new classes of drugs, in particular, calcium-channels blockers and angiotensin-converting enzyme inhibitors, have been shown to be as effective as the originally used diuretics and beta-blockers. Active treatment in the Syst-Eur trial based on nitrendipine as first step, possibly associated with enalapril and/or hydrochlorthiazide reduced not only stroke and cardiovascular complications but also the incidence of dementia including Alzheimer's disease. This important finding must be confirmed by further trials specifically focusing on the prevention of dementia. In addition, the importance of pulse pressure as a risk factor, underlines the need for new drugs which could increase aortic distensibility and decrease systolic blood pressure without greatly reducing diastolic pressure. Improving the management of hypertension offers new opportunities to reduce age-related disease in older people and to promote healthy aging.
----P Journal_Article Review Review__Academic 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Brain_Ischemia_MeSH S_epidemiology_MeSH Brain_Ischemia_epidemiology_MeSH S_etiology_MeSH Brain_Ischemia_etiology_MeSH S_prevention_&_control_MeSH Brain_Ischemia_prevention_&_control_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Dementia_MeSH S_epidemiology_MeSH Dementia_epidemiology_MeSH S_etiology_MeSH Dementia_etiology_MeSH S_prevention_&_control_MeSH Dementia_prevention_&_control_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Incidence_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH 
****** 11094241
----K E
----T Management of mild chronic hypertension during pregnancy: a review.
----A OBJECTIVE: To conduct a systematic review of evidence relating to management of mild chronic hypertension during pregnancy, including associated risks, benefits, and harms of treatment with antihypertensive agents, nonpharmacologic measures, and aspirin and benefits of various monitoring strategies. DATA SOURCES: Using four broad search strategies, we searched English and non-English-language citations in 16 electronic databases from their inception to February 1999 and consulted relevant textbooks, references, and experts. STUDY SELECTION: Reviewers screened 6228 abstracts and found 215 articles that met multiple prespecified patient selection, study population, and design criteria. TABULATION, INTEGRATION, AND RESULTS: Forty-six studies consistently showed that chronic hypertension triples the risk for perinatal mortality (odds ratio [OR] 3.4; 95% confidence interval [CI] 3.0, 3.7) and doubles the risk for placental abruption (OR 2.1; 95% CI 1.1, 3.9). Thirteen small, randomized controlled trials had inadequate power to rule in or rule out moderate-to-large (20%-50%) benefits of antihypertensive treatment. Possible adverse effects were fetal renal failure when angiotensin-converting enzyme inhibitors are used in the second or third trimester and growth restriction when atenolol is used early in pregnancy. Trials showed that aspirin neither reduces nor increases perinatal and maternal morbidity, but they did not rule out possible small-to moderate beneficial or adverse effects. No studies provide guidance on benefits or consequences of various nonpharmacologic therapies or monitoring strategies. CONCLUSION: Mild chronic hypertension is associated with increased maternal and fetal risks. Beneficial treatment and monitoring regimens are not clear, but some treatments, such as angiotensin-converting enzyme inhibitors, are best avoided.
----P Journal_Article Review Review__Academic 
----M M_Abruptio_Placentae_MeSH S_etiology_MeSH Abruptio_Placentae_etiology_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Infant_MeSH M_Infant_Mortality_MeSH M_Patient_Selection_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11099990
----K E
----T Rate-control versus conversion strategy in postoperative atrial fibrillation: a prospective, randomized pilot study.
----A BACKGROUND: Atrial fibrillation remains a frequent complication after heart surgery. The optimal strategy to treat the condition has not been established. Several retrospective studies have suggested that a primary rate-control strategy may be equivalent to a strategy that restores sinus rhythm. METHODS: Fifty patients with atrial fibrillation after heart surgery were randomly assigned to a strategy of antiarrhythmic therapy with or without electrical cardioversion or ventricular rate control. Both arms received anticoagulation with heparin overlapped with warfarin. The primary end point was time to conversion to sinus rhythm analyzed by the Kaplan-Meier method. Atrial fibrillation relapse after the initial conversion was monitored in the hospital over a 2-month period. RESULTS: There was no significant difference between an antiarrhythmic conversion strategy (n = 27) and a rate-control strategy (n = 23) in time to conversion to sinus rhythm (11.2 +/- 3. 2 vs 11.8 +/- 3.9 hours; P =.8). With the use of Cox multivariate analysis to control for the effects of age, sex, beta-blocker usage, and type of surgery, the antiarrhythmic strategy showed a trend toward reducing the time from treatment to restoration of sinus rhythm (P =.08). The length of hospital stay was reduced in the antiarrhythmic arm compared with the rate-control strategy (9.0 +/- 0.7 vs 13.2 +/- 2.0 days; P =.05). In-hospital relapse rates in the antiarrhythmic arm were 30% compared with 57% in the rate-control strategy (P =.24). There were no significant difference in relapse rates at 1 week (24% vs 28%), 4 weeks (6% vs 12%), and 6 to 8 weeks (4% vs 9%). At the end of the study, 91% of the patients in the rate-control arm were in sinus rhythm compared with 96% in the antiarrhythmic arm (P =.6). CONCLUSIONS: This pilot study shows little difference between a rate-control strategy and a strategy to restore sinus rhythm. Regardless of strategy, most patients will be in sinus rhythm after 2 months. A larger randomized, controlled study is needed to assess the impact of restoration of sinus rhythm on length of stay.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Cardiac_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiac_Surgical_Procedures_adverse_effects_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH M_Drug_Administration_Routes_MeSH P_Electric_Countershock_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Length_of_Stay_MeSH M_Male_MeSH M_Pilot_Projects_MeSH M_Procainamide_MeSH S_administration_&_dosage_MeSH Procainamide_administration_&_dosage_MeSH M_Prognosis_MeSH M_Propafenone_MeSH S_administration_&_dosage_MeSH Propafenone_administration_&_dosage_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH 
****** 11103666
----K 1
----T [Intensive treatment of blood pressure in patients with kidney disease and proteinuria]
----A Blood pressure and proteinuria are important determinants of progressive renal failure in patients with renal diseases. In a 53-year-old man with hypertension and nephrotic-range proteinuria, lowering the blood pressure to a value of 125/75 mmHg resulted in a disappearance of the proteinuria. Recent literature data indicate that the treatment of blood pressure in patients with proteinuria, with emphasis on the benefits of reaching a blood pressure target of 125/75 mmHg and the use of angiotensin-converting enzyme inhibitors, may lead to a serious improvement in their prognosis.
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_English_Abstract_MeSH M_Glomerulosclerosis__Focal_MeSH S_etiology_MeSH Glomerulosclerosis__Focal_etiology_MeSH S_urine_MeSH Glomerulosclerosis__Focal_urine_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_etiology_MeSH Obesity_etiology_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH 
****** 11104878
----K E
----T Effectiveness of low dose captopril versus propranolol therapy in infants with severe congestive failure due to left-to-right shunts.
----A To evaluate the therapeutical effects of the angiotensin converting enzyme inhibitor Captopril to the beta-blocker Propranolol in infants with congestive failure due to pulmonary overcirculation, we retrospectively analysed clinical, neurohormonal and hemodynamic data in 22 infants, 11 of whom were treated with Captopril (Group 1), 11 with Propranolol (Group 2). Age, weight, number of palliative operations, plasma renin activities and pulmonary to systemic flow ratios (3.5 vs. 3.5) were not significantly different prior to Captopril or Propranolol therapy. If treatment with digoxin and diuretics did not succeed, the infants were additionally treated with Captopril (1 mg/kg) for a mean of 7.4 months, or with 1.9 mg/kg Propranolol for 9.2 months. RESULTS: 1 mg/kg Captopril did not effectively suppress angiotensin converting enzyme in the steady state at trough level (92+/-52 vs. 87+/-50 nmol/min/ml). In the Propranolol group, the clinical heart failure score (2.6+/-1.5 vs. 7. 4+/-2.5) and plasma renin activities (14+/-10 vs. 101+/-70 ng/ml/h) were significantly lower, compared to the Captopril group. Length of hospital stay (23+/-9 vs. 52+/-24 days) was lower and weight gain (126+/-38 vs. 86+/-84 g/week) was higher within 3 months after starting Propranolol therapy. Significantly lower left atrial pressures (6.2+/-2.2 vs. 13.4+/-9.2 mmHg) and lower endiastolic ventricular pressures (7.6+/-2.5 vs. 12.6+/-4.0 mmHg) during pre-operative cardiac catheterization indicated a better diastolic ventricular function under chronic Propranolol treatment. CONCLUSION: Although high dose Captopril was not evaluated in this study, when compared to patients on low Captopril dosages, infants who received Propranolol treatment showed improvement in heart failure scores, shorter lengths of hospital stay, lower plasma renin activities and better diastolic ventricular functions.
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Defects__Congenital_MeSH S_drug_therapy_MeSH Heart_Defects__Congenital_drug_therapy_MeSH S_physiopathology_MeSH Heart_Defects__Congenital_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Infant_MeSH M_Infant__Newborn_MeSH M_Male_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Retrospective_Studies_MeSH M_Statistics__Nonparametric_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 11113718
----K I
----T Effect of beta 1 blockade with atenolol on progression of heart failure in patients pretreated with high-dose enalapril.
----A BACKGROUND: The survival benefit of beta-blocker treatment in patients with heart failure has been established in recent trials. Yet, the impact of beta-blockers added on high dose angiotensin converting enzyme inhibitors has not been reported. AIMS: To investigate the effect of atenolol, a hydrophilic, selective beta1-adrenergic antagonist, added on enalapril 40 mg/day in patients with advanced left ventricular dysfunction in a double-blind placebo-controlled trial. METHODS: One hundred and nineteen patients with class II or III heart failure, left ventricular ejection fraction < or = 25% and treatment with 40 mg enalapril daily were given an initial challenge dose of atenolol 12. 5 mg. One hundred patients (54 with idiopathic, 28 with ischemic, 18 with other dilated cardiomyopathy) tolerated challenge and were randomized to atenolol (maintenance dose 89+/-11 mg/day, range 50-100 mg/day) or placebo. The primary endpoint was combined worsening heart failure or death within 2 years, the secondary endpoint was hospitalization for cardiac events. RESULTS: After 395+/-266 days interim analysis revealed a significant difference between the atenolol and placebo group (log rank P<0.01) and the trial was concluded. Twenty-seven patients had developed worsening heart failure (8 in the atenolol group vs. 19 in the placebo group) and 13 patients had died (5 in the atenolol vs. 8 in the placebo group). Overall there were 23 hospitalizations for cardiac events (6 in the atenolol group vs. 21 in the placebo group, P=0.07); 17 hospitalizations were due to worsening heart failure (5 in the atenolol group, 12 in the placebo-group, P=0.05) and 10 due to arrhythmias (1 in the atenolol group vs. 9 in the placebo group, P<0.01) CONCLUSIONS: The data suggest that in patients with advanced left ventricular dysfunction, beta-blockers can provide substantial benefits supplementary to that already achieved with high dose enalapril treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Selection_MeSH 
****** 11113722
----K E
----T Baseline demographics of the Valsartan Heart Failure Trial. Val-HeFT Investigators.
----A BACKGROUND: The Valsartan Heart Failure Trial (Val-HeFT) is the first large-scale randomized, multinational clinical study to assess the efficacy and safety of valsartan, an angiotensin II receptor blocker, added to conventional therapy, including angiotensin-converting enzyme inhibitors, in heart failure patients. A total of 5010 patients with an ejection fraction <40% have been randomized to either valsartan titrated to 160 mg b.i.d. or to placebo. AIMS: Baseline characteristics of patients in Val-HeFT are presented and compared with other major clinical trials in heart failure. METHODS: Baseline data were collected and summary statistics calculated. RESULTS: The study population has a mean age of 62.7 years and is 80% male, 90.3% white, 6.9% black, and 2.8% Asian. Antecedent coronary heart disease is reported in 57.2% of patients. Angiotensin-converting enzyme inhibitors are prescribed for 92.7% of patients, diuretics for 85.8%, digoxin for 67.3%, and beta-blockers for 35.6%. Subgroup comparisons by age, sex, race and ejection fraction quartile show small differences in baseline characteristics. CONCLUSION: Overall the Val-HeFT population is generally representative of the population of patients with mild to moderate heart failure in industrialized countries.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Sex_Factors_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 11113724
----K E
----T Clinical trials update: IMPROVEMENT-HF, COPERNICUS, MUSTIC, ASPECT-II, APRICOT and HEART.
----A Important new studies relevant to the field of heart failure reported at the annual congress of the European Society of Cardiology (ESC), held in Amsterdam in August 2000, are reviewed. The IMPROVEMENT of Heart Failure survey investigated the knowledge and perceptions of over 1300 primary care physicians from 14 ESC member nations and the actual practice in over 11000 of their patients. Guidelines and clinical practice were compared. The survey suggested, in this large sample, that the quality of care was higher than previous smaller surveys have suggested but have also identified important deficiencies in knowledge and management that should be rectified. The COPERNICUS study demonstrated that carvedilol was remarkably well tolerated even in patients with very severe heart failure and that treatment was associated with a substantial reduction in mortality even among patients that would conventionally not be considered, by many, for beta-blocker therapy. The MUSTIC trial suggested that cardiac resynchronisation using biventricular pacing improved patients symptomatically whether or not the patient was in atrial fibrillation. Morbidity and mortality studies of cardiac resynchronisation are now underway. The ASPECT-II and APRICOT-II studies investigated the role of warfarin, aspirin and their combination for the long-term management of myocardial infarction. One interpretation of the data from these studies is that the combination of aspirin and warfarin is about as effective as warfarin alone but with a much higher incidence of side effects. Warfarin alone appeared superior to aspirin alone. In summary, the annual congress of the ESC provided important new information for clinical practice and, to date, was, by far, the most important cardiology congress in the world this year.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Coronary_Thrombosis_MeSH S_drug_therapy_MeSH Coronary_Thrombosis_drug_therapy_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Guideline_Adherence_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Myocardial_Diseases_MeSH S_therapy_MeSH Myocardial_Diseases_therapy_MeSH M_Pacemaker__Artificial_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Single-Blind_Method_MeSH M_Thrombolytic_Therapy_MeSH 
****** 11115082
----K E
----T ACEI/ATRA therapy decreases proteinuria by improving glomerular permselectivity in IgA nephritis.
----A BACKGROUND: It has been postulated that angiotensin-converting enzyme inhibitor/angiotensin receptor antagonist (ACEI/ATRA) may decrease proteinuria in patients with glomerulonephritis by its action on the glomerular basement membrane. We therefore studied the relationship between the response of patients with IgA nephritis (IgAN) to ACEI/ATRA therapy by decreasing proteinuria and its effect on the selectivity index (SI) in these patients. METHODS: Forty-one patients with biopsy-proven IgAN entered a control trial, with 21 in the treatment group and 20 in the control group. The entry criteria included proteinuria of 1 g or more and/or renal impairment. Patients in the treatment group received ACEI/ATRA or both with three monthly increases in dosage. In the control group, hypertension was treated with atenolol, hydrallazine, or methyldopa. The following tests were performed at three monthly intervals: serum creatinine, total urinary protein, SI, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and low molecular weight (LMW) proteinuria. RESULTS: After a mean duration of therapy of 13 +/- 5 months, in the treatment group, there was no significant change in serum creatinine, proteinuria, or SI, but in the control group, serum creatinine deteriorated from 1.8 +/- 0.8 to 2.3 +/- 1.1 mg/dL (P < 0.05). Among the 21 patients in the treatment group, 10 responded to ACEI/ATRA therapy determined as a decrease in proteinuria by 30% (responders), and the other 11 did not respond (nonresponders). Among the responders, SI improved from a mean of 0.26 +/- 0.07 to 0.18 +/- 0. 07 (P < 0.001), indicating a tendency toward selective proteinuria. This was associated with an improvement in serum creatinine from mean 1.7 +/- 0.6 to 1.5 +/- 0.6 mg/dL (P < 0.02) and a decrease in proteinuria from a mean of 2.3 +/- 1.1 to 0.7 +/- 0.5 g/day (P < 0. 001). After treatment, proteinuria in the treatment group (1.8 +/- 1. 6 g/day) was significantly less than in the control group (2.9 +/- 1. 8 g/day, P < 0.05). The post-treatment SI in the responder group (0. 18 +/- 0.07) was better than that of the nonresponder group (0.33 +/- 0.11, P < 0.002). Eight out of 21 patients in the treatment group who had documented renal impairment had improved renal function compared with two in the control group (chi2 = 4.4, P < 0. 05). Of the eight patients in the treatment group who improved their renal function, three normalized their renal function compared with one from the control group. CONCLUSION: Our data suggest that ACEI/ATRA therapy may be beneficial in patients with IgAN with renal impairment and nonselective proteinuria, as such patients may respond to therapy with improvement in protein selectivity, decrease in proteinuria, and improvement in renal function. ACEI/ATRA therapy probably modifies pore size distribution by reducing the radius of large unselective pores, causing the shunt pathway to become less pronounced, resulting in less leakage of protein into the urine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Glomerulonephritis__IGA_MeSH S_drug_therapy_MeSH Glomerulonephritis__IGA_drug_therapy_MeSH S_physiopathology_MeSH Glomerulonephritis__IGA_physiopathology_MeSH M_Human_MeSH M_Kidney_MeSH S_physiology_MeSH Kidney_physiology_MeSH M_Losartan_MeSH S_administration_&_dosage_MeSH Losartan_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH S_physiopathology_MeSH Proteinuria_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11503798
----K E
----T Trimetazidine: a second look. Just a placebo.
----A (1) Trimetazidine is licensed in France for the prevention of angina attacks and for symptomatic treatment of vertigo and tinnitus.  (2) In angina the evidence on trimetazidine is sorely lacking.  The only available comparative trial failed to show that trimetazidine monotherapy was even as good as low-dose propranolol.  For want of appropriate assessment, it is not known if trimetazidine can reinforce the activity of betablockers, the reference treatment.  (3) In symptomatic treatment of vertigo and tinnitus, the three available placebo-controlled trials show significant differences in favour of trimetazidine, but these differences are too small to be clinically relevant.  (4) Data on the adverse effect profile of trimetazidine are virtually non existent.  Gastrointestinal disorders and headache have been reported.
----P Journal_Article 
----M M_Angina_Pectoris_MeSH S_prevention_&_control_MeSH Angina_Pectoris_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_France_MeSH M_Human_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Tinnitus_MeSH S_drug_therapy_MeSH Tinnitus_drug_therapy_MeSH M_Treatment_Outcome_MeSH P_Trimetazidine_MeSH S_adverse_effects_MeSH Trimetazidine_adverse_effects_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Vertigo_MeSH S_drug_therapy_MeSH Vertigo_drug_therapy_MeSH 
****** 11053724
----K E
----T Effect of concomitant digoxin and carvedilol therapy on mortality and morbidity in patients with chronic heart failure.
----A We retrospectively performed stepwise logistic regression analysis on 1,509 patients with chronic heart failure in 4 multicenter United States studies and 1 Australia-New Zealand study to examine the effect of digoxin in patients randomized to carvedilol or placebo. Patients receiving digoxin had more advanced heart failure, the incidence of hospitalization for any cause and the combination of all-cause death and all-cause hospitalization were the same in the digoxin versus no-digoxin groups.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Morbidity_MeSH S_trends_MeSH Morbidity_trends_MeSH M_Probability_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Proportional_Hazards_Models_MeSH M_Retrospective_Studies_MeSH M_Survival_Analysis_MeSH 
****** 11129677
----K E
----T Effect of heart failure program on cardiovascular drug utilization and dosage in patients with chronic heart failure.
----A BACKGROUND: Utilization and dosage of angiotensin-converting enzyme (ACE) inhibitors in patients with chronic heart failure (CHF) remain low. Recent data suggest that care of patients with CHF in specialized heart failure programs is associated with improved clinical outcomes. HYPOTHESIS: Specialized heart failure care is associated with better utilization and higher dose of cardiovascular drugs. METHODS: Data from 133 patients with CHF referred to a heart failure program were analyzed. Mean functional class 3.1 +/- 0.5, left ventricular ejection fraction 19 +/- 8. Utilization and doses of cardiovascular drugs were examined at initial evaluation and at last visit, after an average period of 17 +/- 14 months. Hospitalization and survival data were determined. RESULTS: Utilization of ACE inhibitors and angiotensin-receptor blockers increased from 87 to 100% (p < 0.001). Average daily dose increased by 60%, from the equivalent of captopril 105 +/- 78 mg to 167 +/- 86 mg (p < 0.001). Utilization of the following drugs increased significantly: beta blockers (16-37%, p < 0.001), metolazone (10-23%, p = 0.007), spironolactone (1-36%, p < 0.001), amiodarone (7-15%, p = 0.05), hydralazine (1-9%, p = 0.004), and nitrates (20-33%, p = 0.03). One-year survival was 90%. The 3- and 6-month hospitalization rates for heart failure were 4 and 7%, and for all cardiovascular causes they were 6 and 11%, respectively. CONCLUSIONS: Care of patients with CHF in a specialized heart failure program was associated with significant increase in the utilization and doses of all beneficial cardiovascular drugs, especially ACE inhibitors. It was also associated with excellent clinical outcomes.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Drug_Utilization_MeSH M_Female_MeSH P_Guideline_Adherence_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Physician's_Practice_Patterns_MeSH M_Retrospective_Studies_MeSH 
****** 11126860
----K 5
----T Guidelines on migraine: part 4. General principles of preventive therapy.
----A 
----P Journal_Article 
----M M_Analgesics_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Biofeedback_(Psychology)_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH S_therapy_MeSH Migraine_therapy_MeSH M_Practice_Guidelines_MeSH M_Relaxation_Techniques_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11130522
----K I
----T Health outcomes associated with calcium antagonists compared with other first-line antihypertensive therapies: a meta-analysis of randomised controlled trials.
----A BACKGROUND: Several observational studies and individual randomised trials in hypertension have suggested that, compared with other drugs, calcium antagonists may be associated with a higher risk of coronary events, despite similar blood-pressure control. The aim of this meta-analysis was to compare the effects of calcium antagonists and other antihypertensive drugs on major cardiovascular events. METHODS: We undertook a meta-analysis of trials in hypertension that assessed cardiovascular events and included at least 100 patients, who were randomly assigned intermediate-acting or long-acting calcium antagonists or other antihypertensive drugs and who were followed up for at least 2 years. FINDINGS: The nine eligible trials included 27,743 participants. Calcium antagonists and other drugs achieved similar control of both systolic and diastolic blood pressure. Compared with patients assigned diuretics, beta-blockers, angiotensin-converting-enzyme inhibitors, or clonidine (n=15,044), those assigned calcium antagonists (n=12,699) had a significantly higher risk of acute myocardial infarction (odds ratio 1.26 [95% CI 1.11-1.43], p=0.0003), congestive heart failure (1.25 [1.07-1.46], p=0.005), and major cardiovascular events (1.10 [1.02-1.18], p=0.018). The treatment differences were within the play of chance for the outcomes of stroke (0.90 [0.80-1.02], p=0.10) and all-cause mortality (1.03 [0.94-1.13], p=0.54). INTERPRETATION: In randomised controlled trials, the large available database suggests that calcium antagonists are inferior to other types of antihypertensive drugs as first-line agents in reducing the risks of several major complications of hypertension. On the basis of these data, the longer-acting calcium antagonists cannot be recommended as first-line therapy for hypertension.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diastole_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 11130523
----K E
----T Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: results of prospectively designed overviews of randomised trials. Blood Pressure Lowering Treatment Trialists' Collaboration.
----A BACKGROUND: This programme of overviews of randomised trials was established to investigate the effects of angiotensin-converting-enzyme (ACE) inhibitors, calcium antagonists, and other blood-pressure-lowering drugs on mortality and major cardiovascular morbidity in several populations of patients. We did separate overviews of trials comparing active treatment regimens with placebo, trials comparing more intensive and less intensive blood-pressure-lowering strategies, and trials comparing treatment regimens based on different drug classes. METHODS: The hypotheses to be investigated, the trials to be included, and the outcomes to be studied were all selected before the results of any participating trial were known. Individual participant data or group tabular data were provided by each trial and combined by standard statistical techniques. FINDINGS: The overview of placebo-controlled trials of ACE inhibitors (four trials, 12,124 patients mostly with coronary heart disease) revealed reductions in stroke (30% [95% CI 15-43]), coronary heart disease (20% [11-28]), and major cardiovascular events (21% [14-27]). The overview of placebo-controlled trials of calcium antagonists (two trials, 5520 patients mostly with hypertension) showed reductions in stroke (39% [15-56]) and major cardiovascular events (28% [13-41]). In the overview of trials comparing blood-pressure-lowering strategies of different intensity (three trials, 20,408 patients with hypertension), there were reduced risks of stroke (20% [2-35]), coronary heart disease (19% [2-33]), and major cardiovascular events (15% [4-24]) with more intensive therapy. In the overviews comparing different antihypertensive regimens (eight trials, 37,872 patients with hypertension), several differences in cause-specific effects were seen between calcium-antagonist-based therapy and other regimens, but each was of borderline significance. INTERPRETATION: Strong evidence of benefits of ACE inhibitors and calcium antagonists is provided by the overviews of placebo-controlled trials. There is weaker evidence of differences between treatment regimens of differing intensities and of differences between treatment regimens based on different drug classes. Data from continuing trials of blood-pressure-lowering drugs will substantially increase the evidence available about any real differences that might exist between regimens.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11130228
----K I
----T Beta blockers and congestive heart failure.
----A 
----P Comment Editorial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Meta-Analysis_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH 
****** 11130231
----K I
----T The importance of beta blockers in the treatment of heart failure.
----A Heart failure, the only cardiovascular disease with an increasing incidence, is associated with significant mortality and poses a considerable economic burden. Traditionally, beta blockers have been considered to be contraindicated in patients with heart failure. Recently, however, several large randomized, controlled mortality trials have been stopped early because of significant improvement in mortality rates in patients with heart failure who were given beta blockers in addition to angiotensin-converting enzyme inhibitors, diuretics and, sometimes, digoxin. Beta blockers should now be considered standard therapy in patients with New York Heart Association class II or class III heart failure who are hemodynamically stable, who do not have dyspnea at rest and who have no other contraindications to the use of these agents.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH 
****** 11127443
----K E
----T Antiremodeling effects on the left ventricle during beta-blockade with metoprolol in the treatment of chronic heart failure.
----A OBJECTIVES: The purpose of the study was to investigate the effects of beta1-blockade on left ventricular (LV) size and function for patients with chronic heart failure. BACKGROUND: Large-scale trials have shown that a marked decrease in mortality can be obtained by treatment of chronic heart failure with beta-adrenergic blocking agents. Possible mechanisms behind this effect remain yet to be fully elucidated, and previous studies have presented insignificant results regarding suspected LV antiremodeling effects. METHODS: In this randomized, placebo-controlled and double-blind substudy to the Metoprolol CR/XL Randomized Intervention Trial in Heart Failure (MERIT-HF), 41 patients were examined with magnetic resonance imaging three times in a six-month period, assessing LV dimensions and function. RESULTS: Decreases in both LV end-diastolic volume index (150 ml/m2 at baseline to 126 ml/m2 after six months, p = 0.007) and LV end-systolic volume index (107 ml/m2 to 81 ml/m2, p = 0.001) were found, whereas LV ejection fraction increased in the metoprolol CR/XL group (29% to 37%, p = 0.005). No significant changes were seen in the placebo group regarding these variables. Left ventricular stroke volume index remained unchanged, whereas LV mass index decreased in both groups (175 g/m2 to 160 g/m2 in the placebo group [p = 0.005] and 179 g/m2 to 164 g/m2 in the metoprolol CR/XL group [p = 0.011). CONCLUSIONS: This study is the first randomized study to demonstrate that the beta1-blocker metoprolol CR/XL has antiremodeling effects on the LV in patients with chronic heart failure and consequently provides an explanation for the highly significant decrease in mortality from worsening heart failure found in the MERIT-HF trial.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Magnetic_Resonance_Imaging_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 11127843
----K E
----T Effects of antihypertensive drugs on the unborn child: what is known, and how should this influence prescribing?
----A This review discusses the use of antihypertensive drugs in acute and long term treatment of hypertensive disorders of pregnancy, including their placental transfer and adverse effects on the fetus. All antihypertensive agents cross the placental barrier and are present in varying concentrations in the fetal circulation, with varying resultant effects on fetal metabolism. Antihypertensive drugs that are lipid soluble will pass through the placental barrier with ease whereas the most polar will not. Placental transfer diminishes under conditions that decrease the surface area or increase the thickness of the placenta. Highly protein-bound drugs form complexes which impair placental transfer while unbound drugs cross the placenta easily. The ionised drug form is highly charged and cannot cross lipid membranes while the un-ionised form can easily cross the placenta. A decrease in placental blood flow can slow down the transfer of lipid soluble drugs to the fetus. Close monitoring of the fetal and maternal condition is necessary for the rest of the pregnancy after antihypertensive therapy is commenced. Methyldopa is the initial drug of choice for long term oral antihypertensive therapy in pregnancy. Neither short term nor long term use of methyldopa is associated with adverse effects. In the short term (<6 weeks) beta-receptor antagonists are effective and well tolerated provided there are no signs of intrauterine growth impairment. ACE (angiotensin converting enzyme) inhibitors are contraindicated in the second and third trimesters of pregnancy because they are teratogenic. Intravenous dihydralazine is widely used for rapid reductions of severely elevated blood pressure. The use of nifedipine concurrently with MgSO4 must be approached with caution because the combination is associated with severe hypotension, neuromuscular blockade and cardiac depression. In the last decade, knowledge of antihypertensive drugs used in pregnancy has improved and new drugs, e.g. calcium antagonists, which have been shown to have great potential for use in pregnancy, have been introduced. Safety for the fetus with newer drugs has not yet been adequately evaluated. Currently, well established and cost effective drugs such as methyldopa (long term use) and intravenous dihydralazine (rapid reduction) are the agents of choice to treat hypertensive disorders of pregnancy.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Embryo_and_Fetal_Development_MeSH S_drug_effects_MeSH Embryo_and_Fetal_Development_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Maternal-Fetal_Exchange_MeSH M_Placenta_MeSH S_blood_supply_MeSH Placenta_blood_supply_MeSH M_Practice_Guidelines_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications_MeSH S_drug_therapy_MeSH Pregnancy_Complications_drug_therapy_MeSH S_etiology_MeSH Pregnancy_Complications_etiology_MeSH 
****** 11144703
----K I
----T Influence of beta-blockers on mortality in chronic heart failure.
----A OBJECTIVE: To briefly discuss the pathophysiology of heart failure and the rationale for the use of beta-blockers in the treatment of chronic heart failure. Key morbidity reduction trials are briefly mentioned, and recent mortality reduction trials are reviewed. General recommendations regarding the use of beta-blockers in heart failure are also included to guide clinical practice. STUDY SELECTION/DATA EXTRACTION: Randomized, placebo-controlled clinical trials and meta-analyses evaluating mortality reduction with beta-blockers in the treatment of heart failure were identified using a MEDLINE search from January 1993 to March 2000. Abstracts and presented results from recent scientific meetings were also considered. DATA SYNTHESIS: Beta-blockers have been shown to decrease hospitalization for worsening heart failure, decrease the need for heart transplant, improve New York Heart Association (NYHA) functional class, and increase left-ventricular ejection fraction. A mortality benefit has recently been demonstrated for patients with chronic heart failure. Carvedilol, bisoprolol, and controlled-release/extended-release metoprolol decreased the risk of dying by 65%, 34%, and 34%, respectively, in patients with primarily NYHA functional class II or III and systolic dysfunction. The benefit of these agents in patients with class IV heart failure or determining whether one agent has an advantage over another is being investigated in ongoing clinical trials. CONCLUSIONS: Several beta-blockers have demonstrated mortality reduction in the treatment of patients with NYHA functional class II or III heart failure and systolic dysfunction. Beta-blockers should be considered in these patients when they are clinically stable and taking the current standard therapy of a diuretic plus an angiotensin-converting enzyme inhibitor or other vasodilator agent.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Morbidity_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 11225566
----K I
----T Effect of fluoxetine on carvedilol pharmacokinetics, CYP2D6 activity, and autonomic balance in heart failure patients.
----A The objective of this study was to examine the pharmacokinetic and pharmacodynamic consequences of concomitant administration of fluoxetine and carvedilol in heart failure patients. Fluoxetine (20 mg) or matching placebo was administered in a randomized, double-blind, two-period crossover study to 10 patients previously identified as extensive metabolizers of CYP2D6 substrates. Patients were maintained on a carvedilol dose of 25 or 50 mg bid and given fluoxetine/placebo for a minimum of 28 days. Plasma was collected over the 12-hour carvedilol dosing interval, and the concentrations of the R(+) and S(-) enantiomers of carvedilol were measured. CYP2D6 phenotype was assessed during each study period using dextromethorphan (30 mg). Changes in autonomic modulation between study periods were measured by heart rate variability in the time and frequency domains using ambulatory electrocardiographic monitoring. Compared to placebo, fluoxetine coadministration resulted in a 77% increase in mean (+/- SD) R(+) enantiomer AUC0-12 (522 +/- 413 vs. 927 +/- 506 ng.h/mL, p = 0.01) and a nonsignificant increase in S(-) enantiomer AUC (244 +/- 185 vs. 330 +/- 179 ng.h/mL, p = 0.17). Mean apparent oral clearance for both enantiomers decreased significantly with fluoxetine administration (R(+): 10.3 +/- 7.2 vs. 4.5 +/- 2.2 mL/min/kg; S(-): 22.5 +/- 12.3 vs. 12.6 +/- 7.4 mL/min/kg; p = 0.004 and 0.03, respectively). No differences in adverse effects, blood pressure, or heart rate were noted between treatment groups, and there were no consistent changes in heart rate variability parameters. In conclusion, fluoxetine administration resulted in a stereospecific inhibition of carvedilol metabolism, with the R(+) enantiomer increasing to a greater extent than the S(-) enantiomer. However, this interaction was of little clinical significance in our sample population.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH M_Adult_MeSH M_Aged_MeSH M_Antidepressive_Agents__Second-Generation_MeSH S_pharmacology_MeSH Antidepressive_Agents__Second-Generation_pharmacology_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Autonomic_Nervous_System_physiopathology_MeSH M_Carbazoles_MeSH S_pharmacokinetics_MeSH Carbazoles_pharmacokinetics_MeSH M_Cross-Over_Studies_MeSH M_Cytochrome_P-450_CYP2D6_MeSH S_metabolism_MeSH Cytochrome_P-450_CYP2D6_metabolism_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_pharmacology_MeSH Fluoxetine_pharmacology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_enzymology_MeSH Heart_Failure__Congestive_enzymology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacokinetics_MeSH Propanolamines_pharmacokinetics_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_pharmacology_MeSH Serotonin_Uptake_Inhibitors_pharmacology_MeSH M_Stereoisomerism_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11132612
----K E
----T Effect of sildenafil citrate on blood pressure and heart rate in men with erectile dysfunction taking concomitant antihypertensive medication. Sildenafil Study Group.
----A OBJECTIVES: To assess the acute effect of sildenafil citrate on blood pressure and heart rate in men with erectile dysfunction taking concomitant antihypertensive medication. DESIGN: Post-hoc subanalysis of five, 12- or 24-week, prospective, randomized, double-blind, placebo-controlled studies. SETTING: Private-practice and academic urology clinics. PATIENTS: A total of 1685 men with erectile dysfunction of > or = 6 months duration, of whom 667 (sildenafil n = 406, placebo n = 261) were taking antihypertensive medication (diuretic, beta-blocker, alpha-blocker, angiotensin converting enzyme inhibitor, and/or calcium antagonist). Of the patients taking antihypertensive medication, 608 (91%) completed the studies (374 of 406 receiving sildenafil, 234 of 261 receiving placebo). INTERVENTIONS: The last dose of oral sildenafil (25-200 mg) or placebo was taken at home on the morning of the final clinic visit. Patients taking antihypertensive medication maintained usual dosing schedules. MAIN OUTCOME MEASUREMENTS: Sitting systolic (SBP)/diastolic blood pressure (DBP) and heart rate at baseline and after dosing with sildenafil or placebo (end-of-treatment visit). RESULTS: Mean changes from baseline in SBP/DBP for men taking antihypertensive medication were -3.6/-1.9 mmHg for those receiving sildenafil and -0.8/-0.1 mmHg for those receiving placebo compared with -2.2/-2.0 mmHg and -0.1/0.4 mmHg, respectively, for men not taking antihypertensive medication. Mean changes from baseline in heart rate for men taking antihypertensive medication were -0.6 beats/min after sildenafil and 0.9 beats/min after placebo compared with 0.4 beats/min and -0.6 beats/min, respectively, for patients not taking antihypertensive medication. Differences in SBP, DBP, and heart rate between the patients taking and those not taking antihypertensive medication were small. CONCLUSIONS: The acute, short-term effects of oral sildenafil on blood pressure and heart rate in men with erectile dysfunction were small and not likely to be clinically significant in those taking concomitant antihypertensive medication.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Impotence_MeSH S_complications_MeSH Impotence_complications_MeSH S_drug_therapy_MeSH Impotence_drug_therapy_MeSH S_physiopathology_MeSH Impotence_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_administration_&_dosage_MeSH Phosphodiesterase_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Phosphodiesterase_Inhibitors_adverse_effects_MeSH M_Piperazines_MeSH S_administration_&_dosage_MeSH Piperazines_administration_&_dosage_MeSH S_adverse_effects_MeSH Piperazines_adverse_effects_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11139094
----K E
----T Update on recent clinical trials in congestive heart failure.
----A Understanding of the pathophysiology of heart failure has advanced over the last decade, resulting in new therapeutic advances. Convincing data exist that angiotensin-converting enzyme (ACE) inhibition and adrenergic blockade are the most important therapies and have the capacity to improve survival and lower morbidity. Higher doses of both ACE inhibitors and beta-blockers appear to provide additional benefits. The aldosterone antagonist spironolactone, when used in severe heart failure, provides additional survival advantage when added to standard triple therapy. Angiotensin receptor blockers have not been shown to be superior to ACE inhibitors, and their role in heart failure treatment requires further investigation. No trial's data support the use of inotropic agents or calcium channel blockers in heart failure. A number of new therapeutic agents, including vasopressin antagonists and tumor necrosis factor-alpha receptor antibody are in phase II and III clinical trials. If proved beneficial, they may provide new treatment options for patients with heart failure. Nevertheless, the current challenge is to increase the use of proven therapies, namely ACE inhibitors and beta-blockers, to improve outcomes in the rapidly growing population of patients with congestive heart failure.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials__Phase_II_MeSH M_Clinical_Trials__Phase_III_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Stimulation__Chemical_MeSH M_Sympatholytics_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH 
****** 11152373
----K I
----T Antioxidant properties of carvedilol and metoprolol in heart failure: a double-blind randomized controlled trial.
----A Animal and human studies have shown that carvedilol has significant antioxidant properties compared with other beta-blockers. The objective of this study was to determine if these antioxidant effects are detectable in patients with heart failure and to compare carvedilol with the selective beta-blocker metoprolol. Twenty-four patients with chronic heart failure were randomly assigned to receive either carvedilol or metoprolol in a double-blind control trial for 12 weeks in a University teaching hospital clinic. Blood pressure, heart rate, exercise tolerance, left ventricular ejection fraction, plasma total antioxidant status, erythrocyte superoxide dismutase, and glutathione peroxidase activities were determined at baseline and every 4 weeks up to 12 weeks. The results showed that erythrocyte superoxide dismutase and glutathione peroxidase were significantly reduced in carvedilol treated patients after 12 weeks of therapy, whereas metoprolol had no significant effect, although the clinical improvement over the short-term was similar with both drugs. Thus carvedilol, in addition to improving symptoms in heart failure, also possesses significant antioxidant properties. Whether this additional action influences long-term outcome is at present unknown.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Antioxidants_MeSH S_metabolism_MeSH Antioxidants_metabolism_MeSH M_Carbazoles_MeSH S_blood_MeSH Carbazoles_blood_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glutathione_Peroxidase_MeSH S_blood_MeSH Glutathione_Peroxidase_blood_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_blood_MeSH Metoprolol_blood_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_blood_MeSH Propanolamines_blood_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Superoxide_Dismutase_MeSH S_blood_MeSH Superoxide_Dismutase_blood_MeSH 
****** 11151741
----K E
----T The pharmacodynamic and pharmacokinetic profiles of controlled-release formulations of felodipine and metoprolol in free and fixed combinations in elderly hypertensive patients.
----A AIMS: The aims of this study were to study the efficacy and tolerability of felodipine extended release (ER) 5 mg and metoprolol controlled release (CR/ZOC) 50 mg given as a fixed combination (Logimax) or as a free combination in elderly (age greater than 60 years) hypertensive patients, using ambulatory blood pressure (BP) monitoring. A secondary aim was to relate the efficacy of the free and fixed combinations with pharmacokinetic profiles. METHODS: This was a double-blind, placebo-controlled randomised three-way crossover multi-centre study. BP was measured for 26 h using ambulatory blood pressure monitoring (ABPM), which was performed on the last day of the three treatment phases. RESULTS: Mean sitting BPs, measured during the trough period with ABPM, were significantly lower with both the free and fixed combinations of metoprolol and felodipine than placebo (141/83 mmHg free, 140/83 mmHg fixed, 156/93 mmHg placebo). The mean BPs measured over 24 h using ABPM were 143/82 mmHg, 140/82 mmHg and 158/93 mmHg for the free, fixed and placebo treatment arms, respectively. The trough-to-peak ratios (T:P) were 75% and 79% for the systolic BP and 70% and 70% for the diastolic BP for the free and fixed combinations, respectively. Pharmacokinetic evaluation revealed identical plasma concentration-time curves for felodipine given as the free or fixed combination. Comparison of the plasma concentration-time curves for metoprolol revealed a delay in the release rate from the fixed combination formulation. No significant differences in BP control between the active treatments were noted during this period. Of 26 patients entered into the study, 3 withdrew during active phase for non-drug-related reasons. No patient withdrew from active treatment due to treatment-related adverse events. The frequency of adverse event reporting for the fixed combination of felodipine and metoprolol was similar to that for placebo (60% and 58%, respectively). CONCLUSION: The results suggest that once-daily dosing with either the free or fixed combination of felodipine 5 mg and metoprolol 50 mg produces a significant sustained reduction in systolic and diastolic BP with similar plasma concentration profiles over a 24-h period.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_pharmacokinetics_MeSH Felodipine_pharmacokinetics_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH 
****** 11189013
----K E
----T Rationale, design and organization of the Second Chinese Cardiac Study (CCS-2): a randomized trial of clopidogrel plus aspirin, and of metoprolol, among patients with suspected acute myocardial infarction. Second Chinese Cardiac Study (CCS-2) Collaborative Group.
----A Assessing combined anti-platelet therapy in suspected acute myocardial infarction Aspirin has been shown to be effective in the emergency treatment of acute myocardial infarction. It irreversibly inhibits platelet cyclo-oxygenase and thereby prevents the formation of the platelet aggregating agent thromboxane A2. Clopidogrel is an anti-platelet agent that acts by a different mechanism, inhibiting adenosine diphosphate-induced platelet aggregation. Simultaneous inhibition of both of these pathways might produce significantly greater anti-platelet effects than inhibition of either alone. The Second Chinese Cardiac Study (CCS-2) will reliably determine whether adding oral clopidogrel to aspirin for up to 4 weeks in hospital after suspected acute myocardial infarction can produce a greater reduction in the risk of major vascular events than can be achieved by giving aspirin alone. In order to be able to detect a further reduction of 10-15%, some 20,000-40,000 patients in over 1000 Chinese hospitals will be randomized. Assessing early beta-blocker therapy in suspected acute myocardial infarction Although over 27,000 patients have been studied previously in randomized trials of short-term beta-blocker therapy in acute myocardial infarction, the reduction in early mortality (513 (3.7%) for beta-blocker therapy deaths versus 586 (4.3%) for control deaths) was only just conventionally significant (P = 0.02) and, overall, the absolute benefits were small in the relatively low-risk patients studied. Although there might be worthwhile benefit in higher risk patients, there is currently little routine use of beta-blocker therapy in acute myocardial infarction. Hence, patients in CCS-2 will also be randomly allocated to receive metoprolol (intravenous then oral) or matching placebo for up to 4 weeks in hospital in a 2 x 2 factorial design. Such a design allows all patients to contribute fully to assessment of the separate effects of the anti-platelet regimen and the beta-blocker (without any material effect on study cost or sample size requirements) whilst also providing information about their combined effects. A streamlined trial in a wide range of patients In order to randomize 20,000-40,000 patients, the design of CCS-2 has been streamlined: data collection and other extra work for collaborators is minimal, allowing busy hospitals to take part easily. All patients presenting within 24 h of the onset of suspected acute myocardial infarction are eligible for the study provided they have a definite ECG abnormality and are not persistently hypotensive, and provided the doctor responsible considers there to be no clear indication for or contraindication to either of the trial treatments. Apart from administration of the trial treatments, all other aspects of individual patient management are entirely at the discretion of the doctor responsible. By including many different types of patient from many different types of hospital, with wide variation in ancillary management, the CCS-2 results will be of direct clinical relevance to the heterogeneous realities of future clinical practice. The trial began in July 1999 and is expected to be completed by the year 2003.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_China_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Research_Design_MeSH M_Ticlopidine_MeSH S_analogs_&_derivatives_MeSH Ticlopidine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Ticlopidine_therapeutic_use_MeSH 
****** 11191937
----K E
----T Amlodipine versus slow release metoprolol in the treatment of stable exertional angina pectoris (AMSA).
----A OBJECTIVES: To compare the effects of amlodipine and slow release metoprolol on subjective symptoms and signs of ischaemia during bicycle ergometric exercise tests in patients with stable angina pectoris. DESIGN: A randomized double-blind comparison of the two drugs in patients with documented coronary disease required to have at least three attacks of angina per week and to perform a symptom-limited exercise test with significant signs of ischaemia in the ECG. RESULTS: Out of 127 patients, 117 completed the study. Both amlodipine and metoprolol significantly increased total exercise time, total workload, time to onset of angina and time to 1 mm ST-depression with no significant differences between the drugs. Amlodipine was significantly more efficient than metoprolol in reducing ST-depression at maximum workload. Diary data revealed no differences in patients' self-rating of drug effects. CONCLUSIONS: Judged by suppression of subjective symptoms and performance on exercise tolerance tests amlodipine represents a useful alternative to metoprolol as monotherapy in stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Exertion_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11159149
----K E
----T Dementia and disability outcomes in large hypertension trials: lessons learned from the systolic hypertension in the elderly program (SHEP) trial.
----A In the Systolic Hypertension in the Elderly Program (SHEP) trial (1985-1990), active treatment reduced the incidence of cardiovascular events, but not that of dementia and disability, as compared with placebo. This study aims to evaluate if assessment of cognitive and functional outcomes was biased by differential dropout. Characteristics of subjects who did or did not participate in follow-up cognitive and functional evaluations were compared. The relative risks of incident cognitive impairment and disability were assessed in the two treatment groups, with the use of the reported findings and under the assumption that the proportions of cognitive and functional impairment among dropouts increased. Assignment to the placebo group and the occurrence of cardiovascular events independently predicted missed assessments. From the reported findings, the risk of cognitive and functional impairment was similar between the two treatment groups. However, when 20-30% and 40-80% of the subjects who missed the assessment were assumed to be cognitively and, respectively, functionally impaired, assignment to active treatment reduced the risk of these outcomes. In the SHEP, the cognitive and functional evaluations were biased toward the null effect by differential dropout. This might have obscured the appraisal of a protective effect of treatment on the cognitive and functional decline of older hypertensive adults.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bias_(Epidemiology)_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Dementia_MeSH S_epidemiology_MeSH Dementia_epidemiology_MeSH M_Disabled_Persons_MeSH S_statistics_&_numerical_data_MeSH Disabled_Persons_statistics_&_numerical_data_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Incidence_MeSH M_Multicenter_Studies_MeSH S_statistics_&_numerical_data_MeSH Multicenter_Studies_statistics_&_numerical_data_MeSH M_Patient_Dropouts_MeSH S_statistics_&_numerical_data_MeSH Patient_Dropouts_statistics_&_numerical_data_MeSH M_Questionnaires_MeSH S_standards_MeSH Questionnaires_standards_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Reserpine_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 11190416
----K 5
----T Differential pharmacokinetics of digoxin in elderly patients.
----A Digoxin remains one of the most commonly prescribed of all cardiac medications. The main indications for digoxin usage include atrial fibrillation and heart failure; both these conditions are more prevalent in older patients. Given the aging population and the increasing incidence of heart failure we would expect prescribing of digoxin to remain as frequent or to even increase in older patients. Older patients are also more likely to develop toxicity and diagnosis of digoxin toxicity can be difficult in this group. Numerous components contribute to the development of toxicity in older patients, ranging from aging-related changes in renal function or body mass to polypharmacy and possible interactions with digoxin. It is therefore important to understand how the pharmacokinetics of digoxin may be altered in the older population. Application of basic pharmacological principles may be helpful in anticipating these problems. This review describes the pharmacokinetics of digoxin, the changes in pharmacokinetics with increasing age and how concomitant disease states or drug interactions may affect the pharmacokinetics of digoxin. Greater knowledge about the causes and prevention of digoxin toxicity should further reduce the morbidity and mortality arising from digoxin toxicity, especially in the elderly population.
----P Journal_Article Review Review__Tutorial 
----M M_Absorption_MeSH M_Aged_MeSH M_Aging_MeSH S_metabolism_MeSH Aging_metabolism_MeSH M_Biological_Availability_MeSH M_Cardiotonic_Agents_MeSH S_pharmacokinetics_MeSH Cardiotonic_Agents_pharmacokinetics_MeSH M_Digoxin_MeSH S_pharmacokinetics_MeSH Digoxin_pharmacokinetics_MeSH M_Drug_Interactions_MeSH M_Geriatric_Assessment_MeSH M_Human_MeSH M_Tissue_Distribution_MeSH 
****** 11195606
----K E
----T Silent ischemic interval on exercise test is a predictor of response to drug therapy: a randomized crossover trial of metoprolol versus diltiazem in stable angina.
----A BACKGROUND AND HYPOTHESIS: There is no method available to predict the relative antianginal efficacy of beta blockers and calcium-channel antagonists. The present study was undertaken to assess the role of silent ischemic interval (SII) on exercise treadmill test (ETT) as a predictor of response to therapy with metoprolol and diltiazem in patients with stable angina. METHODS: Thirty-four patients with stable angina were divided into two groups depending upon the presence or absence of an SII gap of at least 1 min between onset of ST depression and appearance of angina on ETT. Metoprolol (50-100 mg twice daily) and diltiazem (60-120 mg three times daily) were randomly assigned for 6 weeks to patients in each group, and then patients were crossed over for further 6 weeks after a washout period of 2 weeks. Antianginal efficacy was assessed by clinical and exercise parameters. RESULTS: In patients with SII, the clinical responder rate was better with metoprolol than with diltiazem (90 vs. 60%, respectively), and on ETT, metoprolol produced significant improvement in the total exercise time (p< 0.01), time to 1 mm ST depression (p <0.01), time to angina (p <0.01), and a significant decrease in peak rate-pressure product (p<0.001), whereas diltiazem had no significant effect on exercise parameters. However, in patients without SII, metoprolol and diltiazem had a similar clinical responder rate (57%), and both produced a significant increase in total exercise time (p < 0.01), time to 1 mm ST depression (p < 0.01), and time to angina (p < 0.01). In addition, metoprolol had a significant effect on peak rate-pressure product (p < 0.001). CONCLUSION: Silent ischemic interval on ETT can be a predictor of response to antianginal therapy in stable angina, as patients with SII respond better to metoprolol and those without SII respond equally to both metoprolol and diltiazem.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Electrocardiography_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH M_Random_Allocation_MeSH 
****** 11196552
----K E
----T Importance of the atrial channel for ventricular arrhythmia therapy in the dual chamber implantable cardioverter defibrillator.
----A INTRODUCTION: Performance of dual chamber implantable cardioverter defibrillator (ICD) systems has been judged based on functioning of the ventricular tachycardia:supraventricular tachycardia (VT:SVT) discrimination criteria and DDD pacing. The purpose of this study was to evaluate the use of dual chamber diagnostics to improve the electrical and antiarrhythmic therapy of ventricular arrhythmias. METHODS AND RESULTS: Information about atrial and ventricular rhythm in relation to ventricular arrhythmia occurrence and therapy was evaluated in 724 spontaneous arrhythmia episodes detected and treated by three types of dual chamber ICDs in 41 patients with structural heart disease. Device programming was based on clinically documented and induced ventricular arrhythmias. In ambulatory patients, sinus tachycardia preceded ventricular arrhythmias more often than in the hospital during exercise testing. The incidence of these VTs could be reduced by increasing the dose of a beta-blocking agent in only two patients. In five patients in whom sinus tachycardia developed after onset of hemodynamic stable VT, propranolol was more effective than Class III antiarrhythmics combined with another beta-blocking agent with regard to the incidence of VT and pace termination. In all but three cases, atrial arrhythmias were present for a longer time before the onset of ventricular arrhythmias. During atrial arrhythmias, fast ventricular rates before the onset of ventricular rate were observed more often than RR irregularities and short-long RR sequences. Dual chamber diagnostics allowed proper interpretation of detection and therapy outcome in patients with different types of ventricular arrhythmia. CONCLUSION: The advantages of the dual chamber ICD system go further than avoiding the shortcomings of the single chamber system. Information from the atrial chamber allows better device programming and individualization of drug therapy for ventricular arrhythmia.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Defibrillators__Implantable_MeSH S_standards_MeSH Defibrillators__Implantable_standards_MeSH M_Diagnosis__Differential_MeSH M_Electrocardiography_MeSH M_Electrophysiologic_Techniques__Cardiac_MeSH M_Follow-Up_Studies_MeSH M_Heart_Atria_MeSH S_physiopathology_MeSH Heart_Atria_physiopathology_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Sensitivity_and_Specificity_MeSH M_Tachycardia__Sinus_MeSH S_diagnosis_MeSH Tachycardia__Sinus_diagnosis_MeSH S_physiopathology_MeSH Tachycardia__Sinus_physiopathology_MeSH M_Tachycardia__Supraventricular_MeSH S_diagnosis_MeSH Tachycardia__Supraventricular_diagnosis_MeSH S_etiology_MeSH Tachycardia__Supraventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Supraventricular_physiopathology_MeSH S_therapy_MeSH Tachycardia__Supraventricular_therapy_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 11199945
----K I
----T Augmentation of fluoxetine's antidepressant action by pindolol: analysis of clinical, pharmacokinetic, and methodologic factors.
----A In a controlled trial, the beta-adrenoceptor/5-hydroxytryptamine-1A (5-HT1A) receptor antagonist pindolol accelerated and enhanced the antidepressant effect of fluoxetine. The median times to sustained response (> or = 50% reduction of baseline severity maintained until endpoint) were 19 days for fluoxetine plus pindolol (N = 55) and 29 days for fluoxetine plus placebo (N = 56) (p = 0.01). The response rate at endpoint was 16% greater in patients treated with the combination. The plasma concentration of pindolol remained stable between 3 days (first blood sampling) and 6 weeks. Mean values were approximately 26 nM, a concentration higher than the Ki of (-)pindolol for human 5-HT1A autoreceptors (11 nM). Plasma fluoxetine and norfluoxetine concentrations increased steadily until the fourth week of treatment. Fluoxetine concentrations were lower in patients receiving the combination (p = 0.043), but there was no significant relationship to the clinical response in either group. A reanalysis of the data using a survival analysis revealed that significant differences in the time to sustained response between both groups would have also been detected (1) in a 2-week trial, (2) without a placebo lead-in phase, and (3) with less frequent visits. However, the use of "response" instead of "sustained response" as measure of clinically relevant change would have greatly diminished the difference between treatment arms (p = 0.08 instead of p = 0.01). This emphasizes the need of using stringent outcome criteria in antidepressant drug trials. A comparison of the data of all sustained responders (N = 27) in the fluoxetine-plus-placebo group with the first 27 responders in the fluoxetine-plus-pindolol group (of a total of 38) revealed a highly significant difference in the time to sustained response (18 and 10 days, respectively; p = 0.0002). This indicates that the faster response in the fluoxetine-plus-pindolol group is not a result of the greater proportion of responders.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antidepressive_Agents_MeSH S_adverse_effects_MeSH Antidepressive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antidepressive_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Depression__Involutional_MeSH S_drug_therapy_MeSH Depression__Involutional_drug_therapy_MeSH S_metabolism_MeSH Depression__Involutional_metabolism_MeSH S_mortality_MeSH Depression__Involutional_mortality_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_adverse_effects_MeSH Fluoxetine_adverse_effects_MeSH S_pharmacokinetics_MeSH Fluoxetine_pharmacokinetics_MeSH S_therapeutic_use_MeSH Fluoxetine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Methods_MeSH M_Pindolol_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Pindolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11116286
----K E
----T Tedisamil: master switch of nature?
----A Decreasing heart rate is potentially useful in ischaemic heart disease. Tedisamil is a bradycardic agent resulting from its ability to inhibit transient outward current (I(to)) in atria. Tedisamil inhibits I(to), potassium current (IK), K(ATP) and the protein kinase A-activated chloride channel in ventricles as well as vascular IK and Ca(2+)-activated IK (IK((Ca))). Tedisamil prolongs cardiac action potentials and the corrected QT (QTc) of the ECG and also increases cardiac refractoriness. Tedisamil is anti-arrhythmic in animal models of ventricular arrhythmias and atrial flutter. The bradycardic effect of tedisamil is associated with a reduction in myocardial oxygen demand. On isolated rat ventricle, tedisamil is a positive inotrope and on isolated rabbit atria, tedisamil reverses the negative inotropic effect of pinacidil. Tedisamil contracts the isolated rat portal vein and aorta, reduces cromakalim-induced relaxations of contracted rat aorta and increases blood pressure in animals and humans. Tedisamil is 96% bound to plasma proteins, has a plasma half-life of about 10 h and is cleared from the kidney unchanged. Clinical trials have shown that the electrophysiology of tedisamil is that of a class III anti-arrhythmic. In coronary artery disease, tedisamil has no effect on inotropism and increases the threshold for angina. Potassium channel blockade with tedisamil may have advantages over calcium channel blockers or K(ATP) channel openers as an anti-ischaemic mechanism in coronary artery disease. In exercise-induced myocardial ischaemia, beta-blockers are probably favourable to tedisamil, as they will limit the increase in heart rate, contractility and blood pressure caused by sympathetic stimulation, whereas tedisamil will not. In heart failure patients, tedisamil reduces heart rate, but increases blood pressure. The usefulness of tedisamil as a bradycardic agent is limited by the increase in blood pressure. A drug that is bradycardic without increasing blood pressure would be an improvement on tedisamil as the master switch of nature for ischaemic heart disease.
----P Journal_Article Review Review__Tutorial 
----M M_Action_Potentials_MeSH S_drug_effects_MeSH Action_Potentials_drug_effects_MeSH M_Animals_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Bicyclo_Compounds__Heterocyclic_MeSH S_pharmacokinetics_MeSH Bicyclo_Compounds__Heterocyclic_pharmacokinetics_MeSH S_pharmacology_MeSH Bicyclo_Compounds__Heterocyclic_pharmacology_MeSH S_therapeutic_use_MeSH Bicyclo_Compounds__Heterocyclic_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Cyclopropanes_MeSH S_pharmacokinetics_MeSH Cyclopropanes_pharmacokinetics_MeSH S_pharmacology_MeSH Cyclopropanes_pharmacology_MeSH S_therapeutic_use_MeSH Cyclopropanes_therapeutic_use_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Human_MeSH M_Ion_Channels_MeSH S_antagonists_&_inhibitors_MeSH Ion_Channels_antagonists_&_inhibitors_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11122756
----K E
----T Percutaneous coronary intervention versus medical therapy for coronary heart disease.
----A Medical therapy reduces myocardial infarction and death in patients with stable coronary heart disease (CHD). In contrast, there is little evidence available to evaluate the impact of percutaneous coronary intervention (PCI) on hard endpoints in such patients. Four randomized, controlled trials have compared PCI with medical therapy. These studies have demonstrated that PCI results in an improvement in angina and exercise tolerance compared with medical therapy, but they also suggest that medical therapy may be preferable to PCI with respect to the risk of cardiac events. Interpretation of these studies has been limited by small sample size, exclusion of high-risk subjects, no or reduced use of stents, lack of a cost- effectiveness evaluation, and absence of risk factor intervention (except for Atorvastatin versus Revascularization Treatment, which used aggressive low-density lipoprotein lowering with atorvastatin in the medical group only). The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial will permit better definition of the role of PCI in the treatment of stable or recently stabilized patients with CHD.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Heptanoic_Acids_MeSH S_therapeutic_use_MeSH Heptanoic_Acids_therapeutic_use_MeSH M_Human_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_metabolism_MeSH Lipoproteins__LDL_Cholesterol_metabolism_MeSH M_Male_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Pyrroles_MeSH S_therapeutic_use_MeSH Pyrroles_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11124714
----K E
----T Intravenous antiarrhythmic agents.
----A Intravenous antiarrhythmic drugs can be used as diagnostic tools; for example, adenosine can be used to reveal the underlying rhythm in narrow QRS tachycardia. Newer class III antiarrhythmic agents, like ibutilide and dofetilide, are effective at the conversion of acute atrial fibrillation; however, electrical cardioversion is still the most effective method for restoration of sinus rhythm in persistent atrial fibrillation. Lidocaine and bretylium in the treatment and prevention of ventricular tachyarrhythmia are de-emphasized because of inefficacy, safety concerns (lidocaine), or shortage of drug (bretylium). Procainamide is effective for stable ventricular tachycardia, and amiodarone is effective in the treatment of shock-refractory ventricular fibrillation. Adrenergic blockade is likely important in the management of tachyarrhythmias, particularly in electrical storm, but more data will be necessary to establish its role.
----P Journal_Article Review Review__Tutorial 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_diagnostic_use_MeSH Anti-Arrhythmia_Agents_diagnostic_use_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Procainamide_MeSH S_therapeutic_use_MeSH Procainamide_therapeutic_use_MeSH M_Propafenone_MeSH S_therapeutic_use_MeSH Propafenone_therapeutic_use_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH 
****** 11133211
----K E
----T Prognostic implications of intima-media thickness and plaques in the carotid and femoral arteries in patients with stable angina pectoris.
----A BACKGROUND: Ultrasonographic assessments of intima-media thickness and plaques in the carotid artery are widely used as surrogate markers for coronary atherosclerosis, but prospective evaluations are scarce and appear to be lacking in patients with coronary artery disease. Ultrasonographic evaluations of femoral vascular changes have not been studied prospectively. METHODS AND RESULTS: In the Angina Prognosis Study in Stockholm (APSIS), 809 patients with stable angina pectoris were studied prospectively during double-blind treatment with verapamil or metoprolol. Ultrasonographic assessments of intima-media thickness, lumen diameter and plaques in the carotid and femoral arteries were evaluated in a subgroup of 558 patients (182 females) with a mean age of 60 +/-7 years, and related to the risk of cardiovascular death (n = 18) or non-fatal myocardial infarction (n = 26), or revascularization (n = 70) during follow-up (median 3.0 years). Univariate Cox regression analyses showed that carotid intima-media thickness and plaques were related to the risk of cardiovascular death or myocardial infarction. Femoral intima-media thickness was related to cardiovascular death or myocardial infarction, as well as to revascularization, whereas femoral plaques were only related to the latter. After adjustment for age, sex, smoking, previous cardiovascular disease and lipid status, carotid intima-media thickness failed to predict any cardiovascular event, whereas carotid plaques tended (P = 0.056) to predict the risk of cardiovascular death or myocardial infarction. Femoral intima-media thickness (P < 0.01) and plaques (P < 0.05) were also related to the risk of revascularization after adjustments. CONCLUSIONS: Carotid and femoral vascular changes were differently related to cardiovascular events. Carotid intima-media thickness was a weak predictor of events, whereas femoral intima-media thickness predicted revascularization. Plaques in the carotid artery were related to cardiovascular death or non-fatal myocardial infarction, whereas plaques in the femoral artery were related to revascularization. Evaluations of plaques provided better prediction than assessments of intima-media thickness in patients with stable angina.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_ultrasonography_MeSH Angina_Pectoris_ultrasonography_MeSH M_Arteriosclerosis_MeSH S_epidemiology_MeSH Arteriosclerosis_epidemiology_MeSH S_ultrasonography_MeSH Arteriosclerosis_ultrasonography_MeSH M_Carotid_Arteries_MeSH S_ultrasonography_MeSH Carotid_Arteries_ultrasonography_MeSH M_Carotid_Artery_Diseases_MeSH S_epidemiology_MeSH Carotid_Artery_Diseases_epidemiology_MeSH S_ultrasonography_MeSH Carotid_Artery_Diseases_ultrasonography_MeSH M_Coronary_Arteriosclerosis_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH S_ultrasonography_MeSH Coronary_Arteriosclerosis_ultrasonography_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Femoral_Artery_MeSH S_ultrasonography_MeSH Femoral_Artery_ultrasonography_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH M_Tunica_Intima_MeSH S_pathology_MeSH Tunica_Intima_pathology_MeSH M_Tunica_Media_MeSH S_pathology_MeSH Tunica_Media_pathology_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 11150619
----K I
----T The effects of angiotensin receptor antagonists on mortality and morbidity in heart failure--and an interaction with beta blockade.
----A 
----P Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Drug_Interactions_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11198553
----K E
----T [Cost effectiveness of bisoprolol in treatment of heart failure in Germany. An analysis based on the CIBIS-II study]
----A OBJECTIVES: Economic analysis of bisoprolol plus standard therapy versus placebo plus standard therapy in the treatment of chronic heart failure in Germany. MATERIALS AND METHODS: Prospective analysis of resource use and costs by way of integration into the international, randomized, double-blind CIBIS (Cardiac Insufficiency Bisoprolol Study)-II clinical trial, which treated 1,327 patients with bisoprolol and 1,320 with placebo. Two hundred and fifteen German patients were included in CIBIS-II (bisoprolol: 112, placebo: 103). The German health economic subpopulation comprised 97 patients (bisoprolol: 52, placebo: 45). The economic base analysis valued the resource use of every single patient of this subpopulation in monetary terms, from the perspective of Germany's third party payer (statutory sick funds). RESULTS: Mean observation time was 1.3 years. During this time hospitalization costs of DM 783.--were saved in the bisoprolol group. Total direct medical costs amounted to DM 7,651.--in the bisoprolol group and DM 8,905.--in the placebo group. This means savings of DM 1,254.--per patient, or a 14.1% cost reduction. If mean data of all German CIBIS-II patients are used as a broader basis, bisoprolol therapy saves DM 1,203.--per patient. Bisoprolol therapy induced a mortality rate reduction from 17% to 12% in the overall clinical CIBIS-II population (n = 2,647). This difference is statistically highly significant (p < 0.0001). Altogether 74 lives could be saved by bisoprolol therapy. Saved life years amounted to 0.03 per patient after 65 weeks of therapy (460 days), and to 0.12 per patient after 130 weeks (30 months). As bisoprolol therapy leads to net savings, a formal cost-effectiveness analysis, which would relate incremental clinical efficiency to additional costs, is not needed. CONCLUSION: The use of bisoprolol in the therapy of chronic heart failure is not only clinically effective, it also saves net costs.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Cost-Benefit_Analysis_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Germany_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_National_Health_Programs_MeSH S_economics_MeSH National_Health_Programs_economics_MeSH 
****** 11201012
----K I
----T Treatment of arterial hypertension with diuretics, beta- and calcium channel blockers in old patients.
----A Hypertension increases in prevalence with age. Population based studies suggest that more than 50% of people over the age of 65 years may have chronic hypertension. Hypertension, especially systolic hypertension, is the single most common, powerful, however, treatable risk factor for cardiovascular morbidity and mortality in the elderly. In order to assess the effectiveness of antihypertensive drug therapy among the elderly, with diuretics, beta-blockers and calcium channel blockers, a literature search was performed at the Cochrane Library, Medline and Excerpta medica. The Cochrane Hypertension Group identified 14 randomised controlled trials of at least one year duration with 21,785 elderly subjects where diuretics, beta-blockers or calcium channel blockers were used in the treatment group as first line drugs. In their meta-analysis (including one small trial with a central acting antiadrenergic drug) there was a decrease in total mortality (111 vs 129 deaths) and cardiovascular morbidity and mortality (126 vs 177 events) within the treatment group. The three trials restricted to persons with isolated systolic hypertension indicated beneficial effects in the treatment group with regard to cardiovascular morbidity and mortality (104 vs 157 events). Trial data on adverse effects is limited. In three studies, where adverse effects were reported, no substantial differences between treatment and control groups in measures of physical, cognitive and emotional function were found. Cardiovascular benefits of treatment with low dose diuretics or beta-blockers are cleared for elderly subjects with either diastolic or isolated systolic hypertension. Treatment with a long-acting dihydropyridine calcium channel blocker shows beneficial effects in reducing cardiovascular morbidity and mortality for elderly people with isolated systolic hypertension. Due to inconsistent findings in a subgroup meta-analysis of antihypertensive drug treatment in very old people, the efficacy of antihypertensive treatment in these subjects still remains unclear.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 11201013
----K 1
----T The role of ACE inhibitors in the treatment of hypertensive elderly patients.
----A Hypertension has a high prevalence among elderly patients. Randomised trials have already demonstrated that treating healthy older persons with hypertension is highly efficacious. Nevertheless some questions have arisen. On the one hand the generalizability of these trial results, particularly for older persons with serious medical comorbidities and poor functional status, is not clear. On the other hand different antihypertensive drugs have shown to be effective. Which drug for which patient? Even data from randomised intervention trials showing that the treatment affects cardiovascular morbidity and mortality, were missing, ACE inhibitors have been used for more than a decade to treat high blood pressure. For a younger population the captopril prevention project showed no differences between ACE inhibitors and conventional antihypertensive treatment (diuretics, beta-blocker) concerning the primary endpoints (myocardial infarction, stroke and other cardiovascular death). The STOP-2 study also confirmed these results for elderly patients. When treating elderly patients one must be aware of physiological changes with age and the comorbidities. Of significance among this patient group is declining renal function. Admissions for uraemia that are related to the use of ACE inhibitors are still commonplace, although many cases are preventable by monitoring renal function, but guidelines are still missing. Concerning the comorbidities ACE inhibitors have benefits compared to other antihypertensive drugs, especially in cases of heart failure, diabetes and coronary heart disease.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 11204288
----K 5
----T Antihypertensive pharmacogenetics: getting the right drug into the right patient.
----A Pharmacogenetic investigation seeks to identify genetic factors that contribute to interpatient and interdrug variation in responses to antihypertensive drug therapy. Classical studies have characterized single gene polymorphisms of drug metabolizing enzymes that are responsible for large interindividual differences in pharmacokinetic responses to several antihypertensive drugs. Progress is being made using candidate gene and genome scanning approaches to identify and characterize many additional genes influencing pharmacodynamic mechanisms that contribute to interindividual differences in responses to antihypertensive drug therapy. Knowledge of polymorphic variation in these genes will help to predict individual patients' blood pressure responses to antihypertensive drug therapy and may also provide new insights into molecular mechanisms responsible for elevation of blood pressure.
----P Evaluation_Studies Journal_Article Review Review__Academic 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Biotransformation_MeSH S_genetics_MeSH Biotransformation_genetics_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calmodulin-Binding_Proteins_MeSH S_genetics_MeSH Calmodulin-Binding_Proteins_genetics_MeSH S_metabolism_MeSH Calmodulin-Binding_Proteins_metabolism_MeSH M_Clinical_Trials_MeSH M_Cytoskeletal_Proteins_MeSH S_genetics_MeSH Cytoskeletal_Proteins_genetics_MeSH S_metabolism_MeSH Cytoskeletal_Proteins_metabolism_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Pharmacogenetics_MeSH S_methods_MeSH Pharmacogenetics_methods_MeSH M_Polymorphism_(Genetics)_MeSH M_Renin-Angiotensin_System_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11206674
----K I
----T Sexual activity in hypertensive men treated with valsartan or carvedilol: a crossover study.
----A The aim of this study was to compare the effect of antihypertensive treatment with valsartan or cavedilol on sexual activity in hypertensive men who were never treated for hypertension. A total of 160 newly diagnosed hypertensive men (diastolic blood pressure [DBP] > or = 95 mm Hg and < 110 mm Hg), aged 40 to 49 years, all married and without any previous sexual disfunction, were enrolled. After a 4-week placebo period, the patients were divided into two groups: a) 120 patients were randomized to receive carvedilol 50 mg once daily or valsartan 80 mg once daily for 16 weeks according to a double-blind, cross-over design; after another 4-week placebo period, patients were crossed over to the alternative regimen for a further 16 weeks; b) 40 patients were treated with placebo according to a single-blind design for 16 weeks. At the screening visit and every 4 weeks thereafter, blood pressure (BP) was evaluated and patients were interviewed by a questionnaire about their sexual activity. Blood pressure was significantly lowered by both treatments, with a 48% of normalization with valsartan and 45% with carvedilol. During the first month of therapy, sexual activity (assessed as number of sexual intercourse episodes per month) declined with both drugs as compared with baseline, although the decrease was statistically significant in the carvedilol (from 8.2 to 4.4 sexual intercourse episodes, P < .01) but not in the valsartan-treated patients (from 8.3 to 6.6 sexual intercourse episodes, not significant). Ongoing with the treatment the sexual activity further worsened with carvedilol (3.7 sexual intercourse episodes per month) while fully recovered and also improved with valsartan (10.2 sexual intercourse episodes per month). The results were confirmed by the cross-over. Erectile dysfunction was a complaint of 15 patients with carvedilol (13.5%), one patient with valsartan (0.9%), and one patient in the placebo group. These findings suggest that carvedilol induces a chronic worsening of sexual activity, whereas valsartan not only does not significantly worsen sexual activity but may even improve it.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Sexual_Behavior_MeSH S_drug_effects_MeSH Sexual_Behavior_drug_effects_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 11211903
----K E
----T Daily variation of azygos and portal blood flow and the effect of propranolol administration once an evening in cirrhotics.
----A BACKGROUND/AIMS: Esophageal variceal bleeding occur more often at night, however, the mechanism for this remains unclear. This study investigated the daily variation of azygos blood flow (AzBF) and portal blood flow (PBF) and the effects of propranolol administration given once in evening in cirrhotics. METHODS: Blood flow were measured using magnetic resonance imaging. Hemodynamic parameters were determined at 08:00, 16:00 24:00 and again 08:00 h, and were measured at baseline and after 14 days oral administration of propranolol (30 mg, n = 7) or placebo (n = 7) at 19:00 h in 14 patients. RESULTS: A daily fluctuation of AzBF and PBF was observed, peaking at 24:00 h in nine patients. In three other patients, peak AzBF and PBF were observed both at 16:00 and 24:00 h. Two patients were constant throughout the day. When the daily variation was compared, ANOVA showed a significant difference (P < 0.001). Propranolol administration at 19:00 h reduced AzBF (-40.7 +/- 17.9% vs. baseline, P < 0.001) and PBF (-26.5 +/- 10.7% vs. baseline, P < 0.01) at 24:00 h. CONCLUSIONS: We found that in most cirrhotics, AzBF and PBF peaks at midnight. Dosing of propranolol in the evening may be important for its role in preventing variceal bleeding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Azygos_Vein_MeSH S_drug_effects_MeSH Azygos_Vein_drug_effects_MeSH S_physiopathology_MeSH Azygos_Vein_physiopathology_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Magnetic_Resonance_Imaging_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_Vein_MeSH S_drug_effects_MeSH Portal_Vein_drug_effects_MeSH S_physiopathology_MeSH Portal_Vein_physiopathology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH 
****** 11212064
----K E
----T Long-term renal and cardiovascular effects of antihypertensive treatment regimens based upon isradipine, perindopril and thiazide.
----A The aim of this study was to describe the renal function (renal hemodynamics, water and sodium handling) and its relation to cardiovascular structural changes in a population of essential hypertensive patients before and after antihypertensive treatment. Glomerular filtration rate and renal plasma flow were measured by a constant infusion technique. The reference substances used were [131I]iodohippurate (Hippuran) and [125I]iothalamate. The lithium clearance method was used for measuring renal water and sodium handling. Microalbuminuria was measured. A subcutaneous gluteal biopsy was taken and the media thickness to lumen diameter ratio of small resistance vessels was determined. Left ventricular mass index was determined by echocardiography. Thirty-seven patients with newly diagnosed or poorly controlled essential hypertension were randomized to treatment with regimens based upon either isradipine, perindopril or hydrochlorothiazide-amiloride. Atenolol and hydralazine were added as secondary and tertiary drugs, respectively, when needed for normalization of diastolic blood pressure. Investigations were performed before and after 9 months of normalization of blood pressure. Renal function in untreated hypertensive patients was characterized by increased renal vascular resistance, decreased renal blood flow, normal glomerular filtration fraction and normal serum creatinine. No association was found between peripheral resistance vessel structure in subcutaneous vessels and renal hemodynamic parameters. Patients with severe left ventricular hypertrophy (left ventricular mass >360 g) had lower glomerular filtration fraction, greater renal vascular resistance, lower renal blood flow and increased microalbuminuria in comparison with patients with less pronounced cardiac changes. After 1 year of treatment, which had a profound effect on heart and vessel structure, renal hemodynamics were unchanged in patients receiving antihypertensive treatment regimens based on the ACE inhibitor perindopril or the Ca-antagonist isradipine, whereas renal plasma flow was reduced, glomerular filtration rate preserved and filtration fraction significantly increased in those treated with a regimen based on diuretics. The serum creatinine concentration was decreased in the former group, whereas it was unchanged in the latter two. Significantly detrimental effect on uric acid homeostasis was only found in patients treated with a regimen based on diuretics.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Creatine_MeSH S_blood_MeSH Creatine_blood_MeSH S_drug_effects_MeSH Creatine_drug_effects_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH M_Isradipine_MeSH S_administration_&_dosage_MeSH Isradipine_administration_&_dosage_MeSH S_pharmacology_MeSH Isradipine_pharmacology_MeSH M_Kidney_Function_Tests_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH S_pharmacology_MeSH Perindopril_pharmacology_MeSH M_Renal_Circulation_MeSH S_drug_effects_MeSH Renal_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11214707
----K E
----T Development of heart failure in bradycardic sick sinus syndrome.
----A Mounting evidence shows that elevated resting sinus rate is an independent predictor of cardiovascular morbidity and mortality in the general population, in elderly subjects, and in patients with myocardial infarction or hypertension. Therefore, a rather slow sinus rate appears to be a protecting factor acting through several mechanisms. The present contribution focuses on the relationship between sinus rate and heart failure. Its major objectives are to discuss whether in patients with heart failure a rather slow heart rate is advisable and whether a sinus bradycardia secondary to sinus node dysfunction can facilitate the development of heart failure. It has been reported that among patients with left ventricular dysfunction, increased sinus rate was a predictor of cardiovascular death at univariate analysis; however, a multivariate analysis to verify whether sinus rate was an independent predictor of mortality was not performed. Randomized trials carried out by utilizing beta-blockers or amiodarone in patients with heart failure showed that heart rate reduction by these drugs was a marker of their ability to reduce mortality. However, beta-blockers and amiodarone have additional pharmacological effects which interfere with the disease substrate. So, at present, though the results of these trials show that a rather slow sinus rate is advisable, we do not know whether in patients with heart failure sinus rate represents an independent predictor of mortality as in patients with myocardial infarction or hypertension and whether the reduction of sinus rate per se is beneficial. The results of the recent randomized THEOPACE trial showed, for the first time, that in a patient population with symptomatic sinus bradycardia (sinus rate < 50 b/min), an increase in heart rate, induced by DDD pacing or oral theophylline, reduced the incidence of overt heart failure. Therefore, sinus bradycardia seems to play a role in the genesis of heart failure. In a post-hoc analysis of the results of this trial it emerged that in the control (not treated) group, the subjects with sinus bradycardia more prone to develop heart failure were those of old age, about 80 years, with organic heart disease and severe chronotropic incompetence. However, this conclusion needs further validation.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Bradycardia_MeSH S_complications_MeSH Bradycardia_complications_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Risk_Factors_MeSH M_Sick_Sinus_Syndrome_MeSH S_complications_MeSH Sick_Sinus_Syndrome_complications_MeSH S_drug_therapy_MeSH Sick_Sinus_Syndrome_drug_therapy_MeSH M_Survival_Analysis_MeSH 
****** 11214769
----K E
----T Blood pressure responses to whole-body cold exposure: effect of carvedilol.
----A OBJECTIVE: The aim of this study was to test the effects of carvedilol on blood pressure (BP) and heart rate (HR) during whole-body cold exposure in hypertensive and normotensive subjects. METHODS: Ten hypertensive and twelve normotensive subjects were exposed to cold (-15 degrees C, wind 3.5 m/s) three times for 15 min with a 1-week interval between the exposures. The study design was made according to a randomised double-blind, crossover method. Before the cold exposures the subjects ingested carvedilol or placebo once a day (carvedilol 12.5 mg/day for 2 days and then 25 mg/day for 5 days) for 1 week. The systolic (SBP) and diastolic (DBP) blood pressure and HR were measured every 3 min during the test procedures using an indirect ambulatory blood pressure monitor device (ABPM-02, Meditech Co.). RESULTS: In the hypertensive group, the cold exposure increased SBP/DBP from 119/75 mmHg to 143/96 mmHg during carvedilol treatment (P<0.001) and from 132/85 mmHg to 159/106 mmHg during placebo (P<0.001). In the normotensive group the cold exposure increased SBP/DBP from 112/72 mmHg to 142/93 mmHg during carvedilol treatment (P<0.001) and from 121/75 mmHg to 147/98 mmHg during placebo (P<0.001). In the hypertensive group, the levels of SBP, DBP and MAP (mean arterial pressure) were significantly lower with carvedilol than with placebo during the cold exposure although carvedilol did not affect the cold-induced rise of the BP. The BPs were lower also with carvedilol in the normotensive group than the placebo during the cold exposure, but the differences were smaller than in the hypertensive group. Carvedilol decreased the BP more the higher the initial mean SBP/DBP was with placebo during the cold exposure. CONCLUSION: Carvedilol reduced the BP during the cold exposure, especially in the hypertensive subjects but also in normotensive ones, without effect on the cold-induced rise of the BP.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH P_Cold_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heat_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11216954
----K E
----T Dilated cardiomyopathy in dialysis patients--beneficial effects of carvedilol: a double-blind, placebo-controlled trial.
----A OBJECTIVES: The aim of this study was to investigate in dialysis patients with symptomatic heart failure New York Heart Association (NYHA) functional class II or III whether the addition of carvedilol to conventional therapy is associated with beneficial effects on cardiac architecture, function and clinical status. BACKGROUND: Congestive heart failure (CHF) in chronic hemodialyzed patients, particularly when associated with dilated cardiomyopathy, represents an ominous complication and is an independent risk factor for cardiac mortality. METHODS: We enrolled 114 dialysis patients with dilated cardiomyopathy. All patients were treated with carvedilol for 12 months in a double-blind, placebo-controlled, randomized trial. The patients underwent M-mode and two-dimensional echocardiography at baseline, 1, 6 and 12 months after the randomization. Each patient's clinical status was assessed using an NYHA functional classification that was determined after 6 and 12 months of treatment. RESULTS: Carvedilol treatment improved left ventricular (LV) function. In the active-treatment group, the increase in LV ejection fraction (from 26.3% to 34.8%, p < 0.05 vs. basal and placebo group) and the reduction of both LV end-diastolic volume (from 100 ml/m2 to 94 ml/m2, p < 0.05 vs. basal and placebo group) and end-systolic volume (from 74 ml/m2 to 62 ml/m2, p < 0.05 vs. basal and placebo group) reached statistical significance after six months of therapy, compared with baseline and corresponding placebo values, and they remained constant at one year of treatment (p < 0.05 vs. basal and placebo group). The clinical status of patients, assessed by NYHA functional classification, improved during the treatment period. Moreover, at the end of the trial, there were no patients in NYHA functional class IV in the carvedilol group, compared with 5.9% of the patients in the placebo arm. CONCLUSIONS: One year of therapy with carvedilol in dialysis patients with CHF and dilated cardiomyopathy reduces LV volumes and improves LV function and clinical status.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH P_Renal_Dialysis_MeSH 
****** 11216965
----K E
----T Reduction of exercise-induced myocardial ischemia during add-on treatment with the angiotensin-converting enzyme inhibitor enalapril in patients with normal left ventricular function and optimal beta blockade.
----A OBJECTIVES: We sought to study the effect of angiotensin-converting enzyme inhibition on exercise-induced myocardial ischemia. BACKGROUND: Although angiotensin-converting enzyme inhibitors have been shown to reduce ischemic events after myocardial infarction, few data are available regarding their direct anti-ischemic effects in patients with coronary artery disease. METHODS: We studied 43 patients (average age 63 +/- 8 years) with exercise-induced myocardial ischemia (> or =0.1 mV ST depression, despite optimal beta blockade) and normal left ventricular function (ejection fraction >0.50). In a double-blind, placebo-controlled parallel design, patients were treated with angiotensin-converting enzyme inhibitor (enalapril 10 mg twice daily) or placebo. Assessments were made after three weeks (short-term) and 12 weeks (long-term). RESULTS: At baseline, the groups were well matched for all clinical characteristics. After three weeks, there was a slight but not significant increase in time to 0.1 mV ST depression in both groups (p = NS); rate pressure product (RPP = heart rate x systolic blood pressure) was also unaffected. After 12 weeks, however, time to 0.1 mV ST depression further increased in the enalapril group (5.6 +/- 1.9 min) but was unchanged in the placebo group (4.4 +/- 1.3 min; p < 0.05 between groups). In contrast, RPP was not affected. Concentrations of both atrial and brain natriuretic peptides at peak exercise tended to be lower by enalapril, if compared to placebo (p = NS). CONCLUSIONS: Angiotensin-converting enzyme inhibition may reduce exercise-induced myocardial ischemia in patients with normal left ventricular function. Further studies are needed to elucidate the mechanisms involved.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11216977
----K E
----T Efficacy and safety of out-of-hospital self-administered single-dose oral drug treatment in the management of infrequent, well-tolerated paroxysmal supraventricular tachycardia.
----A OBJECTIVES: We tested the efficacy of two drug treatments, flecainide (F) and the combination ofdiltiazem and propranolol (D/P), administered as a single oral dose for termination of the arrhythmic episodes. BACKGROUND: Both prophylactic drug therapy and catheter ablation are questionable as first-line treatments in patients with infrequent and well-tolerated episodes of paroxysmal supraventricular tachycardia (SVT). METHODS: Among 42 eligible patients (13% of all screened for SVT) with infrequent (< or =5/year), well-tolerated and long-lasting episodes, 37 were enrolled and 33 had SVT inducible during electrophysiological study. In the latter, three treatments (placebo, F, and D/P) were administered in a random order 5 min after SVT induction on three different days. RESULTS: Conversion to sinus rhythm occurred within 2 h in 52%, 61%, and 94% of patients on placebo, F and D/P, respectively (p < 0.001). The conversion time was shorter after D/P (32 +/- 22 min) than after placebo (77 +/- 42 min, p < 0.001) or F (74 +/- 37 min, p < 0.001). Four patients (1 placebo, 1 D/P, and 2 F) had hypotension and four (3 D/P and 1 F) a sinus rate <50 beats/min following SVT interruption. Patients were discharged on a single oral dose of the most effective drug treatment (F or D/P) at time of acute testing. Twenty-six patients were discharged on D/P and five on F. During 17 +/- 12 months follow-up, the treatment was successful in 81% of D/P patients and in 80% of F patients, as all the arrhythmic episodes were interrupted out-of-hospital within 2 h. In the remaining patients, a failure occurred during one or more episodes because of drug ineffectiveness or drug unavailability. One patient had syncope after D/P ingestion. During follow-up, the percentage of patients calling for emergency room assistance was significantly reduced as compared to the year before enrollment (9% vs. 100%, p < 0.0001). CONCLUSIONS: The episodic treatment with oral D/P and F, as assessed during acute testing, appears effective in the management of selected patients with SVT. This therapeutic strategy minimizes the need for emergency room admissions during tachycardia recurrences.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Ambulatory_Care_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Flecainide_MeSH S_administration_&_dosage_MeSH Flecainide_administration_&_dosage_MeSH S_adverse_effects_MeSH Flecainide_adverse_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Readmission_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Self_Administration_MeSH P_Self_Care_MeSH M_Tachycardia__Paroxysmal_MeSH S_drug_therapy_MeSH Tachycardia__Paroxysmal_drug_therapy_MeSH M_Tachycardia__Supraventricular_MeSH S_drug_therapy_MeSH Tachycardia__Supraventricular_drug_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 11216978
----K E
----T Lack of efficacy of atenolol for the prevention of neurally mediated syncope in a highly symptomatic population: a prospective, double-blind, randomized and placebo-controlled study.
----A OBJECTIVES: This study was designed to evaluate the efficacy of atenolol for the long-term management of patients with vasovagal syncope. The primary hypothesis was that atenolol is not superior to placebo for the treatment of vasovagal syncope. BACKGROUND: There is no definitive well-controlled analysis of the efficacy of beta-adrenergic blocking agents in patients with recurrent vasovagal syncope. METHODS: This is a prospective, randomized, double-blind, placebo-controlled study. Fifty patients with recurrent vasovagal syncope were included (at least two episodes in the last year). A baseline tilt test was performed. Twenty patients (40%) had a positive tilt test. Intravenous atenolol prevented a second positive tilt in five patients. The patients were randomized to receive either atenolol or a placebo (26 patients atenolol 50 mg/day, 24 patients placebo). The follow-up procedure lasted one year. The primary end point of the study was the time to first recurrence of syncope. RESULTS: In the intention-to-treat analysis, the group treated with atenolol had a similar number of patients with recurrent syncopal episodes as the placebo group. The Kaplan-Meier actuarial estimates of time to first syncopal recurrence showed that the probability of remaining free of syncope drops similarly in both groups and that there was no statistical difference between both curves (patients treated with atenolol vs. the placebo) with a log-rank test p value of 0.4517. CONCLUSIONS: The recurrence of neurocardiogenic syncope in highly symptomatic patients treated with atenolol is similar to that of patients treated with placebo.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Support__Non-U_S__Gov't_MeSH M_Syncope__Vasovagal_MeSH S_etiology_MeSH Syncope__Vasovagal_etiology_MeSH S_prevention_&_control_MeSH Syncope__Vasovagal_prevention_&_control_MeSH M_Tilt-Table_Test_MeSH M_Treatment_Failure_MeSH 
****** 11219471
----K I
----T Comparison of 26-week efficacy and tolerability of telmisartan and atenolol, in combination with hydrochlorothiazide as required, in the treatment of mild to moderate hypertension: a randomized, multicenter study.
----A OBJECTIVE: This study was undertaken to compare the efficacy and tolerability of telmisartan, a novel antihypertensive agent, and atenolol, a well-established beta-blocker, in the treatment of mild to moderate hypertension. METHODS: This 26-week, multicenter, randomized, double-blind, double-dummy, parallel-group, titration-to-response study compared doses of telmisartan (40 mg titrated to 80 mg titrated to 120 mg) with atenolol (50 mg titrated to 100 mg) required to achieve diastolic blood pressure (DBP) control (< or = 90 mm Hg or a decrease from baseline of > or = 10 mm Hg). Open-label hydrochlorothiazide (HCTZ) 12.5 or 25 mg was added if needed according to a prespecified titration rule. Men and women aged > 18 years with mild to moderate hypertension (morning mean supine DBP [SDBP] > or = 95 mm Hg and < or = 114 mm Hg) were eligible to participate. Patients with significant cardiovascular, metabolic, hepatic, or renal dysfunction or chronic obstructive pulmonary disease were excluded. The primary efficacy end point was trough SDBP response at 26 weeks; secondary efficacy end points included changes from baseline at trough in both standing and supine DBP and systolic blood pressure (SBP), and heart rate after 4, 8, 16, and 26 weeks; SBP control (reduction from baseline of > or = 10 mm Hg); normalization of supine SDBP to < or = 90 mm Hg; and the need for add-on HCTZ. Changes in quality of life were also examined. Adverse events were obtained from spontaneous reporting and recorded. Serious adverse events were reported to the sponsor according to predefined timelines. RESULTS: A total of 533 patients from 49 centers participated. Patients' mean age was 57.9 years (range, 22-79 years); 55.9% (298/533) of the population was male and 98.1% (523/533) was white. Of the 533 patients randomly assigned to treatment and included in the safety analysis, 520 (97.6%) were included in the efficacy analysis; 346 received telmisartan and 174 received atenolol. A total of 489 patients (91.7%) completed the study (325 [93.9%], telmisartan; 164 [94.2%], atenolol). Full SDBP response (trough SDBP < or = 90 mm Hg and/or a reduction from baseline of > or = 10 mm Hg) was observed in 84% and 78% of telmisartan- and atenolol-treated patients, respectively; this difference was not statistically significant. Final SBP/DBP reductions of 20.9/14.4 mm Hg were observed for the telmisartan regimen versus 16.7/13.3 mm Hg for the atenolol regimen; only the difference in SBP was significant (P = 0.005). Reduction from baseline in SBP of > or = 10 mm Hg was achieved by 80% of telmisartan-treated and 68% of atenolol-treated patients (P = 0.003). Adverse events were reported by 52.7% of patients given telmisartan and 61.2% of patients given atenolol; this difference was not statistically significant. Most events were mild or moderate. Although fatigue and male impotence were more common in atenolol-treated patients (3.4% and 4.0%, respectively), the incidence of these adverse events was too low to differentiate statistically. CONCLUSIONS: Telmisartan appears to be at least as effective as atenolol in the treatment of mild to moderate hypertension and may be better tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Benzimidazoles_MeSH S_administration_&_dosage_MeSH Benzimidazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Benzimidazoles_adverse_effects_MeSH M_Benzoates_MeSH S_administration_&_dosage_MeSH Benzoates_administration_&_dosage_MeSH S_adverse_effects_MeSH Benzoates_adverse_effects_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11271956
----K I
----T Sotalol vs metoprolol for ventricular rate control in patients with chronic atrial fibrillation who have undergone digitalization: a single-blinded crossover study.
----A AIMS: To compare the effects of sotalol and metoprolol on heart rate, during isotonic (ITE) and isometric (IME) exercise and daily activities, in digitalized patients with chronic atrial fibrillation. METHODS AND RESULTS: The study had a randomized, single-blinded, crossover design. Twenty-three patients with chronic atrial fibrillation received placebo for 4 weeks, followed by a 4-week period of treatment with sotalol and metoprolol in random order. At the end of each period, the patients were assessed with 24-h ECG monitoring, a cardiopulmonary exercise test and a handgrip manoeuvre. Both agents produced a lower heart rate than placebo at rest and at all levels of isotonic exercise (P < 0.001) without affecting oxygen uptake. Sotalol produced a lower heart rate than metoprolol only at submaximal exercise (116 +/- 9 bpm for sotalol vs 125 +/- 11 bpm for metoprolol, P < 0.001). During isometric exercise, sotalol produced a lower maximum heart rate than did metoprolol (113 +/- 22 vs 129 +/- 18 bpm, respectively). Both agents produced a lower mean heart rate than placebo over 24 h (P < 0.001 for all), while sotalol produced a lower mean heart rate than metoprolol during the daytime (P < 0.01). CONCLUSION: Sotalol is a safe and effective agent for control of heart rate in digitalized patients with atrial fibrillation. Sotalol is superior to metoprolol at submaximal exercise, resulting in better rate control during daily activities.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Chronic_Disease_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH 
****** 11174349
----K E
----T Effect of metoprolol on rest and exercise left ventricular systolic and diastolic function in idiopathic dilated cardiomyopathy.
----A OBJECTIVE: To further characterize the effects of heart rate on systolic and diastolic function in patients with idiopathic dilated cardiomyopathy (IDCM), it was hypothesized that the relationship between heart rate and left ventricular systolic and diastolic function would be unaltered by beta-blockade and exercise. METHODS: Eighteen patients with IDCM were randomized in a double-blind manner to receive either metoprolol or placebo for 3 months. Before and after 3 months of therapy, resting and exercise radionuclide left ventriculograms were obtained for assessment of left ventricular systolic and diastolic function. RESULTS: At rest, metoprolol treatment compared with placebo was associated with decreased heart rate (61 +/- 11 vs 99 +/- 10 beats/min, P <.0001) and an increased left ventricular ejection fraction (0.32% +/- 0.10% vs 0.17% +/- 0.08%, P =.01). With exercise, metoprolol compared with placebo caused a decreased heart rate (86 +/- 18 vs 126 +/- 43 beats/min, P =.056), an increase in left ventricular ejection fraction (0.32% +/- 0.14% vs 0.19% +/- 0.07%, P =.052), a longer time to peak filling rate (164 +/- 21 vs 127 +/- 17 ms, P =.005), and a decreased peak filling rate (5.41 +/- 1.71 vs 8.40 +/- 1.85 stroke volumes/s, P =.012). Before beta-blockade, heart rate at rest was negatively correlated to left ventricular ejection fraction and positively correlated to peak filling rate; with exercise, the relationships of heart rate to left ventricular ejection fraction and peak filling rate were similar. After metoprolol treatment, the heart rate continued to have a similar positive correlation with the peak filling rate at rest and with exercise. CONCLUSIONS: In patients with IDCM, systolic and diastolic cardiac function, at rest and with exercise, was related to heart rate. After beta-blockade, at rest and with exercise, diastolic function continued to be related to heart rate.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Cardiomyopathy__Congestive_radionuclide_imaging_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH P_Exercise_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Radionuclide_Ventriculography_MeSH P_Rest_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11165547
----K I
----T Community-wide coronary heart disease mortality in Mexican Americans equals or exceeds that in non-Hispanic whites: the Corpus Christi Heart Project.
----A PURPOSE: Previous comparisons of coronary heart disease mortality between Mexican Americans and non-Hispanic whites have given paradoxic results: despite their adverse cardiovascular risk profiles, especially a greater prevalence of diabetes, Mexican Americans are reported to have lower rates of mortality from coronary heart disease. SUBJECTS AND METHODS: We performed a community-based surveillance among all residents of Nueces County, Texas, aged 25 to 74 years, from 1990 to 1994. All death certificates were obtained and coded, and deaths potentially related to coronary heart disease were selected and validated by standardized methods blinded to ethnicity. Validated in-hospital and out-of-hospital coronary heart disease mortality was compared between 785 Mexican Americans and 862 non-Hispanic white women and men. RESULTS: Validated coronary heart disease mortality in Mexican Americans exceeded that for non-Hispanic whites in the same community. Among women, definite coronary heart disease mortality was 40% greater among Mexican Americans (rate ratio [RR] 1.43, 95% confidence interval [CI]: 1.12 to 1.82), as was all coronary heart disease mortality (RR, 1.32, 95% CI: 1.08 to 1.63). Among men, Mexican Americans had greater rates of all (RR, 1.11; 95% CI: 0.96 to 1.28) and definite coronary heart disease mortality (RR, 1.16; 95% CI: 0.91 to 1.47), but the associations were not statistically significant. CONCLUSIONS: When community-wide mortality rates from coronary heart disease are properly validated, Mexican Americans have rates equal to or higher than those of non-Hispanic whites. Community-based surveillance with validation of coronary heart disease as the cause of death is necessary to avoid the errors that occur with the use of death certificates alone.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_ethnology_MeSH Coronary_Disease_ethnology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_European_Continental_Ancestry_Group_MeSH S_statistics_&_numerical_data_MeSH European_Continental_Ancestry_Group_statistics_&_numerical_data_MeSH M_Female_MeSH M_Hospital_Mortality_MeSH S_trends_MeSH Hospital_Mortality_trends_MeSH M_Human_MeSH M_Male_MeSH M_Mexican_Americans_MeSH S_statistics_&_numerical_data_MeSH Mexican_Americans_statistics_&_numerical_data_MeSH M_Middle_Aged_MeSH M_Population_Surveillance_MeSH M_Reproducibility_of_Results_MeSH M_Sensitivity_and_Specificity_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Texas_MeSH S_epidemiology_MeSH Texas_epidemiology_MeSH 
****** 11176759
----K I
----T Treatment of congestive heart failure: guidelines for the primary care physician and the heart failure specialist.
----A During the past 10 years, the philosophy of heart failure treatment has evolved from symptom control to a combined prevention and symptom-management strategy. Recent clinical trials have proved that early detection can delay progression. Treatment of asymptomatic left ventricular dysfunction is as important as treatment of symptomatic disease. The purpose of this review is to simplify recent guidelines for pharmacological management of chronic systolic heart failure for the primary care physician and the heart failure specialist. Early recognition and prevention therapies, combined with lifestyle modification, are essential in the treatment of heart failure. Therapy with angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics is now standard. Digoxin is added to improve clinical symptoms, especially in patients with atrial fibrillation. Aldosterone antagonists may be recommended in select patients with stable New York Heart Association class III or IV heart failure. If angiotensin-converting enzyme inhibitors are not tolerated, angiotensin receptor blockers, hydralazine hydrochloride, and isosorbide dinitrate are recommended. The data on antiarrhythmic and anticoagulation therapies are inconclusive.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Life_Style_MeSH M_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 11165421
----K E
----T Operational aspects of terminating the doxazosin arm of The Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
----A The Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is a randomized, practice-based trial sponsored by the National Heart, Lung, and Blood Institute (NHLBI). The double-blind, active-controlled component of ALLHAT was designed to determine whether the rate of the primary outcome-a composite of fatal coronary heart disease and nonfatal myocardial infarction-differs between diuretic (chlorthalidone) treatment and each of three other classes of antihypertensive drugs: a calcium antagonist (amlodipine), an angiotensin-converting enzyme inhibitor (lisinopril), and an alpha-adrenergic blocker (doxazosin) in high-risk hypertensive persons ages 55 years and older. In addition, 10,377 ALLHAT participants with mild to moderate hypercholesterolemia were also enrolled in a randomized, open-label trial designed to determine whether lowering serum LDL cholesterol with an HMG CoA reductase inhibitor (pravastatin) will reduce all-cause mortality as compared to a control group receiving "usual care." In January 2000, an independent data review committee recommended discontinuing the doxazosin treatment arm. The NHLBI director promptly accepted the recommendation. This article discusses the steps involved in the orderly closeout of one arm of ALLHAT and the dissemination of trial results. These steps included provisional preparations; the actual decision process; establishing a timetable; forming a transition committee; preparing materials and instructions; informing 65 trial officers and coordinators, 628 active clinics and satellite locations, 313 institutional review boards, over 42,000 patients, and the general public; reporting detailed trial results; and monitoring the closeout process. Control Clin Trials 2001;22:29-41
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M P_Adverse_Drug_Reaction_Reporting_Systems_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Databases__Factual_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_adverse_effects_MeSH Doxazosin_adverse_effects_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_chemically_induced_MeSH Heart_Failure__Congestive_chemically_induced_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_mortality_MeSH Hypercholesterolemia_mortality_MeSH S_prevention_&_control_MeSH Hypercholesterolemia_prevention_&_control_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Pravastatin_MeSH S_adverse_effects_MeSH Pravastatin_adverse_effects_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH M_Risk_Assessment_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH 
****** 11161946
----K 4
----T Therapeutic options for the management of patients with cardiac syndrome X.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aminophylline_MeSH S_therapeutic_use_MeSH Aminophylline_therapeutic_use_MeSH M_Analgesics_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Estrogen_Replacement_Therapy_MeSH M_Human_MeSH M_Imipramine_MeSH S_therapeutic_use_MeSH Imipramine_therapeutic_use_MeSH M_Nicorandil_MeSH S_therapeutic_use_MeSH Nicorandil_therapeutic_use_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Syndrome_X_MeSH S_drug_therapy_MeSH Syndrome_X_drug_therapy_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11161949
----K E
----T Cardiac risk factors, medication, and recurrent clinical events after acute coronary disease; a prospective cohort study.
----A AIMS: Systematic data are sparse on clinical outcome after acute coronary disease followed by cardiac rehabilitation therapy. Therefore, our objective was to determine the long-term development of cardiac risk factors, recurrent clinical events, and cardiac medication in patients undergoing routine in hospital cardiac rehabilitation therapy. METHODS AND RESULTS: In the prospective PIN Study (Post Infarct Care), 2441 consecutive patients (78% men, 60+/-10 years, 22% women, 65+/-10 years) were enrolled in 18 inpatient rehabilitation centres in Germany following myocardial infarction (56%), coronary artery bypass graft (38%) or percutaneous transluminal coronary angioplasty (6%). Cardiac risk factors, pre-specified clinical end-points, and the prescription of cardiac medication were prospectively documented on admission to and at discharge from rehabilitation therapy, and 3, 6 and 12 months later by obtaining information with standardized questionnaires from the patients and their physicians. The cardiac risk factors improved initially during cardiac rehabilitation therapy, but deteriorated within the following 12 months: 39% patients smoked at the beginning vs 5% at the end of in hospital rehabilitation vs 10% at 12 months follow-up (P<0.001). The respective numbers for patients with blood pressure >140 and/or 90 mmHg were 24 vs 8 vs 25% (P<0.01) and with plasma cholesterol >200 mg. dl(-1)57 vs 29 vs 51% (P<0.01). A total of 886 patients experienced one or more recurrent clinical events during the first year, 69% of those within the initial 6 months. At 12 months follow-up, 77% of patients received aspirin, 70% beta-blockers, 62% lipid lowering medication, and 53% angiotensin converting enzyme inhibitors. CONCLUSION: The present results indicate that the benefit of cardiac rehabilitation therapy following acute coronary events is only partially maintained during the following year. Continuous strategies of medical care need to be developed to improve the long-term outcome in coronary patients.
----P Journal_Article 
----M M_Aged_MeSH M_Blood_Pressure_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_rehabilitation_MeSH Coronary_Disease_rehabilitation_MeSH M_Female_MeSH M_Human_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_analysis_MeSH Lipoproteins__HDL_Cholesterol_analysis_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_analysis_MeSH Lipoproteins__LDL_Cholesterol_analysis_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11179247
----K 5
----T Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Ascites_MeSH S_therapy_MeSH Ascites_therapy_MeSH M_Bacterial_Infections_MeSH S_therapy_MeSH Bacterial_Infections_therapy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Hepatorenal_Syndrome_MeSH S_therapy_MeSH Hepatorenal_Syndrome_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Peritonitis_MeSH S_therapy_MeSH Peritonitis_therapy_MeSH M_Recurrence_MeSH 
****** 11182177
----K E
----T Effect of bisoprolol on QT dispersion in patients with congestive heart failure--the etiology-dependent response.
----A AIMS: To evaluate the effect of beta1-selective blocker bisoprolol on the QT and QTc dispersion in patients with chronic heart failure and to compare the responses to bisoprolol in patients with different etiologies. METHODS AND RESULTS: Eighty-one patients with heart failure secondary to ischemic heart disease (n=47) or idiopathic dilated cardiomyopathy (n=34) were stratified by etiology and then randomly assigned to the bisoprolol and control group (no tablet) on top of the conventional treatment. QT dispersion was calculated by subtracting the shortest QT from the longest QT, in absolute value (Qtmax-Qtmin). It was also corrected with Bazett's formula (QTc dispersion). After 6 weeks of treatment, QT and QTc dispersion were significantly decreased in the bisoprolol group (QT dispersion: 66.5+/-13.4 ms vs. 49.1+/-16.8 ms for ischemic heart disease (P<0.01); 67.5+/-12.4 ms vs. 59.4+/-14.4 ms for dilated cardiomyopathy (P<0.05); QTc dispersion: 78.3+/-15.2 ms vs. 53.3+/-18.1 ms for ischemic heart disease (P<0.01); 79.1+/-14.2 ms vs. 69.0+/-17.9 ms for dilated cardiomyopathy (P<0.05)), but there was no significant decrease of QT and QTc dispersion in the control group. Linear regression analysis showed that patients with ischemic heart disease tend to have lower 6-week QT dispersion than patients with dilated cardiomyopathy (coefficient beta=-0.283, P=0.009) after controlling for their baseline values in the bisoprolol group. CONCLUSION: These findings suggested that bisoprolol reduces QT and QTc dispersion in patients with chronic heart failure, but the etiology of heart failure affects the response of patients to bisoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH M_Female_MeSH M_Heart_Conduction_System_MeSH S_drug_effects_MeSH Heart_Conduction_System_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH 
****** 11175972
----K E
----T Endoscopic treatment of patients with portal hypertension.
----A This article discusses endoscopic treatment of patients with sequelae from portal hypertension. The literature on endoscopic therapy for primary and secondary prophylaxis of esophageal varices is reviewed. Therapeutic approaches to less commonly seen entities, such as portal gastropathy and portal colopathy, are discussed.
----P Journal_Article Review Review__Tutorial 
----M P_Endoscopy__Gastrointestinal_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_surgery_MeSH Gastrointestinal_Hemorrhage_surgery_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_surgery_MeSH Hypertension__Portal_surgery_MeSH M_Ligation_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Sclerotherapy_MeSH 
****** 11182704
----K E
----T Iodine-123 MIBG imaging before treatment of heart failure with carvedilol to predict improvement of left ventricular function and exercise capacity.
----A BACKGROUND. We examined whether cardiac sympathetic imaging with iodine-123 metaiodobenzylguanidine (MIBG) would predict improvement of left ventricular (LV) function and exercise capacity in patients with heart failure after treatment with carvedilol. METHODS AND RESULTS. Eighteen patients with heart failure and 5 control subjects underwent I-123 MIBG imaging. Heart-to-mediastinum ratios at 20 minutes and 3 hours and myocardial washout rates (WR) were measured. Of the 18 patients, 11 were randomized to receive carvedilol medication, whereas the remaining 7 received a placebo. Only the carvedilol group demonstrated a significant improvement in both heart failure functional class and LV ejection fraction (EF) 1 year after the start of medication. Within the carvedilol group, MIBG WR showed a significant inverse correlation with improvement in LVEF (rho = -0.74, P =.02). The diagnostic accuracy of WR for predicting EF response to carvedilol was 91%. WR also appeared to be inversely related to the peak oxygen consumption rate (rho = -0.65, P =.08), although this did not reach statistical significance. CONCLUSION. I-123 MIBG imaging appears useful in predicting which patients with heart failure are likely to show the most improvement in LV function and exercise capacity after carvedilol treatment. Further studies in this area appear to be warranted.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_3-Iodobenzylguanidine_MeSH S_diagnostic_use_MeSH 3-Iodobenzylguanidine_diagnostic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Echocardiography_MeSH M_Exercise_Test_MeSH P_Exercise_Tolerance_MeSH M_Female_MeSH M_Gated_Blood-Pool_Imaging_MeSH M_Heart_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Failure__Congestive_radionuclide_imaging_MeSH M_Human_MeSH M_Iodine_Radioisotopes_MeSH S_diagnostic_use_MeSH Iodine_Radioisotopes_diagnostic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11157688
----K E
----T Sex differences in the prognosis of congestive heart failure: results from the Cardiac Insufficiency Bisoprolol Study (CIBIS II).
----A BACKGROUND: Whether female sex is associated with a better prognosis in patients with congestive heart failure (CHF) remains uncertain. The Cardiac Insufficiency Bisoprolol Study (CIBIS) II showed that bisoprolol reduced all-cause mortality and morbidity rates in CHF patients treated with diuretics and ACE inhibitors. We examined whether survival was different in men (n=2132) and women (n=515) enrolled in CIBIS II. METHODS AND RESULTS: Women differed from men with regard to age, NYHA functional classification, primary cause of CHF, and risk factors such as left bundle-branch block. After adjustment for baseline differences, the probability of all-cause mortality was significantly reduced by 36% in women compared with that in men (hazard ratio 0.64, 95% CI 0.47 to 0.86, P:=0.003). Women also had a 39% reduction in cardiovascular deaths (hazard ratio 0.64, 95% CI 0.45 to 0.91, P:=0.01) and a 70% reduction in deaths from pump failure (hazard ratio 0.30, 95% CI 0.13 to 0.70, P:=0.005) compared with men. Kaplan-Meier survival analysis revealed a significant reduction in all-cause mortality among women treated with bisoprolol compared with men (6% versus 12% P:=0.01) but not among women treated with placebo (13% versus 18%, P:=0.10). However, this sex/ss-blocker effect was not significant in multivariate analysis. CONCLUSIONS:These results indicate that regardless of ss-blocker treatment and baseline clinical profile, female sex is a significant independent predictor of survival in patients with CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Prognosis_MeSH M_Sex_Factors_MeSH M_Survival_Analysis_MeSH 
****** 11171788
----K I
----T Effects of early use of atenolol or captopril on infarct size and ventricular volume: A double-blind comparison in patients with anterior acute myocardial infarction.
----A BACKGROUND: beta-Blockers and ACE inhibitors reduce early mortality when either one is started in the first hours after myocardial infarction (MI). Considering the close correlation between morphological changes and prognosis, we aimed to investigate whether the benefit of both beta-blockers and ACE inhibitors might reside in a similar protective effect on infarct size or ventricular volume. METHODS AND RESULTS: In a randomized, double-blind comparison between early treatment with captopril or atenolol in 121 patients with acute anterior MI, both drugs showed a similar reduction in mean blood pressure. However, only the atenolol-treated patients showed a significant early reduction in heart rate. Infarct size, obtained from the perfusion defect in resting single photon emission imaging, was higher in captopril-treated patients than in atenolol-treated patients: 29.8+/-12% versus 20.8+/-12% (P:<0.01) by polar map and 28.3+/-13% versus 20.0+/-13% (P:<0.01) by tomography. Changes from baseline to 1 week and to 3 months in ventricular end-diastolic volume, assessed by echocardiography, were as follows: 58+/-14 versus 64+/-19 (P<0.05) and 65+/-21 mL/m(2) (P<0.05), respectively, with captopril, and 58+/-18 versus 64+/-18 (P<0.05) and 69+/-30 mL/m(2) (P<0.05), respectively, with atenolol. Neither group showed significant changes in end-systolic volume. Among patients with perfusion defect >18% (n=51), those treated with atenolol showed a significant increase of end-systolic and end-diastolic ventricular volumes, whereas captopril-treated patients did not. CONCLUSIONS: Although early treatment with atenolol or captopril results in similar overall short- and medium-term preservation of ventricular function and volumes, in patients with larger infarctions, a beta-blocker alone does not adequately protect myocardium from ventricular dilatation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_radionuclide_imaging_MeSH Myocardial_Infarction_radionuclide_imaging_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH M_Tomography__Emission-Computed__Single-Photon_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH 
****** 11163733
----K E
----T Autonomic dysfunction in patients with mild heart failure and coronary artery disease and the effects of add-on beta-blockade.
----A AIM: Autonomic impairment is related to the incidence of sudden death in chronic heart failure (CHF). Our objective was to study autonomic profiles in patients with mild CHF due to coronary artery disease, and to investigate the value of add-on beta-blockade. METHODS AND RESULTS: Measures of autonomic function (plasma norepinephrine, heart rate [HR] variability, autonomic function testing), and exercise capacity, were compared between 24 patients with mild CHF, and 24 healthy controls. In this mechanistic study, we assessed the effect of 26 weeks metoprolol treatment in a double-blind, randomized, placebo-controlled design. All patients received metoprolol sustained release (200 mg; n=12) or placebo (n=12). Assessments were made at baseline and after 10 and 26 weeks' treatment. At baseline, norepinephrine levels were elevated, while HR variability parameters were decreased in patients vs. controls (both P<0.05). Autonomic function testing showed only small differences, although significant alterations were observed with deep breathing and head up tilting (both P<0.05). After 26 weeks', metoprolol did not affect exercise capacity or norepinephrine concentrations. In contrast, HR variability was markedly improved in metoprolol-treated patients vs. placebo-treated patients (P<0.05). In particular, a shift toward normal in the sympathovagal balance was observed (P<0.05). Autonomic function testing showed only small, and generally non-significant trends after metoprolol. CONCLUSIONS: Marked autonomic abnormalities are already present in mild CHF, which may be (partially) reversed by metoprolol. These observations support the reported reduction of sudden death by beta-blockade in patients with CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Autonomic_Nervous_System_physiopathology_MeSH M_Case-Control_Studies_MeSH M_Chronic_Disease_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11163746
----K I
----T Clinical trials update: highlights of the scientific sessions of the American Heart Association year 2000: Val HeFT, COPERNICUS, MERIT, CIBIS-II, BEST, AMIOVIRT, V-MAC, BREATHE, HEAT, MIRACL, FLORIDA, VIVA and the first human cardiac skeletal muscle myoblast transfer for heart failure.
----A This article continues a series of reports summarising recent research developments pertinent to the topic of heart failure. This is a summary of presentations made at scientific sessions of the American Heart Association in November 2000. Clinical studies of particular interest to people caring for patients with heart failure include Val-HeFT, AMIOVIRT and V-MAC. New data from beta-blockers trials are reviewed, highlights from some important developments in post-infarction care, including MIRACL and FLORIDA, discussed and results of some early studies of gene therapy reported.
----P Clinical_Trial Congresses Randomized_Controlled_Trial 
----M M_Animals_MeSH P_Clinical_Trials_MeSH M_Defibrillators__Implantable_MeSH M_Gene_Therapy_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Muscle__Skeletal_MeSH S_cytology_MeSH Muscle__Skeletal_cytology_MeSH 
****** 11220350
----K E
----T Sulphonylurea dose-response relationships: relation to clinical practice.
----A AIM: The evaluation of serum triglyceride levels has played an important role as an independent method for assessing the risk factor for coronary atherosclerosis. Fibrates, nicotinic acid, and omega-3 polyunsaturated fish oils are the pharmacological tools most used today against hypertriglyceridaemia. Acarbose is a pseudotetrasaccharide of microbial origin which exerts a competitive, selective and reversible inhibition of the intestinal alpha glucoside-hydrolase. We evaluated the efficacy and side-effects of acarbose as a new and alternative drug in the treatment of hypertriglyceridaemia in non-diabetic patients. METHODS: We enrolled 30 non-diabetic patients (18 men, 12 women; mean age 59.23 +/- 6.27 years) without a family history of diabetes mellitus affected by familial hypertriglyceridaemia. The study covered a total period of 6.5 months: half of the patients were on 1.5 months of 'run in' diet only followed by 5 months of therapeutic diet plus acarbose; and half were on the therapeutic diet plus placebo. We gave 30 dividable pills to all patients. The administration was as follows: half a pill before lunch and half a pill before dinner while on the 'run in' diet. Fifteen patients (group A) took acarbose while the reminder (group B) took a placebo (50 mg of starch); these were distributed randomly and the test was double blind. The 20 weeks of study were divided in five 4-week periods. Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-c), LDL-cholesterol (LDL-c) and glucose were determined at the starting of the study and after each treatment cycle. Glucose values were determined 2 h after lunch at the beginning of the study and at the end of the first, third and fifth month of treatment. All parameters assessed have been analysed by anova. RESULTS: The serum total cholesterol, LDL-c levels observed in the two groups did not change during the course of treatment. We observed a noteworthy progressive reduction of mean baseline triglyceride levels until the fourth month (p < 0.05) in acarbose-treated patients, with an increase in HDL-c (p < 0.008). CONCLUSIONS: We maintain that acarbose may be a useful therapeutic tool in addition to the diet in order to reduce triglyceride serum levels in non-diabetic patients.
----P Journal_Article Review Review__Tutorial 
----M M_Area_Under_Curve_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Human_MeSH M_Hypoglycemic_Agents_MeSH S_adverse_effects_MeSH Hypoglycemic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Safety_MeSH M_Sulfonylurea_Compounds_MeSH S_adverse_effects_MeSH Sulfonylurea_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonylurea_Compounds_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11273288
----K E
----T Angiotensin converting enzyme inhibitors and cough--a north Indian study.
----A Cough is an important side effect of Angiotensin Converting Enzyme Inhibitor (ACEI) therapy. The incidence of cough was investigated in a prospective 8 week study in 250 hypertensive patients receiving ACEI alone or in combination with other agents. Enalapril (5-20 mg/day), Lisinopril (5-20 mg/day), Captopril (25-75 mg/day) or Ramipril (5-15 mg/day) was prescribed to patients, who were followed up at weekly visits. Cough developed in 73 of the 250 patients i.e. an incidence of 29.2%. Females had a higher incidence of cough as compared to males--37.9% versus 15.5% (p < 0.001) and there was no significant difference in the cough incidence in the various age groups. A dry, non-productive cough developed in all patients within 4 weeks of ACEI initiation. Increased nocturnal intensity of cough was reported by 79.4% patients. Cough incidence was 34.4%, 24.3% and 18.1% in patients on Enalapril, Ramipril and Lisinopril, respectively. Cough was not dose related and was not related to smoking. There was no statistically significant difference among patients on ACEI alone or in combination with beta blockers, calcium channel blockers or diuretics. Of the 18 patients with ACEI induced cough who received Indomethacin, 50 mg bid, 8 reported complete cure and cough was reduced in intensity in the remaining ten.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cough_MeSH S_chemically_induced_MeSH Cough_chemically_induced_MeSH S_drug_therapy_MeSH Cough_drug_therapy_MeSH S_epidemiology_MeSH Cough_epidemiology_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_India_MeSH S_epidemiology_MeSH India_epidemiology_MeSH M_Indomethacin_MeSH S_administration_&_dosage_MeSH Indomethacin_administration_&_dosage_MeSH M_Lisinopril_MeSH S_adverse_effects_MeSH Lisinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Ramipril_MeSH S_adverse_effects_MeSH Ramipril_adverse_effects_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Risk_Assessment_MeSH 
****** 11224723
----K 4
----T The pros and cons of different prostanoids in the medical management of glaucoma.
----A The prostaglandin analogs are new exciting drugs added to the therapeutic armamentarium for patients with glaucoma. Several studies have evaluated the ocular hypotensive properties and side effects of latanoprost in different forms of glaucoma. This drug, seems to be the most effective intraocular pressure (IOP)-reducing agent currently available, and has a low incidence of ocular and systemic side effects. Fewer data are available regarding unoprostone, but the IOP-reducing effect of this drug seems to be comparable or slightly inferior to that of timolol and it produces fewer side effects. When compared with unoprostone, latanoprost has been shown to effect a greater reduction in IOP. A major drawback to the use of prostaglandin analogues is the lack of long-term experience such as that currently available for other classes of agents.
----P Evaluation_Studies Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Dinoprost_MeSH S_administration_&_dosage_MeSH Dinoprost_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Dinoprost_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Dinoprost_therapeutic_use_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Ophthalmic_Solutions_MeSH M_Prognosis_MeSH M_Prostaglandins_MeSH S_administration_&_dosage_MeSH Prostaglandins_administration_&_dosage_MeSH S_therapeutic_use_MeSH Prostaglandins_therapeutic_use_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11224003
----K E
----T Improvement of patients' knowledge by a single educational meeting on hypertension.
----A OBJECTIVES: A poor therapeutic compliance is a major cause of insufficient control of hypertension. As education of patients is fundamental in order to improve their compliance, we organised two pilot educational meetings aimed at (1) assessing the support of patients to this kind of meetings, and (2) verifying the impact on patient's education. METHODS: We invited 225 consecutive patients referred to our Hypertension Clinic (some of them regularly followed up and some referred for the first time) to participate to an educational meeting on hypertension. Patients were divided in two groups, for organising reasons each attending a single meeting. Each meeting included four sessions: (1) the first session included a multiple choice questionnaire (nine questions, with answers collected by an interactive electronic system) in order to evaluate the degree of patient's information about hypertension (definition, prevalence, aetiology, complications and treatment), (2) a traditional teaching session, (3) an interactive phase aimed to assess the improvement of knowledge in which the same questions as in the first session have been asked again, and (4) a general discussion session. RESULTS: A total of 144 patients (mean age 54 +/- 12 years; 76 M, 68 F) of the 225 invited attended the meeting. The answers to our questions in the initial session were correct in a percentage ranging from 60% to 80%. During the third phase immediately after the teaching session, the percentage of correct answers increased significantly (range: 75--98%, P < 0.05 at least in all questions). CONCLUSIONS: This study shows: (1) a satisfactory adherence of patients to this educational initiative; (2) a positive impact of a single educational meeting on patient's knowledge about issues related to hypertension. The potential role of improving patient's education on clinical outcomes such as blood pressure levels and the rate of blood pressure control requires future controlled studies. Journal of Human Hypertension (2001) 15, 57-61
----P Journal_Article 
----M M_Human_MeSH M_Hypertension_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Italy_MeSH P_Patient_Education_MeSH M_Prevalence_MeSH 
****** 11222470
----K E
----T Beneficial effects of pentoxifylline in patients with idiopathic dilated cardiomyopathy treated with angiotensin-converting enzyme inhibitors and carvedilol: results of a randomized study.
----A BACKGROUND: We previously reported beneficial effects of pentoxifylline, a xanthine-derived agent known to inhibit the production of tumor necrosis factor-alpha, in patients with idiopathic dilated cardiomyopathy treated with diuretics, digoxin, and ACE inhibitors. Since then, 3 large clinical trials showed important clinical benefits of beta-blockers in this population. Therefore, we designed the present study to establish whether in patients with heart failure already receiving treatment with ACE inhibitors and beta-blockers, the addition of pentoxifylline would have an additive beneficial effect. METHODS AND RESULTS: In a single-center, prospective, double-blind, randomized, placebo-controlled study, 39 patients with idiopathic dilated cardiomyopathy were randomized to pentoxifylline 400 mg TID (n=20) or placebo (n=19) if they had a left ventricular ejection fraction <40% after 3 months of therapy with digoxin, ACE inhibitors, and carvedilol. Primary end points were New York Heart Association functional class, exercise tolerance, and left ventricular function. Patients were followed up for 6 months. Five patients died (3 in the placebo group). Patients treated with pentoxifylline had a significant improvement in functional class compared with the placebo group (P:=0.01), with an increment in exercise time from 9.5+/-5 to 12.3+/-6 minutes (P:=0.1). Left ventricular ejection fraction improved from 24+/-9% to 31+/-13%, P:=0.03, in the treatment group. CONCLUSIONS: In patients with idiopathic dilated cardiomyopathy, the addition of pentoxifylline to treatment with digoxin, ACE inhibitors, and carvedilol is associated with a significant improvement in symptoms and left ventricular function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antigens__CD95_MeSH S_metabolism_MeSH Antigens__CD95_metabolism_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_immunology_MeSH Cardiomyopathy__Congestive_immunology_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pentoxifylline_MeSH S_therapeutic_use_MeSH Pentoxifylline_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Tumor_Necrosis_Factor_MeSH S_metabolism_MeSH Tumor_Necrosis_Factor_metabolism_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11239855
----K E
----T Assessing and reducing cardiac risks of noncardiac surgery.
----A 
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Human_MeSH M_Postoperative_Complications_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Risk_Factors_MeSH 
****** 11246837
----K E
----T Hypertension control improved through patient education. Chinese PEP Investigators.
----A OBJECTIVE: To evaluate the effects of patient education for hypertension on hypertension control. METHODS: Of 169 eligible patients (systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg), 60 were assigned to educational group (group E, antihypertensive drug treatment with an addition of patient education) and 109 to routine group (group R, antihypertensive drug treatment alone). The average follow-up approximated to 3 years. RESULTS: The blood pressure was reduced from at baseline and sustained in the three-year follow-up by 20/13 mmHg in group E and by 22/13 mmHg in group R. For this similar blood pressure reduction, about 10 mg less of metoprolol and 6 mg less of nitrendipine were used in group E than in group R. The percentage of the patients in whom goal blood pressure (under 160/90 mmHg) was achieved during follow-up was higher and progressively increased in group E (1st year: 65%, 2nd year: 72%) in comparison with in group R (1st year: 45%; 2nd year: 55%). Body weight was significantly reduced by 1.36 and 1.81 kg from at baseline to at the 1st and 2nd year repeated measurements in group E. The significant reduction from at baseline to at the 2nd year was significantly different from that in group R (P = 0.02). For 24-hour urinary sodium excretion, it was decreased in the group E, whereas it was increased in the group R. The cumulative rates of hypertension-related complications were 4.43% in group E and 7.02% in group R (absolute difference = 2.59%, P = 0.48). The rate of missed appointments was somewhat higher in group R (10%) than in group E (7%) during the first year but lower in the 2nd and 3rd year (R vs E: 10% vs 2% in the 2nd year; 8% vs 2% in the 3rd year). Four patients lost to follow-up in group R (6.87%) and 1 patient in group E (1.74%, P = 0.08). CONCLUSION: The findings of this study suggest that patient education is of some benefits to the hypertension control.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nitrendipine_MeSH S_therapeutic_use_MeSH Nitrendipine_therapeutic_use_MeSH P_Patient_Education_MeSH M_Relaxation_Techniques_MeSH 
****** 11244515
----K E
----T Further insights into coronary debulking: the EUROCARE trial of directional atherectomy and the PACT trial of pullback atherectomy.
----A Although the principle of reducing plaque load in the coronary artery remains very appealing, clinical benefit from debulking devices has not been demonstrated unequivocally. Other approaches to prevent restenosis had been the application of various pharmacological agents. Unfortunately, the majority of clinical studies have not reproduced the promising results observed in the experimental laboratories. New frontiers in improving atherectomy devices and in optimizing concomitant medical treatment are currently being explored. We report on the EUROCARE trial investigating the possible benefit of carvedilol after coronary atherectomy, and the Pullback Atherectomy (PAC) pilot trial using a novel atherectomy device.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antioxidants_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH P_Atherectomy__Coronary_MeSH S_instrumentation_MeSH Atherectomy__Coronary_instrumentation_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Coronary_Arteriosclerosis_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH S_therapy_MeSH Coronary_Arteriosclerosis_therapy_MeSH M_Equipment_Design_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11246060
----K E
----T Perceived benefit after participating in positive or negative/neutral heart failure trials: the patients' perspective.
----A BACKGROUND: Clinical trials, the gold standard for the evaluation of new therapeutic strategies, may prove a drug to be beneficial, harmful or neutral according to its effect on the end-point(s) under study. AIMS: To study the reaction and perspective of the patients participating in a clinical heart failure trial, particularly in relation to whether the trial subsequently proved to be positive, negative or neutral. METHODS: Anonymous self-completed questionnaire was sent to 78 and returned by 70 consecutive patients 1--6 months after participating in six clinical heart failure trials. The trial was neutral or negative regarding the primary end-point in four (47 patients) of the six studies (MACH-1 trial of mibefradil, REACH trial of bosentan, CASCO trial of calcium sensitizer, ecadotril trial of neutral endopeptidase inhibitor) and positive in two (23 patients) (ICARUS Israel carvedilol study, exercise study of candesartan cilexetil). RESULTS: Most patients reported subjective global clinical benefit (78% for positive, 74% for negative or neutral trial, NS) after participating in a clinical trial. After adjustment for age, sex, level of education, previous research, perceived comprehension, and treatment allocation (active drug/placebo) in a stepwise regression model, perceived global improvement was greater in older patients (P=0.02), after participation in a positive trial (P=0.05) and in females (P=0.07). The major reason given by the patient for perceived clinical improvement was better follow-up, some believed it was due to change in medication, particularly those who had participated in a positive trial. CONCLUSIONS: More than 70% of patients participating in clinical trials of new drugs for heart failure reported perceived global improvement. Clinical improvement was greater in, but not limited to, patients who participated in positive trials. These salutary findings support the continued recruitment of patients to clinical heart failure trials.
----P Journal_Article 
----M M_Aged_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_psychology_MeSH Heart_Failure__Congestive_psychology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Education_MeSH P_Patient_Participation_MeSH P_Patient_Satisfaction_MeSH M_Placebo_Effect_MeSH P_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 11246064
----K E
----T Poles apart, but are they the same? A comparative study of Australian and Scottish patients with chronic heart failure.
----A This paper reports on an international comparison of the characteristics, treatment and health outcomes of chronic heart failure (CHF) patients discharged from acute hospital care in Australia and Scotland. The baseline characteristics and treatment of 200 CHF patients recruited to a randomised study of a non-pharmacological intervention in Australia and 157 CHF patients concurrently recruited to a similar study in Scotland were compared. Subsequent health outcomes (including survival and readmission) within 3 months of discharge in those patients who received usual post-discharge care in Australia (n=100) and Scotland (n=75) were also compared. Individuals in both countries were predominantly old and frail with significant comorbidity likely to complicate treatment. Similar proportions of Australian and Scottish patients were prescribed either a 'high' (20 vs. 18%) or medium (64 vs. 66%) dose of an angiotensin-converting enzyme inhibitor. Proportionately more Australian patients were prescribed a long-acting nitrate, digoxin and/or a beta-blocker. At 3 months post-discharge, 57 of the 100 (57%: 95% CI 47--67%) Australian and 37 of the 75 (49%: 95% CI 38--61%) Scottish patients assigned to 'usual care' remained event-free (NS). Similarly, 15 vs. 12% required > or =2 unplanned readmission (NS) and 16 vs. 19% of Australian and Scottish patients, respectively, died (NS). Australian and Scottish patients accumulated a median of 0.6 vs. 0.9 days, respectively, of hospitalisation/patient/month (NS). On multivariate analysis (including country of origin), unplanned readmission or death was independently correlated with severe renal impairment (adjusted odds ratio 4.4, P<0.05), a previous hospitalisation for CHF (2.3, P<0.05), longer index hospitalisation (2.7 for >10 days, P<0.05) and greater comorbidity (1.3 for each incremental unit of the Charlson Index, P=0.05). Health outcomes among predominantly old and frail CHF patients appear to be independent of the health-care system in which the patient is managed and more likely to be dependent on the syndrome itself.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Australia_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH M_Chronic_Disease_MeSH M_Comorbidity_MeSH M_Comparative_Study_MeSH P_Cross-Cultural_Comparison_MeSH M_Disease_Progression_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Scotland_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 11252291
----K E
----T A systematic review of the use of triptans in acute migraine.
----A OBJECTIVE: A systematic review of the literature was undertaken, to consolidate evidence concerning the efficacy and safety of triptans currently available in Canada (sumatriptan, rizatriptan, naratriptan, zolmitriptan), and to provide guidelines for selection of a triptan. METHODS: Data from published, randomized, placebo-controlled trials were pooled and a combined number needed to treat (NNT) and number needed to harm (NNH) was generated for each triptan. Direct comparative trials of triptans were also examined. RESULTS: The lowest NNT for headache response/pain-free at one/two hours is observed with subcutaneous sumatriptan. Among the oral formulations, the lowest NNT is observed with rizatriptan and the highest NNT with naratriptan. The lowest NNH is observed with subcutaneous sumatriptan. CONCLUSIONS: Triptans are relatively safe and effective medications for acute migraine attacks. However, differences among them are relatively small. Considerations in selecting a triptan include individual patient response/tolerance, characteristics of the attacks, relief of associated symptoms, consistency of response, headache recurrence, delivery systems and patient preference.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Serotonin_Agonists_MeSH S_adverse_effects_MeSH Serotonin_Agonists_adverse_effects_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Sumatriptan_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Sumatriptan_pharmacokinetics_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11251129
----K E
----T What is the optimal medical management of ischemic heart failure?
----A Ischemic heart disease is an important and common contributor to the development of heart failure. Theoretically, all patients with heart failure may benefit from treatment designed to retard progressive ventricular dysfunction and arrhythmias. Patients with ischemic heart disease may also theoretically benefit from the relief of ischemia, the prevention of coronary occlusion, and revascularization. However, there is little evidence to show that the presence or absence of coronary disease modifies the benefits of effective treatments such as angiotensin-converting enzyme inhibitors and beta-blockers. Moreover, there is no evidence that treatment directed specifically at myocardial ischemia or coronary disease alters outcome in patients with heart failure. Treatments aimed at relieving painless myocardial ischemia have not been shown to alter prognosis. Lipid-lowering therapy is theoretically attractive for patients with heart failure and coronary disease; however, theoretical concerns also exist about the safety of such agents, and patients with heart failure have been excluded from large outcome studies very effectively. Some agents, such as aspirin, designed to reduce the risk of coronary occlusion seem ineffective or harmful in patients with heart failure, although warfarin may be safe and possibly effective. There is no evidence yet that revascularization improves prognosis in patients with heart failure, even in patients who are shown to have extensive myocardial hibernation. On current evidence, revascularization should be reserved for the relief of angina. Large-scale, randomized controlled trials are currently underway that are investigating the role of specific treatments targeted at coronary syndromes. The Carvedilol Hibernation Reversible Ischemia Trial: Marker of Success study is investigating the effects of carvedilol in a large cohort of patients with and without hibernating myocardium. The Warfarin and Antiplatelet Therapy in Chronic Heart Failure study is comparing the efficacy of aspirin, clopidogrel, and warfarin. The Heart Revascularization Trial-United Kingdom study is assessing the effect of revascularization on mortality in patients with heart failure and myocardial hibernation. Smaller scale studies are assessing the safety and efficacy of statin therapy in patients with heart failure. Only once the outcomes to these and other planned trials are known can the medical community know how best to treat their patients.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Arrhythmia_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 11256540
----K E
----T Additional beneficial effects of canrenoate in patients with anterior myocardial infarction on ACE-inhibitor treatment. A pilot study.
----A BACKGROUND: Recent evidence suggests that, via the mineralocorticoid receptors present in cardiovascular tissues, aldosterone exerts profibrotic effects, and that partial aldosterone escape occurs during ACE-inhibitor treatment. METHODS: A double-blind, randomized study was performed in order to evaluate the feasibility, tolerability, and the effects of the administration of 25 mg/day of canrenoate plus captopril versus captopril alone to patients with anterior acute myocardial infarction (AMI) unsuitable for or not receiving thrombolytic treatment and to patients in whom such treatment resulted or did not result in reperfusion. One hundred eighty-seven patients with anterior AMI were included in the present study. In all cases serum creatinine concentrations and serum K concentrations were < 2.0 mg/dl and < 5.5 mmol/l respectively. The patients were randomized in two groups: the canrenoate group included 94 patients who received captopril and 25 mg i.v. of canrenoate (1 mg/hour for the first 72 hours and then orally 25 mg/day) whereas the placebo group (93 patients) received captopril and placebo. On admission and on days 10, 90 and 180 all patients underwent echocardiography in order to determine the end-systolic volume (ESV), the ejection fraction (EF), the end-diastolic diameter, the E/A ratio, the E deceleration time as well as the isovolumetric relaxation time (IVRT) and the E and A peak velocities. RESULTS: Unreperfused patients did not show patency of the infarct-related artery whereas in reperfused patients this vessel was patent (7-10 days after AMI). The two groups were similar in age, sex, incidence of diabetes, smoking habits, hypertension, creatine kinase enzymatic peak, adjuvant therapy, baseline EF, ESV, and incidence of coronary artery bypass grafting/coronary angioplasty. Following 10 days of treatment (canrenoate group), only 9 patients presented with serum K and creatinine concentrations respectively > 5.5 mmol/l and > 2.0 mg/dl. Among those patients receiving canrenoate, the mitral E/A ratio was higher compared to the placebo group (p = 0.001) whereas the ESV was significantly reduced (p < 0.05). The deceleration time for reperfused patients receiving canrenoate was higher than that observed for reperfused patients in the placebo group. The intragroup EF was significantly increased (p = 0.042). Compared to the placebo group, the IVRT was significantly higher for unreperfused patients receiving canrenoate than in the placebo group (p = 0.001). Serum creatinine, blood urea and K levels as well as the incidence and extent of vessel disease were similar for both groups. No side effects were observed during the study period. CONCLUSIONS: Our data suggest that the combination of captopril plus canrenoate is feasible for the initial treatment of patients presenting with AMI. Besides, compared to captopril alone it is more efficacious in improving the E/A ratio, the ESV, the EF, and the IVRT.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Canrenoate_Potassium_MeSH S_therapeutic_use_MeSH Canrenoate_Potassium_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Feasibility_Studies_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_ultrasonography_MeSH Myocardial_Infarction_ultrasonography_MeSH M_Myocardial_Reperfusion_MeSH S_methods_MeSH Myocardial_Reperfusion_methods_MeSH M_Pilot_Projects_MeSH M_Thrombolytic_Therapy_MeSH M_Treatment_Failure_MeSH 
****** 11255718
----K 1
----T [Comparative study between bisoprolol and metoprolol, combined with hydrochlorothiazide, as antihypertensive therapy]
----A The main objective of this research was to compare the efficacy and security of bisoprolol (B), a new cardioselective beta-blocker, that does not have intrinsic sympathomimetic activity, and metoprolol associated to hydrochlorothiazide (HCTZ), in the treatment of patients with mild to moderate hypertension. Sixty-two hypertensive patients (47 females and 15 males) aged 20 to 70 years (mean 52.5 +/- 10.4) were included in a double-blind, placebo controlled and randomized clinical trial. After a two-weeks wash out period and a similar placebo phase, patients were randomly assigned to receive either a once-daily dosing of B (10 mg) with 6.25 mg of HCTZ, or M (100 mg) plus 6.25 mg of HCTZ during four-weeks. If there was no reduction below 90 mmHg at the end of this period, the dosing of either beta-blocker was doubled. After eight weeks of treatment, the mean decreases in systolic/diastolic blood pressures from baseline were 31.8/21.2 and 28.0/20.6 mmHg for B/HCTZ and M/HCTZ, respectively (p < 0.0001). There were no clinically significant changes from baseline in laboratory parameters in either group. Reduction in blood pressure with B/HCTZ is associated with adverse events and metabolic changes similar to those observed with other antihypertensive drugs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 11231439
----K E
----T Effect of metoprolol on cytokine levels in chronic heart failure--a substudy in the Metoprolol Controlled-Release Randomised Intervention Trial in Heart Failure (MERIT-HF).
----A BACKGROUND: Enhanced immune activation has been suggested to be involved in the pathogenesis of congestive heart failure (CHF). There is evidence for interactions between the sympathetic nervous system and the immune system. We therefore examined the effect of the selective beta(1)-receptor blocker metoprolol on various immunologic variables in CHF. METHODS: Eighty-one patients with CHF were randomized to metoprolol or placebo in a double-blind trial. Plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, soluble IL-2 receptor (sIL-2R), monocyte chemoattractant peptide-1, and IL-8 were measured at baseline, after 3 months, and at the end of the study (11.4 +/- 0.4 months). RESULTS: Our main findings were (1) at baseline TNF-alpha, IL-6, IL-8, monocyte chemoattractant peptide-1, and sIL-2R but not IL-10 levels were markedly elevated in patients with CHF compared with controls; (2) during treatment with metoprolol, but not with placebo, there was a significant decrease in sIL-2R after 3 months, with a return to baseline at the end of the study; and (3) levels of all other immunologic variables remained unchanged throughout the study in both the metoprolol and the placebo groups. CONCLUSIONS: Our findings suggest that metoprolol treatment in CHF is associated with a significant but temporary decrease in sIL-2R, possibly reflecting down-modulation of T-cell activation. However, an enhanced immune activation also persisted in the metoprolol group, suggesting a potential for more specific immunomodulatory therapy in CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Cytokines_MeSH S_blood_MeSH Cytokines_blood_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Interleukins_MeSH S_analysis_MeSH Interleukins_analysis_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tumor_Necrosis_Factor_MeSH S_analysis_MeSH Tumor_Necrosis_Factor_analysis_MeSH 
****** 11255522
----K E
----T Warfarin therapy for an octogenarian who has atrial fibrillation.
----A In North America, atrial fibrillation is associated with at least 75 000 ischemic strokes each year. Most of these strokes occur in patients older than 75 years of age. The high incidence of stroke in very elderly persons reflects the increasing prevalence of atrial fibrillation that occurs with advanced age, the high incidence of stroke in elderly patients, and the failure of physicians to prescribe antithrombotic therapy in most of these patients. This failure is related to the increased risk for major hemorrhage with advanced age, obfuscating the decision to institute stroke prophylaxis with antithrombotic therapy.This case-based review describes the risk and benefits of prescribing antithrombotic therapy for a hypothetical 80-year-old man who has atrial fibrillation and hypertension, and it offers practical advice on managing warfarin therapy. After concluding that the benefits of warfarin outweigh its risks in this patient, we describe how to initiate warfarin therapy cautiously and how to monitor and dose the drug. We then review five recent randomized, controlled trials that document the increased risk for stroke when an international normalized ratio (INR) of less than 2.0 is targeted among patients with atrial fibrillation. Next, we make the case that cardioversion is not needed for this asymptomatic patient with chronic atrial fibrillation. Instead, we choose to leave the patient in atrial fibrillation and to control his ventricular rate with atenolol. Later, when the INR increases to 4.9, we advocate withholding one dose of warfarin and repeating the INR test. Finally, when the patient develops dental pain, we review the analgesic agents that are safe to take with warfarin and explain why warfarin therapy does not have to be interrupted during a subsequent dental extraction.
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analgesics_MeSH S_administration_&_dosage_MeSH Analgesics_administration_&_dosage_MeSH M_Anticoagulants_MeSH S_administration_&_dosage_MeSH Anticoagulants_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Dental_Care_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Monitoring_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_International_Normalized_Ratio_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Surgical_Procedures__Operative_MeSH M_Warfarin_MeSH S_therapeutic_use_MeSH Warfarin_therapeutic_use_MeSH 
****** 11231847
----K E
----T The case for beta-adrenergic blockade as prophylaxis against perioperative cardiovascular morbidity and mortality.
----A Perioperative morbidity and mortality are frequently cardiac in origin. Many studies have prospectively attempted to define risk factors for cardiac ischemic events. Although we can now identify high-risk patients, optimal cardioprotective management strategies remain unclear. Treatment with beta-adrenergic antagonists decreases myocardial oxygen consumption and is generally well tolerated. This article reviews the physiologic and clinical basis for using these agents as prophylaxis against cardiovascular events in high-risk surgical patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Animals_MeSH M_Arrhythmia_MeSH S_mortality_MeSH Arrhythmia_mortality_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Heart_Failure__Congestive_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Premedication_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH 
****** 11230280
----K 5
----T Hypothesis: Beta-adrenergic receptor blockers and weight gain: A systematic analysis.
----A One of the arguments put forward against the primary use of beta-blockers has been concern about adverse metabolic effects, such as unfavorable effects on lipids or insulin sensitivity. Another less-appreciated potential drawback is their propensity to cause weight gain in some patients. In 8 evaluable prospective randomized controlled trials that lasted >/=6 months, body weight was higher in the beta-blocker than in the control group at the end of the study. The median difference in body weight was 1.2 kg (range -0.4 to 3.5 kg). A regression analysis suggested that beta-blockers were associated with an initial weight gain during the first few months. Thereafter, no further weight gain compared with controls was apparent. There was no relationship between demographic characteristics and changes in body weight. Based on these observations, the first-line use of beta-blockers in obese hypertensive patients should be reviewed. Obesity management in overweight hypertensive patients may be more difficult in the face of beta-blocker treatment.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Weight_Gain_MeSH S_drug_effects_MeSH Weight_Gain_drug_effects_MeSH 
****** 11230298
----K E
----T Left ventricle and arteries: structure, function, hormones, and disease.
----A The observation in the 1970s that the performance of the dysfunctional left ventricle was under the influence of aortic impedance led us to exploration of the role of the renin-angiotensin system and other hormonal systems in the progression of heart failure. The apparent efficacy of vasodilator drugs led to the first randomized, controlled trial in heart failure that demonstrated that all impedance-lowering drugs did not exert the same long-term benefit. Differences on the structural remodeling process in the myocardium and arterial vasculature were shown to account for the differential long-term response. We now recognize that the remodeling process in the left ventricle may be inhibited by nitrates, converting enzyme inhibitors, and beta-blockers, and this growth process leads to adverse outcomes. The impedance load on the left ventricle is influenced by vascular remodeling that also may be inhibited by drugs such as converting enzyme inhibitors. Thus, progression of cardiovascular disease is largely a consequence of structural changes that are hormonally mediated and may be inhibited by drug therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Argipressin_MeSH S_blood_MeSH Argipressin_blood_MeSH M_Comparative_Study_MeSH M_Drug_Combinations_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Hydralazine_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Nitroprusside_MeSH S_therapeutic_use_MeSH Nitroprusside_therapeutic_use_MeSH M_Prazosin_MeSH S_therapeutic_use_MeSH Prazosin_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Stroke_Volume_MeSH M_Survival_Analysis_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 11255611
----K E
----T Hypertension control in a community health centre at Riyadh, Saudi Arabia.
----A OBJECTIVE: This study was carried out to determine the degree of control of hypertension and the most commonly used drugs for hypertensive patients attending our community health center. METHODS: A cross sectional study carried out by randomly examining the case notes of patients attending our primary care clinics. RESULTS: Case notes of 3747 patients were examined, 2064 (55%) females (mean age 23.76 years) and 1683 (45%) males (mean age 24.63 years). Prevalence of hypertension was 3% (108 patients), 3% (63 patients) and 3% (45 patients) for females and males respectively. Majority of patients 16 (35%) males and 32 (51%) females had blood pressure of 141-160/90-100 mmHg. Seventeen (37%) males and 15 (24%) female patients had blood pressure < 140/90 mm Hg. Among 108 hypertensive patients, 29 (65%) males and 44 (69%) females were on single drug. The most commonly used drugs were ACE inhibitors (35%), calcium channel blockers (17.5%) and beta- blockers (14%). CONCLUSION: This study like some other studies shows that control of hypertension falls short of recommended goals. There is need to adopt a strategy that incorporates health education about life style and proper protocol as this has been found useful in other studies.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Community_Health_Centers_MeSH M_Community_Health_Services_MeSH M_Cross-Sectional_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Saudi_Arabia_MeSH 
****** 11207505
----K 5
----T Review article: a drug therapy for the prevention of variceal haemorrhage.
----A The development of varices is a major complication of cirrhosis, and variceal haemorrhage has a high mortality. There have been major advances in the primary and secondary prevention of variceal haemorrhage over the last 20 years involving endoscopic, radiological and pharmacological approaches. This review concentrates principally on drug therapy, particularly on the numerous haemodynamic studies. Many of these drugs have not been studied in clinical trials, but provide data about the underlying pathogenesis of portal hypertension. Also covered in this review are the randomized controlled trials and meta-analyses that involve a large number of patients. These trials involve relatively few drugs such as non-selective beta-blockers and nitrates. Correlations between haemodynamic and clinical parameters are discussed. Despite the recent increase in the use of alternative endoscopic therapies, an effective and well tolerated drug remains a clinically important research goal.
----P Journal_Article Review Review__Tutorial 
----M M_Hemodynamic_Processes_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Liver_MeSH S_blood_supply_MeSH Liver_blood_supply_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Randomized_Controlled_Trials_MeSH M_Varicose_Veins_MeSH S_drug_therapy_MeSH Varicose_Veins_drug_therapy_MeSH S_etiology_MeSH Varicose_Veins_etiology_MeSH S_prevention_&_control_MeSH Varicose_Veins_prevention_&_control_MeSH 
****** 11259143
----K E
----T Lifestyle and risk factor management and use of drug therapies in coronary patients from 15 countries; principal results from EUROASPIRE II Euro Heart Survey Programme.
----A AIMS: The principal aim of the second EUROASPIRE survey was to determine in patients with established coronary heart disease whether the Joint European Societies' recommendations on coronary prevention are being followed in clinical practice. METHODS: This survey was undertaken in 1999-2000 in 15 European countries: Belgium, Czech Republic, Finland, France, Germany, Greece, Hungary, Ireland, Italy, the Netherlands, Poland, Slovenia, Sweden, Spain and the U.K., in selected geographical areas and 47 centres. Consecutive patients, men and women < or =70 years were identified retrospectively with the following diagnoses: coronary artery bypass graft, percutaneous transluminal coronary angioplasty, acute myocardial infarction and myocardial ischaemia. Data collection was based on a review of medical records and interview and risk assessment at least 6 months after hospital admission. RESULTS: 8181 medical records (25% women) were reviewed and 5556 patients (adjusted participation rate 76%) interviewed. Recording of risk factor history and risk factor measurement in hospital notes was incomplete, particularly for discharge documents. At interview (median time 1.4 years after hospital discharge), 21% of patients smoked cigarettes, 31% were obese, 50% had raised blood pressure (systolic blood pressure > or =140 mmHg and/or diastolic blood pressure > or =90 mmHg), 58% had elevated serum total cholesterol (total cholesterol > or =5 mmol x l(-1)) and 20% reported a medical history of diabetes. Glucose control in these diabetic patients was poor with 87% having plasma glucose >6.0 mmol x l(-1)and 72% > or =7.0 mmol x l(-1). Among the patients interviewed the use of prophylactic drug therapies on admission, at discharge and at interview was as follows: aspirin or other antiplatelets drugs 47%, 90% and 86%; beta-blockers 44%, 66% and 63%; ACE inhibitors 24%, 38% and 38%; and lipid-lowering drugs 26%, 43% and 61%, respectively. With the exception of antiplatelet drugs, wide variations in the use of prophylactic drug therapies exist between countries. CONCLUSIONS: This European survey of coronary patients shows a high prevalence of unhealthy lifestyles, modifiable risk factors and inadequate use of drug therapies to achieve blood pressure and lipid goals. There is considerable potential throughout Europe to raise the standard of preventive cardiology through more effective lifestyle intervention, control of other risk factors and optimal use of prophylactic drug therapies in order to reduce coronary morbidity and mortality.
----P Journal_Article 
----M M_Aged_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Europe_MeSH M_Female_MeSH M_Guideline_Adherence_MeSH M_Health_Care_Surveys_MeSH M_Human_MeSH M_International_Cooperation_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Practice_Guidelines_MeSH M_Prevalence_MeSH M_Retrospective_Studies_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11259147
----K E
----T Specialty-related differences in the epidemiology, clinical profile, management and outcome of patients hospitalized for heart failure; the OSCUR study. Oucome dello Scompenso Cardiaco in relazione all'Utilizzo delle Risore.
----A AIMS: This study was designed to identify potential specialty-related differences in the epidemiology, clinical profile, management and outcome of patients hospitalized for congestive heart failure in departments of cardiology or internal medicine. METHODS AND RESULTS: From 1 July to 31 December 1998, we prospectively recorded epidemiological and clinical data from patients with congestive heart failure consecutively admitted to 11 departments of cardiology and 12 departments of internal medicine in Liguria, a northern area of Italy. The overall study population included 749 patients; 22% were treated by cardiologists and 78% by internists (P<0.0001). Patients managed by cardiologists were more likely to undergo echocardiography (92% vs 37%), Holter monitoring (25% vs 3%) and exercise stress testing (20% vs 0.5%) than those managed by internists (P=0.001). At discharge, patients treated by cardiologists were more likely to be prescribed beta-blockers (41% to 4%) and ACE inhibitors (100% to 74%) than those treated by internists (P<0.0001), and the latter medication at higher dosages by cardiologists than internists. In addition, patients followed by cardiologists were younger (70+/-9 to 79+/-1 years;P<0.0001), more likely to be male (61% to 50%;P=0.011) and to have coronary artery disease (57% to 45%;P<0.006) than those followed by internists. Conversely, patients followed by internists were more likely to have diabetes, chronic obstructive pulmonary disease, atrial fibrillation and renal failure (P<0.03). In the overall study population, 53 patients (7%) died during hospitalization. Patients treated by cardiologists had a mortality not significantly different from that of patients treated by internists (10% and 6%, respectively;P=0.067), although congestive heart failure was more severe on admission in patients treated by cardiologists. CONCLUSION: Cardiologists follow published guidelines for congestive heart failure more strictly than internists, but treat a smaller number of patients who are younger, have more severe congestive heart failure and fewer co-morbidities than those managed by internists.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiology_MeSH S_standards_MeSH Cardiology_standards_MeSH M_Echocardiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Internal_Medicine_MeSH S_standards_MeSH Internal_Medicine_standards_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Physician's_Practice_Patterns_MeSH M_Prospective_Studies_MeSH P_Quality_of_Health_Care_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11249904
----K I
----T Effect of beta blockers on incidence of new coronary events in older persons with prior myocardial infarction and diabetes mellitus.
----A Of 613 persons, mean age 79 +/- 9 years, with prior myocardial infarction and diabetes mellitus, 68 (11%) had contraindications to beta blockers; 289 of 545 persons (53%) without contraindications to beta blockers were treated with beta blockers. The Cox regression model showed that significant independent predictors of new coronary events were age (risk ratio 1.02 for an increment of 1 year of age), systemic hypertension (risk ratio 2.0), serum low-density lipoprotein cholesterol > or =125 mg/dl (risk ratio 1.4), serum high-density lipoprotein cholesterol < or =35 mg/dl (risk ratio 1.6), and use of beta blockers (risk ratio 0.73).
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Death__Sudden__Cardiac_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_classification_MeSH Hypertension_classification_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Risk_Factors_MeSH 
****** 11263853
----K E
----T Management of asymptomatic left ventricular dysfunction.
----A Asymptomatic left ventricular dysfunction should be treated as an early stage on the continuum that is chronic heart failure. The author presents the clinical trial data on which current management with angiotensin-converting enzyme inhibitors and beta-blockers is based. Issues surrounding screening are also discussed.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Ramipril_MeSH S_administration_&_dosage_MeSH Ramipril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH M_Ventricular_Function__Left_MeSH 
****** 11265951
----K E
----T Oral amiodarone for prevention of atrial fibrillation after open heart surgery, the Atrial Fibrillation Suppression Trial (AFIST): a randomised placebo-controlled trial.
----A BACKGROUND: Beta-blockers and amiodarone reduce the frequency of atrial fibrillation after open-heart surgery but the effectiveness of oral amiodarone in older patients already receiving beta-blockers is unknown. We have assessed the efficacy of oral amiodarone in preventing atrial fibrillation in patients aged 60 years or older undergoing open-heart surgery. METHODS: We did a randomised, double-blind placebo-controlled trial in which patients undergoing open-heart surgery (n=220, average age 73 years) received amiodarone (n=120) or placebo (n=100). Patients enrolled less than 5 days before surgery received 6 g of amiodarone or placebo over 6 days beginning on preoperative day 1. Patients enrolled at least 5 days before surgery received 7 g over 10 days beginning on preoperative day 5. FINDINGS: Patients on amiodarone had a lower frequency of any atrial fibrillation (22.5% vs 38.0%; p=0.01; absolute difference 15.5% [95% CI 3.4-27.6%]), and there were significant differences in favour of the active drug for symptomatic atrial fibrillation (4.2% vs 18.0%, p=0.001), cerebrovascular accident (1.7% vs 7.0%, p=0.04), and postoperative ventricular tachycardia (1.7% vs 7.0%, p=0.04). Beta-blocker use (87.5% amiodarone vs 91.0% placebo), nausea (26.7% vs 16.0%), 30-day mortality (3.3% vs 4.0%), symptomatic bradycardia (7.5% vs 7.0%), and hypotension (14.2% vs 10.0%) were similar. INTERPRETATION: Oral amiodarone prophylaxis in combination with beta-blockers prevents atrial fibrillation and symptomatic fibrillation and reduces the risk of cerebrovascular accidents and ventricular tachycardia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Cardiac_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiac_Surgical_Procedures_adverse_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11265558
----K 1
----T [Economic study of carvedilol in heart failure. A cost effectiveness study in France]
----A A programme of four phase III clinical trials carried out in the USA on 1094 patients showed that Carvedilol, associated with the usual bitherapy and eventually with digitalis, reduced the mortality and number of hospital admissions of patients with cardiac failure. These results, transposed to the French population, may be used to evaluate the economic advantages of Carvedilol by developing a cost-effectiveness study which consists in relating the direct expenses (drugs and hospital admissions) of each of the two strategies, with or without Carvedilol, to their respective mortalities. Hospital expenses were estimated with respect to the H.M.G. corresponding to each hospital stay at 1997-1998 values. The cost in the Carvedilol group was 2,823 FF per patient (including 1,491 FF for the drug itself) but 2,056 FF were economised in hospital expenses. With an increased cost of 767 FF but a 50% reduction in mortality corresponding to a difference in mortality of 45@1000, the cost-effectiveness of Carvedilol was 17,040 per life saved and 2,130 FF per additional year of life expectancy. A study of the sensitivity produced even more favourable results of Carvedilol. An evaluation of hospital expenses on the basis of AP-HP data indicates that the addition of Carvedilol is associated with a 4,425 FF reduction in hospital expenses, which makes it a cost saving strategy.
----P Clinical_Trial Clinical_Trial__Phase_III Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_economics_MeSH Carbazoles_economics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Digitalis_MeSH S_therapeutic_use_MeSH Digitalis_therapeutic_use_MeSH M_Economics__Hospital_MeSH M_English_Abstract_MeSH M_France_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Life_Expectancy_MeSH M_Phytotherapy_MeSH M_Plants__Medicinal_MeSH M_Plants__Toxic_MeSH M_Propanolamines_MeSH S_economics_MeSH Propanolamines_economics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 11264544
----K E
----T Predicting response to carvedilol for the treatment of heart failure: a multivariate retrospective analysis.
----A BACKGROUND: Carvedilol has been shown to decrease the progression of heart failure and improve left ventricular function and survival in patients with a left ventricular ejection fraction (LVEF) less than 35%. However, not all patients respond uniformly to this therapy. We proposed to identify variables that could, potentially, be used to predict response to carvedilol therapy as measured by the change in LVEF after treatment (Delta LVEF), and to identify pretreatment variables associated with hospitalization for heart failure after carvedilol therapy. METHODS AND RESULTS: A retrospective analysis of 98 patients treated with open-label carvedilol for a mean period of 16 months was performed by using bivariate and step-wise multivariate analyses. Bivariate analysis showed a positive correlation of Delta LVEF with heart rate at baseline (P =.001). There was a negative correlation of Delta LVEF with baseline LVEF (P <.01), diabetes mellitus (P =.04), and ischemic cardiomyopathy (P =.0002). Multivariate analysis showed a positive correlation of Delta LVEF with heart rate at baseline (P =.01) and a negative correlation with initial LVEF (P =.02) and ischemic cardiomyopathy (P =.006). Variables associated with hospitalization after initiation of carvedilol therapy were New York Heart Association (NYHA) classification (P =.001), lower extremity edema (P =.001), presence of an S3 (P =.02), hyponatremia (P =.02), elevated blood urea nitrogen (BUN) (P =.002), atrial fibrillation (P =.001), diabetes mellitus (P =.02), and obstructive sleep apnea (P =.009). CONCLUSIONS: Heart failure patients with the lowest LVEF or the highest heart rate at baseline had the greatest gain in LVEF after treatment with carvedilol. Patients with ischemic cardiomyopathy derived less benefit. Patients with clinical evidence of decompensated heart failure were at greater risk for hospitalization after initiation of carvedilol therapy.
----P Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gated_Blood-Pool_Imaging_MeSH S_drug_effects_MeSH Gated_Blood-Pool_Imaging_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11277474
----K I
----T Clinical use of beta-blocker therapy in patients with heart failure: a practical guide.
----A 
----P Evaluation_Studies Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 11275919
----K E
----T Testing the effectiveness of converting patients to long-acting antianginal medications: The Quality of Life in Angina Research Trial (QUART).
----A OBJECTIVE: Our purpose was to test the hypothesis that converting patients with stable angina to long-acting antianginal medications would improve their functional status, symptom control, treatment satisfaction, and quality of life. METHODS AND RESULTS: A single-blind randomized trial of 100 patients with stable coronary artery disease was performed in the outpatient clinic of a Veterans Affairs Health System. Outpatients with chronic stable angina taking at least 2 antianginal medications were studied. Patients were randomized to one of two treatments: optimal adjustment of their usual antianginal medications or conversion to solely long-acting medications (long-acting diltiazem +/- nitroglycerin patches +/- atenolol) with subsequent optimization. The primary outcome was the 3-month change in Seattle Angina Questionnaire scores. Although no differences in physical limitation scores were noted, patients randomized to receive long-acting medications had improved symptom control (3-month improvement in anginal stability [19.1 vs 5.6, P =.02] and anginal frequency [17.8 vs 5.5, P =.006]), more treatment satisfaction (3-month improvement of 8.2 vs 3.0, P =.057), and better quality of life (3-month improvement of 11.2 vs 5.6, P =.09) compared with patients whose pretrial medications were optimized. The improvement in symptom control was statistically significant. CONCLUSION: Converting patients with chronic, stable angina to long-acting antianginal medications resulted in substantial improvements in symptom control with a trend toward better treatment satisfaction and quality of life.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Chronic_Disease_MeSH M_Health_Status_Indicators_MeSH M_Human_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH M_Prospective_Studies_MeSH P_Quality_of_Life_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11273985
----K E
----T How many medicines do patients with heart failure need?
----A 
----P Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Cytokines_MeSH S_antagonists_&_inhibitors_MeSH Cytokines_antagonists_&_inhibitors_MeSH S_metabolism_MeSH Cytokines_metabolism_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Disease_Models__Animal_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Endothelins_MeSH S_antagonists_&_inhibitors_MeSH Endothelins_antagonists_&_inhibitors_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH M_Human_MeSH M_Immunoglobulin_G_MeSH S_therapeutic_use_MeSH Immunoglobulin_G_therapeutic_use_MeSH M_Immunosuppressive_Agents_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH M_Mice_MeSH M_Mice__Transgenic_MeSH M_Neprilysin_MeSH S_antagonists_&_inhibitors_MeSH Neprilysin_antagonists_&_inhibitors_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Receptors__Tumor_Necrosis_Factor_MeSH S_therapeutic_use_MeSH Receptors__Tumor_Necrosis_Factor_therapeutic_use_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Tumor_Necrosis_Factor_MeSH S_antagonists_&_inhibitors_MeSH Tumor_Necrosis_Factor_antagonists_&_inhibitors_MeSH S_metabolism_MeSH Tumor_Necrosis_Factor_metabolism_MeSH 
****** 11273991
----K I
----T Pharmacogenetic interactions between beta-blocker therapy and the angiotensin-converting enzyme deletion polymorphism in patients with congestive heart failure.
----A BACKGROUND: Activation of the renin-angiotensin and sympathetic nervous systems adversely affect heart failure progression. The ACE deletion allele (ACE D) is associated with increased renin-angiotensin activation; however, its influence on patient outcomes remains uncertain, and the pharmacogenetic interactions with beta-blocker therapy have not been previously evaluated. METHODS AND RESULTS: We prospectively followed 328 patients (age, 56.1+/-11.9 years) with systolic dysfunction (left ventricular ejection fraction, 0.24+/-0.08) to assess the impact of the ACE D allele on transplant-free survival (median follow-up, 21 months). Transplant-free survival was compared by genotype for the whole cohort and separately in patients with (n=120) and those without beta-blocker therapy (n=208) at the time of entry. Transplant-free survival was significantly poorer for patients with the D: allele (1-year percent survival II/ID/DD=94/77/75; 2-year=78/65/60; ordered log-rank test, P:=0.044). In patients not treated with beta-blockers, the adverse impact of ACE D allele was dramatically increased (1-year percent survival II/ID/DD=95/75/67; 2-year=81/61/48; P:=0.005). In contrast, in patients receiving beta-blocker therapy, no influence of ACE genotype on transplant-free survival was evident (1-year percent survival II/ID/DD=91/80/86; 2-year=70/71/77; P:=0.73). CONCLUSIONS: In a cohort of patients with systolic dysfunction, the ACE D allele was associated with a significantly poorer transplant-free survival. This effect was primarily evident in patients not treated with beta-blockers and was not seen in patients receiving therapy. These findings suggest a potential pharmacogenetic interaction between the ACE D/I polymorphism and therapy with beta-blockers in the determination of heart failure survival.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Disease-Free_Survival_MeSH M_Female_MeSH M_Genetic_Screening_MeSH M_Genotype_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_genetics_MeSH Heart_Failure__Congestive_genetics_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_genetics_MeSH Peptidyl-Dipeptidase_A_genetics_MeSH M_Pharmacogenetics_MeSH M_Polymorphism_(Genetics)_MeSH S_genetics_MeSH Polymorphism_(Genetics)_genetics_MeSH M_Prospective_Studies_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH M_Sequence_Deletion_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 11281235
----K I
----T ACE inhibitors, beta-blockers, calcium blockers, and diuretics for the control of systolic hypertension.
----A The objective of this study was to determine which of the common groups of antihypertensive drugs is most effective at lowering systolic blood pressure (SBP) in elderly patients with previously untreated hypertension and the percentage of patients controlled with single or sequential monotherapy. Subjects were recruited from patients attending other outpatient clinics and entered into the study if their SBP was more than 150 mm Hg after three visits. Patients were given a low and high dose of each of the main classes of drugs or placebo for 1 month each. The study was a balanced, randomized crossover design with five periods: placebo; angiotensin converting enzyme inhibitors; beta-blocking drugs; calcium-blocking drugs; and thiazide diuretics. Blood pressure (BP) was measured 24 to 26 h after the previous dose. A questionnaire for side effects was administered at each visit. Seventy-four patients entered the study. beta-Blockers could not be used in 15 patients because of asthma or bronchospasm and these had two placebo periods. There were 9 of 66 patients on P, 9 of 46 on beta-blockers, 4 of 65 on calcium-blocking drugs, 4 of 65 on diuretic, and 1 of 62 patients on ACE inhibitors who did not progress to the higher dose because of side effects. Decreases in SBP compared to randomized placebo were calcium-blocking drugs 15 mm Hg = diuretic 13 mm Hg > ACE inhibitors 8 mm Hg = beta-blockers 5 mm Hg. Blood pressure decrease correlated with placebo BP (P < .0005, r = 0.53 to 0.70). When corrected for placebo, target SBP (<140 mm Hg) was reached in between 6% to 15% of patients on monotherapy. Sequential monotherapy achieved target in 29%. Angiotensin converting enzyme inhibitors, calcium-blocking drugs, and diuretics had no more side effects than placebo. Patients on beta-blockers had more side effects and the well-being score was reduced. Diuretics and calcium-blocking drugs are more effective in elderly patients at lowering SBP pressure. beta-Blockers were relatively ineffective, were frequently contraindicated, and had more side effects. Monotherapy achieved control in only a small number of patients. In elderly people with essential hypertension, therapy should be instituted with diuretics or calcium-blocking drugs, but combination therapy will usually be required to achieve goal.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH 
****** 11281737
----K I
----T Beta-blockers in congestive heart failure. A Bayesian meta-analysis.
----A PURPOSE: Congestive heart failure is an important cause of patient morbidity and mortality. Although several randomized clinical trials have compared beta-blockers with placebo for treatment of congestive heart failure, a meta-analysis quantifying the effect on mortality and morbidity has not been performed recently. DATA SOURCES: The MEDLINE, Cochrane, and Web of Science electronic databases were searched from 1966 to July 2000. References were also identified from bibliographies of pertinent articles. STUDY SELECTION: All randomized clinical trials of beta-blockers versus placebo in chronic stable congestive heart failure were included. DATA EXTRACTION: A specified protocol was followed to extract data on patient characteristics, beta-blocker used, overall mortality, hospitalizations for congestive heart failure, and study quality. DATA SYNTHESIS: A hierarchical random-effects model was used to synthesize the results. A total of 22 trials involving 10 135 patients were identified. There were 624 deaths among 4862 patients randomly assigned to placebo and 444 deaths among 5273 patients assigned to beta-blocker therapy. In these groups, 754 and 540 patients, respectively, required hospitalization for congestive heart failure. The probability that beta-blocker therapy reduced total mortality and hospitalizations for congestive heart failure was almost 100%. The best estimates of these advantages are 3.8 lives saved and 4 fewer hospitalizations per 100 patients treated in the first year after therapy. The probability that these benefits are clinically significant (>2 lives saved or >2 fewer hospitalizations per 100 patients treated) is 99%. Both selective and nonselective agents produced these salutary effects. The results are robust to any reasonable publication bias. CONCLUSIONS: beta-Blocker therapy is associated with clinically meaningful reductions in mortality and morbidity in patients with stable congestive heart failure and should be routinely offered to all patients similar to those included in trials.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bayes_Theorem_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Research_Design_MeSH S_standards_MeSH Research_Design_standards_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 11283842
----K I
----T A meta-analysis of endoscopic variceal ligation for primary prophylaxis of esophageal variceal bleeding.
----A Despite publication of several randomized trials of prophylactic variceal ligation, the effect on bleeding-related outcomes is unclear. We performed a meta-analysis of the trials, as identified by electronic database searching and cross-referencing. Both investigators independently applied inclusion and exclusion criteria, and abstracted data from each trial. Standard meta-analytic techniques were used to compute relative risks and the number needed to treat (NNT) for first variceal bleed, bleed-related mortality, and all-cause mortality. Among 601 patients in 5 homogeneous trials comparing prophylactic ligation with untreated controls, relative risks of first variceal bleed, bleed-related mortality, and all-cause mortality were 0.36 (0.26-0.50), 0.20 (0.11-0.39), and 0.55 (0.43-0.71), with respective NNTs of 4.1, 6.7, and 5.3. Among 283 subjects from 4 trials comparing ligation with beta-blocker therapy, the relative risk of first variceal bleed was 0.48 (0.24-0.96), with NNT of 13; however, there was no effect on either bleed-related mortality (relative risk [RR], 0.61; confidence interval [CI], 0.20-1.88) or all-cause mortality (RR, 0.95; CI, 0.56-1.62). In conclusion, compared with untreated controls, prophylactic ligation reduces the risks of variceal bleeding and mortality. Compared with beta-blockers, ligation reduces the risk for first variceal bleed but has no effect on mortality. Prophylactic ligation should be considered for patients with large esophageal varices who cannot tolerate beta-blockers. Subsequent research should further compare ligation and beta-blockers to determine the effect on mortality, and measure ligation's cost-effectiveness.
----P Journal_Article Meta-Analysis 
----M M_Esophageal_and_Gastric_Varices_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Ligation_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11288822
----K E
----T Follow-up of renal function in treated and untreated older patients with isolated systolic hypertension. Systolic Hypertension in Europe (Syst-Eur) Trial Investigators.
----A BACKGROUND: In the outcome trials that provided information on renal function in older hypertensive patients, diuretics and beta-blockers were mostly used as first-line drugs. The long-term renal effects of calcium-channel blockers remain unclear. OBJECTIVE: To compare the changes in renal function in 2,258 treated and 2,148 untreated patients with isolated systolic hypertension, of whom 455 had diabetes mellitus and 390 had proteinuria. METHODS: We performed a post-hoc analysis of the double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) Trial. Active treatment was initiated with nitrendipine (10-40 mg/day) with the possible addition of enalapril (5-20 mg/day), hydrochlorothiazide (12.5-25 mg/day), or both, titrated or combined to reduce the sitting systolic blood pressure by at least 20 mmHg, to less than 150 mmHg. The main outcome measures were serum creatinine concentration and creatinine clearance calculated by the formula of Cockroft and Gault. RESULTS: Serum creatinine concentration at the time when participants were randomly allocated to study groups was less than 176.8 micromol/l (2.0 mg/dl), averaging 88 micromol/l. At the time of the last serum creatinine measurement, the blood pressure difference (P< 0.001) between the two groups was 11.6/4.1 mmHg. In the intention-to-treat analysis (11,427 patient-years), serum creatinine and the calculated creatinine clearance were not influenced by active treatment. However, in the patients assigned randomly to receive active treatment, the incidence of mild renal dysfunction (serum creatinine at least 176.8 mmol/l) decreased by 64% (P= 0.04) and that of proteinuria by 33% (P= 0.03). Active treatment reduced the risk of proteinuria more in diabetic than in non-diabetic patients: by 71%, compared with 20% (P= 0.04). In non-proteinuric patients, active treatment did not influence serum creatinine, whereas in patients with proteinuria at entry to the study, serum creatinine decreased on active treatment (P< 0.001). Furthermore, in on-randomized treatment comparison stratified for risk at baseline, serum creatinine concentration did not change (P= 0.98) in patients continuing to receive monotherapy with nitrendipine, whereas it increased by 6.73 mmol/l (P < 0.001) in patients who received hydrochlorothiazide alone or in combination with other study medication (P < 0.001 for difference in trends). CONCLUSIONS: In older patients with isolated systolic hypertension, antihypertensive treatment starting with the dihydropyridine calcium-channel blocker, nitrendipine, did not decrease blood pressure at the expense of renal function and prevented the development of proteinuria, especially in diabetic patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Europe_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Male_MeSH M_Nitrendipine_MeSH S_therapeutic_use_MeSH Nitrendipine_therapeutic_use_MeSH M_Proteinuria_MeSH S_complications_MeSH Proteinuria_complications_MeSH S_prevention_&_control_MeSH Proteinuria_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH 
****** 11288962
----K E
----T Angiotensin receptor blockers: evidence for preserving target organs.
----A Hypertension is a major problem throughout the developed world. Although current antihypertensive treatment regimens reduce morbidity and mortality, patients are often noncompliant, and medications may not completely normalize blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood pressure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart failure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) inhibit the activity of the RAS, but these two classes of antihypertensive medications have different mechanisms of action and different pharmacologic profiles. Angiotensin-converting enzyme inhibitors block a single pathway in the production of angiotensin II (Ang II). In addition, angiotensin I is not the only substrate for ACE. The ACE inhibitors also block the degradation of bradykinin that may have potential benefits in cardiovascular disease. Bradykinin is, however, the presumed cause of cough associated with ACE inhibitor therapy. Data from clinical trials on ACE inhibitors serve to support the involvement of the RAS in the development of cardiovascular disease. Angiotensin receptor blockers act distally in the RAS to block the Ang II type 1 (AT1) receptor selectively. Thus, ARBs are more specific agents and avoid many side effects. Experimental and clinical trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maximal benefit may be obtained with Ang II blockade using both ARBs and ACE inhibitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature.
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11288383
----K E
----T Hypertension clinical guideline 2000.
----A OUTCOMES: Extensive data from many randomised controlled trials have shown the benefit of treating hypertension. The target blood pressure (BP) for antihypertensive management should be systolic < 140 mmHg and diastolic < 90 mmHg, with minimal or no drug side-effects. However, a lesser reduction will elicit benefit, although this is not optimal. The reduction of BP in the elderly and in those with severe hypertension should be achieved gradually over 6 months. Stricter BP control is required for patients with end-organ damage, coexisting risk factors and co-morbidity, e.g. diabetes mellitus. Coexistent risk factors should also be controlled. BENEFITS: Reduction in risk of stroke, cardiac failure, renal insufficiency and probably coronary artery disease. The major precautions and contraindications to each antihypertensive drug recommended are listed. RECOMMENDATIONS: Correct BP measurement procedure is described. Evaluation of cardiovascular risk factors and recommendations for antihypertensive therapy are stipulated. The total cardiovascular disease risk profile should be determined for all patients and this should inform management strategies. Lifestyle modification and patient education play an essential role in the management strategy. DRUG THERAPY: First line--low-dose diuretics; second line--add one of the following: reserpine, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers; third line--add another second-line drug or hydralazine or an alpha-blocker. The guideline includes management of specific situations, e.g. hypertensive emergency or urgency, severe hypertension with target organ damage and refractory hypertension (BP > 160/95 mmHg on triple therapy), hypertension in diabetes mellitus, etc. VALIDATION. The guideline was developed by the Executive Committee of the Southern African Hypertension Society with consensus meeting endorsement, and is endorsed by the South African Medical Association Guideline Commitee.
----P Guideline Journal_Article Practice_Guideline 
----M M_Blood_Pressure_Determination_MeSH S_standards_MeSH Blood_Pressure_Determination_standards_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_diagnosis_MeSH Pregnancy_Complications__Cardiovascular_diagnosis_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH M_Societies__Medical_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11292228
----K 5
----T Preventive therapy in pediatric migraine.
----A Preventive therapy for migraine headache includes identification of migraine precipitants, possible adjustments in lifestyle, appropriate management of acute headache, and, when necessary, the use of pharmacologic agents. There are no well-controlled clinical trials with sufficient patient numbers to support the use of any agent in the prevention of migraine headache in children. Data on the use of amitriptyline and divalproex sodium in open-label studies suggest that these agents may be efficacious. The mechanism of action for these agents is unknown but may be related to the 5-hydroxytyptamine-2 (5-HT2) receptor antagonism or regulation of ion channels. A review of the pertinent literature on migraine prophylaxis in children is presented. Dosing guidelines are presented based on the limited data available and clinical experience.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_administration_&_dosage_MeSH Anti-Inflammatory_Agents__Non-Steroidal_administration_&_dosage_MeSH M_Anticonvulsants_MeSH S_administration_&_dosage_MeSH Anticonvulsants_administration_&_dosage_MeSH M_Antidepressive_Agents__Tricyclic_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents__Tricyclic_administration_&_dosage_MeSH M_Child_MeSH M_Diagnosis__Differential_MeSH M_Diet_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Histamine_H1_Antagonists_MeSH S_administration_&_dosage_MeSH Histamine_H1_Antagonists_administration_&_dosage_MeSH M_Human_MeSH M_Life_Style_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Practice_Guidelines_MeSH M_Primary_Prevention_MeSH S_methods_MeSH Primary_Prevention_methods_MeSH 
****** 11293353
----K 1
----T [Are the newer antihypertensive agents better and more effective than diuretics?]
----A BACKGROUND: In recent years, the expenses for medical antihypertensive therapy have increased considerably, the main reason being the switchover to newer and more expensive antihypertensive drugs. RESULTS: Several recent studies which have compared the efficacy of the older, conventional drugs (thiazid diuretics and beta-blockers) with the newer agents (calcium blockers, angiotensin-converting enzyme (ACE) inhibitors), have shown that they are almost equipotent with regard to effects on blood pressure, morbidity and mortality. At lower doses, the metabolic effects of thiazide diuretics are minimal and probably without clinical significance, and the risk of developing diabetes mellitus type 2 does not seem to be increased. INTERPRETATION: The cheaper thiazide diuretics are still valuable drugs in the treatment of hypertension. If more than one agent is necessary to reduce blood pressure to the desired level, they can be combined with other antihypertensive agents.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH P_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_economics_MeSH Calcium_Channel_Blockers_economics_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Controlled_Clinical_Trials_MeSH P_Diuretics__Thiazide_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_economics_MeSH Diuretics__Thiazide_economics_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Costs_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11296462
----K 1
----T [Does diabetes change the anti-ischemic therapeutic options in the symptomatic coronary patient?]
----A The assessment of results of medical treatment, angioplasty and coronary bypass surgery in diabetic coronary patients is difficult because of the absence of distinction in the subgroups of type 1 and 2 diabetes and of stable and unstable angina. With respect to medical therapy, betablockers are practically without deleterious effects and are effective in diabetic populations. The same is true of other antianginal drugs. Conventional coronary angioplasty is associated with poorer results than the general population in the long-term, partly because of progression of the coronary artery disease and partly because of an increased incidence of restenosis. The use of stents improves these results, which are similar to those of the general population with single vessel disease or those without proteinuria. Coronary bypass surgery, despite a certain perioperative morbidity, is associated with an identical survival rate at 5 years as non-diabetics, providing the internal mammary artery is grafted. The comparison between these methods is resumed in the ACIP study which opposes the 3 strategies, in Morris et al's study comparing medical and surgical approaches and, finally, in the recent BARI trial where patients were randomly allocated to angioplasty or surgery. It would appear that the surgical strategy gives better results in multivessel disease. However, many reserves have been voiced because of the small numbers of patients, the high number of excluded patients and the fact that recent progress in angioplasty with widespread use of stenting associated with the prescription of new antiaggregant drugs was not taken into account.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_statistics_&_numerical_data_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_statistics_&_numerical_data_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comorbidity_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH S_statistics_&_numerical_data_MeSH Coronary_Artery_Bypass_statistics_&_numerical_data_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH M_Diabetic_Nephropathies_MeSH S_complications_MeSH Diabetic_Nephropathies_complications_MeSH M_English_Abstract_MeSH M_Graft_Occlusion__Vascular_MeSH S_epidemiology_MeSH Graft_Occlusion__Vascular_epidemiology_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_epidemiology_MeSH Hyperlipidemia_epidemiology_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Internal_Mammary-Coronary_Artery_Anastomosis_MeSH S_statistics_&_numerical_data_MeSH Internal_Mammary-Coronary_Artery_Anastomosis_statistics_&_numerical_data_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Postoperative_Complications_MeSH S_epidemiology_MeSH Postoperative_Complications_epidemiology_MeSH M_Proteinuria_MeSH S_complications_MeSH Proteinuria_complications_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_epidemiology_MeSH Smoking_epidemiology_MeSH M_Stents_MeSH M_Treatment_Outcome_MeSH 
****** 11300246
----K I
----T Effect of beta blockers on mortality and morbidity in persons treated for congestive heart failure.
----A 
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Function_Tests_MeSH M_Human_MeSH M_Intervention_Studies_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Severity_of_Illness_Index_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11298665
----K I
----T Lack of pharmacokinetic interaction between the antimigraine compound, almotriptan, and propranolol in healthy volunteers.
----A This study was designed to assess the pharmacokinetics of almotriptan, a 5-HT1B/1D agonist, when administered in the presence and absence of propranolol. Healthy male (n = 10) and female (n = 2) volunteers received (i) 80 mg propranolol twice daily for 7 days and 12.5 mg almotriptan on day 7, and (ii) 12.5 mg almotriptan on day 7, according to a two-way crossover design. Plasma and urinary almotriptan concentrations were measured by high performance liquid chromatography (HPLC) methods. Treatment effects on pharmacokinetic parameters were assessed by analysis of variance (ANOVA). Statistically significant differences between treatments in area under the curve (AUC), clearance, and half-life were observed (P < 0.03), but these differences were < 7%. Ninety percent confidence interval analysis of log-transformed pharmacokinetic parameters showed that the treatments were equivalent. Adverse events were mild to moderate in intensity, and no treatment effects on vital signs were observed. The results show that propranolol has no effect on the pharmacokinetics of almotriptan. Concomitant administration of the two drugs is well tolerated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Area_Under_Curve_MeSH M_Cross-Over_Studies_MeSH M_Drug_Interactions_MeSH M_Female_MeSH M_Half-Life_MeSH M_Human_MeSH M_Indoles_MeSH S_pharmacokinetics_MeSH Indoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Metabolic_Clearance_Rate_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Propranolol_MeSH S_pharmacokinetics_MeSH Propranolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Reference_Values_MeSH M_Serotonin_Agonists_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_pharmacokinetics_MeSH Vasodilator_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11298666
----K E
----T Cyclandelate in the prophylaxis of migraine: a placebo-controlled study.
----A The prophylactic action of cyclandelate was investigated in a multicentre, randomized, placebo-controlled, parallel group study. A 4-week baseline period was followed by a 4-week placebo phase and a 16-week treatment period with either 1600 mg cyclandelate or placebo. Patients (n = 251) with two to six migraine attacks/month were randomized. Neither the primary study endpoint (reduction of migraine days from baseline to the last 28 days) nor most of the secondary endpoints (reduction in the number of migraine attacks, severity or duration of attacks, frequency of autonomic disturbances, medication for treatment of attacks) showed a difference between cyclandelate and placebo. Cyclandelate, however, was superior to placebo in a global impression of efficacy rated by the patients and the treating physicians. Both treatments were well tolerated. In conclusion, cyclandelate was not superior to placebo in the prophylaxis of migraine with regard to parameters usually used in migraine prophylaxis trials.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Cyclandelate_MeSH S_therapeutic_use_MeSH Cyclandelate_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11303005
----K E
----T A cardiac prevention and rehabilitation programme for all patients at first presentation with coronary artery disease.
----A OBJECTIVE: To develop and test a cardiac prevention and rehabilitation programme for achieving sustained lifestyle, risk factor, and therapeutic targets in patients presenting for the first time with exertional angina, acute coronary syndromes, or coronary revascularisation. DESIGN: A descriptive study. SETTING: A hospital based 12 week outpatient programme. INTERVENTIONS: A multiprofessional family based programme of lifestyle and risk factor modification. MAIN OUTCOME MEASURES: Non-smoking status, body mass index, blood pressure, plasma cholesterol, use of prophylactic drugs. RESULTS: 158 patients (82% of 194 possible cases) were recruited over 15 months, with 72% completing the programme. Targets for achieving non-smoking status, blood pressure < 140/90 mm Hg, and total cholesterol < 4.8 mmol/l were achieved in 92%, 73%, and 62%, respectively, and the proportion on aspirin, beta blockers, and lipid lowering treatment was 95%, 58%, and 64% on referral back to general practice for continuing care. CONCLUSIONS: A comprehensive cardiac prevention and rehabilitation programme can be offered to all patients presenting for the first time with coronary heart disease, including those with exertional angina who are normally managed in primary care. Lifestyle, risk factor, and therapeutic targets can be successfully achieved in most patients with such a hospital based programme.
----P Evaluation_Studies Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Ambulatory_Care_MeSH S_methods_MeSH Ambulatory_Care_methods_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_rehabilitation_MeSH Coronary_Disease_rehabilitation_MeSH M_England_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Health_Behavior_MeSH M_Health_Promotion_MeSH S_methods_MeSH Health_Promotion_methods_MeSH M_Human_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Program_Evaluation_MeSH M_Risk_Factors_MeSH M_Smoking_Cessation_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11305807
----K E
----T Strategies and feasibility of hypertension control in a prevalent hemodialysis cohort.
----A BACKGROUND: There are few data to demonstrate the feasibility of long-term blood pressure (BP) control using short dialysis sessions as practiced in the US. Control of hypertension in hemodialysis patients may reduce the risk of cardiovascular events. METHODS: Forty-two dialysis patients had BPs and weights recorded before and after dialysis for two consecutive weeks and were followed by one physician over three years. Patients were treated by ultrafiltration and conventional antihypertensive drugs and BPs were repeated at three years in the 32 survivors. RESULTS: 93% of the patients (39/42) were African-American. At inception, 85% of the patients were hypertensive with BPs of 154 +/- 23/83 +/- 14 mmHg and 137 +/- 22/74 +/- 14 mmHg pre- and post-dialysis, respectively. The response to ultrafiltration was dependent upon gender, with women having a greater BP reduction compared to men. At three-year follow-up, the BP had dropped significantly in the survivors a mean of 9.4/6.7 mmHg. Pre- and post-dialysis weights, post dialysis BP and interdialytic weight-gain were unchanged. The BP reduction was achieved by an increase in the number of antihypertensive medications from 0.91 +/- 0.86 medications to 1.41 +/- 1.16. Improved BP control did not worsen the efficiency of dialysis (Kt/V). The use of beta-blockers doubled during the period of follow-up. Compared to the USRDS average cardiovascular death rate, the risk of cardiovascular deaths was improved 80% over three years. CONCLUSION: Long-term BP reduction can be achieved through the use of antihypertensive agents and volume control in a predominantly African-American hemodialysis population. This may impact cardiovascular mortality.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_African_Continental_Ancestry_Group_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Body_Weight_MeSH M_Cohort_Studies_MeSH M_Feasibility_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Kidney_Failure__Chronic_MeSH S_therapy_MeSH Kidney_Failure__Chronic_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH P_Renal_Dialysis_MeSH S_methods_MeSH Renal_Dialysis_methods_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH M_Ultrafiltration_MeSH 
****** 11312480
----K E
----T A beta-blocker, not magnesium, is effective prophylaxis for atrial tachyarrhythmias after coronary artery bypass graft surgery.
----A OBJECTIVE: To evaluate magnesium as a sole or adjuvant agent with currently used prophylactic drugs in suppressing postoperative atrial tachyarrhythmias (POAT) after coronary artery bypass graft (CABG) surgery. DESIGN: Single-center prospective, randomized clinical trial. SETTING: University hospital. PARTICIPANTS: Patients (n = 400) undergoing CABG surgery. INTERVENTIONS: Patients were randomized among 6 prophylaxis regimens: (1) control (no antiarrhythmics), (2) magnesium only, (3) digoxin only, (4) magnesium and digoxin, (5) propranolol only, and (6) magnesium and propranolol. Patients randomized to a regimen including magnesium received 12 g given during 96 hours postoperatively. Patients in a digoxin regimen received 1 mg after cardiopulmonary bypass and 0.25 mg daily. Patients in a propranolol regimen received 1 mg intravenously every 6 hours until able to take 10 mg orally 4 times a day. Prophylaxis regimens were discontinued after 4 days postoperatively. MEASUREMENTS AND MAIN RESULTS: The primary outcome was a sustained POAT or discharge from the hospital. Control patients had an incidence of POAT (38%) not significantly different from patients in magnesium-only (38%), digoxin-only (31%), and magnesium with digoxin (37%) regimens. Patients treated with propranolol had a significant reduction in POAT. Nearly identical POAT rates in the propranolol-only (18%) and propranolol with magnesium (19%) groups support the lack of efficacy of magnesium in this trial. Study design allowed analysis of and showed a beta-blocker withdrawal effect in addition to suppressive benefit of postoperative beta-blockers. CONCLUSION: beta-Blocker prophylaxis is indicated to reduce the incidence of POAT in CABG surgery patients and to prevent a beta-blocker withdrawal effect in patients receiving these medications preoperatively. Digoxin and magnesium as sole or adjuvant agents do not offer suppressive or ventricular rate reduction benefits in POAT.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Magnesium_MeSH S_therapeutic_use_MeSH Magnesium_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Tachycardia__Supraventricular_MeSH S_etiology_MeSH Tachycardia__Supraventricular_etiology_MeSH S_prevention_&_control_MeSH Tachycardia__Supraventricular_prevention_&_control_MeSH 
****** 11333992
----K I
----T Race and the response to adrenergic blockade with carvedilol in patients with chronic heart failure.
----A BACKGROUND: The benefits of angiotensin-converting-enzyme inhibitors and beta-blockers may be smaller in black patients than in patients of other races, but it is unknown whether race influences the response to carvedilol in patients with chronic heart failure. METHODS: In the U.S. Carvedilol Heart Failure Trials Program, 217 black and 877 nonblack patients (in New York Heart Association class II, III, or IV and with a left ventricular ejection fraction of no more than 0.35) were randomly assigned to receive placebo or carvedilol (at doses of 6.25 to 50 mg twice daily) for up to 15 months. The effects of carvedilol on ejection fraction, clinical status, and major clinical events were retrospectively compared between black and nonblack patients. RESULTS: As compared with placebo, carvedilol lowered the risk of death from any cause or hospitalization for any reason by 48 percent in black patients and by 30 percent in nonblack patients. Carvedilol reduced the risk of worsening heart failure (heart failure leading to death, hospitalization, or a sustained increase in medication) by 54 percent in black patients and by 51 percent in nonblack patients. The ratios of the relative risks associated with carvedilol for these two outcome variables in black as compared with nonblack patients were 0.74 (95 percent confidence interval, 0.42 to 1.34) and 0.94 (95 percent confidence interval, 0.43 to 2.05), respectively. Carvedilol also improved functional class, ejection fraction, and the patients' and physicians' global assessments in both the black patients and the nonblack patients. For all these measures of outcome and clinical status, carvedilol was superior to placebo within each racial cohort (P<0.05 in all analyses), and there was no significant interaction between race and treatment (P> 0.05 in all analyses). CONCLUSIONS: The benefit of carvedilol was apparent and of similar magnitude in both black and nonblack patients with heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_Antagonists_therapeutic_use_MeSH P_African_Continental_Ancestry_Group_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Continental_Population_Groups_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Mortality_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 11317188
----K I
----T Does treatment of non-malignant hypertension reduce the incidence of renal dysfunction? A meta-analysis of 10 randomised, controlled trials.
----A OBJECTIVE: It remains controversial whether non-malignant 'benign' hypertension causes renal dysfunction. The effect of lowering blood pressure on the incidence of renal dysfunction among patients with non-malignant hypertension is not clear. This meta-analysis was conducted to determine whether antihypertensive drug therapy reduces the incidence of renal dysfunction in patients with non-malignant hypertension. METHODS: Randomised, controlled trials of antihypertensive drug therapy of more than 1 year duration that reported renal dysfunction as an outcome were identified through MEDLINE search and literature review. A random effects model was used to obtain summary estimates. RESULTS: Ten trials were identified, involving 26, 521 individuals and 114 000 person-years. All excluded subjects with advanced baseline renal disease. Definition of renal dysfunction outcome varied among trials but within each trial was applied similarly to both treatment and control groups. Drug treatment consisted mostly of diuretics and adrenergic blockers. Overall, treated patients had lower blood pressure and fewer cardiovascular events. There were a total of 317 cases of renal dysfunction. Patients randomised to antihypertensive therapy (or more intensive therapy) did not have a significant reduction in their risk of developing renal dysfunction (relative risk = 0.97; 95% confidence interval (CI) 0.78-1.21; P = 0.77). CONCLUSIONS: Among patients with non-malignant hypertension enrolled in randomised trials, treated patients did not have a lower risk of renal dysfunction. The 95% CI suggests that a 25% or more true protective effect of antihypertensive drugs is unlikely.
----P Journal_Article Meta-Analysis 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Kidney_Diseases_MeSH S_complications_MeSH Kidney_Diseases_complications_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11317198
----K E
----T Using medication history to measure confounding by indication in assessing calcium channel blockers and other antihypertensive therapy.
----A Reported findings of elevated risk of adverse events associated with calcium channel blocker use in hypertensives may be due partly to unmeasured confounding by indication. To determine if such confounding occurs, we conducted a retrospective cohort analysis of 77 196 Pennsylvania Medicaid recipients aged 18 to 61 who were treated with antihypertensive medication between 1990 and 1992. All diagnoses and dispensed prescriptions during the year prior to study entry were examined. Prior recipients of multitherapy (n = 18 763) were more likely to have had previously diagnosed risk factors (OR = 1.31 [95% CI, 1.30-1.33]) than subjects with prior monotherapy (n = 11141). New initiators (n = 47292) were less likely to have had previously diagnosed risk factors (OR = 0.48 (95% CI, 0.47-0.49)) than previous users (n = 29904). The likelihood of being prescribed calcium channel blocker rather than other monotherapy was significantly higher for subjects diagnosed during the previous week with arteriosclerotic cardiovascular disease OR = 7.78 (95% CI, 2.72-22.28), P < 0.0001; angina OR = 2.92 (95% CI, 1.77-4.83), (P < 0.0001); diabetes OR = 1.49 (95% CI, 1.07-2.06), (P = 0.0004); and hypertension OR = 1.57 (95% CI 1.35-1.82), (P < 0.0001). Calcium channel blockers were selectively prescribed to subjects at elevated risk of adverse events. Confounding by indication was found in this large indigent population. Unmeasured confounding may contribute to overestimated relative risk of adverse events associated with calcium channel blocker therapy vs diuretics or beta-blockers. At least 1 full year of subjects' medical and prescription drug history should be examined prior to study entry; shorter observation periods will miss clinically relevant information about risk.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Male_MeSH M_Medical_History_Taking_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11317165
----K E
----T Renal safety and tolerability of celecoxib, a novel cyclooxygenase-2 inhibitor.
----A The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. Conventional treatment for these debilitating conditions routinely involves the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonspecific inhibitors of COX-1 and COX-2. Numerous studies suggest that inhibition of renal prostaglandin synthesis by NSAIDs is deleterious to kidney function, particularly in high-risk patients. As celecoxib inhibits COX-2 and spares COX-1 at therapeutic doses, we hypothesized that it may offer an improved renal safety profile in patients at risk for NSAID-induced renal toxicity. This article represents a post hoc analysis of the renal safety of celecoxib, using the safety database generated during its clinical development program. This analysis includes data from more than 50 clinical studies involving more than 13,000 subjects. Most subjects were enrolled in randomized, controlled trials (of up to 12 weeks' duration); however, more than 5000 subjects received celecoxib for as long as 2 years in a long-term, open-label study at as much as twice the maximum recommended dosage. The overall incidence of renal adverse events after celecoxib was greater than that after placebo but similar to that after NSAIDs. The most common events reported after celecoxib, namely, peripheral edema (2.1%), hypertension (0.8%), and exacerbation of preexisting hypertension (0.6%), were not time- or dose-related. Peripheral edema was not associated with increased weight or blood pressure. Furthermore, there was no evidence of drug-drug interactions between celecoxib and concomitant angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics. We conclude that celecoxib is well tolerated by patients who may be at risk for NSAID-induced renal toxicity, such as the elderly and those with hypertension or preexisting chronic heart disease.
----P Journal_Article Review Review__Tutorial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH M_Arthritis__Rheumatoid_MeSH S_drug_therapy_MeSH Arthritis__Rheumatoid_drug_therapy_MeSH M_Cyclooxygenase_Inhibitors_MeSH S_adverse_effects_MeSH Cyclooxygenase_Inhibitors_adverse_effects_MeSH S_pharmacokinetics_MeSH Cyclooxygenase_Inhibitors_pharmacokinetics_MeSH S_pharmacology_MeSH Cyclooxygenase_Inhibitors_pharmacology_MeSH M_Databases__Factual_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Interactions_MeSH M_Edema_MeSH S_chemically_induced_MeSH Edema_chemically_induced_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_chemically_induced_MeSH Hypertension_chemically_induced_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_pathology_MeSH Kidney_pathology_MeSH M_Osteoarthritis_MeSH S_drug_therapy_MeSH Osteoarthritis_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Sulfonamides_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_pharmacokinetics_MeSH Sulfonamides_pharmacokinetics_MeSH S_pharmacology_MeSH Sulfonamides_pharmacology_MeSH 
****** 11321866
----K E
----T The cost-effectiveness of doxazosin for the treatment of hypertension in type II diabetic patients in the UK and Italy.
----A The objective of this analysis was to assess the cost-effectiveness of achieving 'tight control' versus 'less tight control' of blood pressure, as defined in the UK Prospective Diabetics Study 38, in type II diabetic patients in the UK and Italy. The effect of including doxazosin in a 'tight control' combination therapy was analysed. Given doxazosin's positive impact on lipid levels in addition to its antihypertensive effect, it is hypothesised that treatment including doxazosin will reduce the incidence of macrovascular complications. For each country, a Markov model was constructed to simulate macrovascular outcomes of patients on various drug combinations. Transitional probabilities were based on the risk rates presented in UKPDS 38. Risk rates were adjusted for the ageing of the cohort and the lipid-lowering properties of doxazosin using Framingham risk equations. Incremental cost-effectiveness ratios ranged from 2224 Pounds to 4867 Pounds (US$3225-7057) per life-year saved for the UK and from L1.8-9.3 million (US$818-4159) per life-year saved for Italy. Doxazosin is a cost-effective agent when included in a combination therapy in the treatment of hypertension in the diabetic populations of the UK and Italy.
----P Journal_Article Multicenter_Study 
----M M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cost-Benefit_Analysis_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_economics_MeSH Diabetes_Mellitus__Type_II_economics_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_economics_MeSH Diabetic_Angiopathies_economics_MeSH M_Doxazosin_MeSH S_economics_MeSH Doxazosin_economics_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Italy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Assessment_MeSH 
****** 11324677
----K 5
----T Beta-blockers in the management of hypertension in patients with type 2 diabetes mellitus: is there a role?
----A It has been conclusively established that treatment of hypertension in patients with type 2 (non-insulin-dependent) diabetes mellitus will significantly reduce the incidence of stroke, heart failure and progression of diabetic complications. Beta-blockers are effective antihypertensive agents which, in long term studies, have proven beneficial in reducing important clinical end-points. However nonselective beta-blockers may have a negative effect on lipid profiles and contribute to hypoglycaemic unawareness, thus preventing their use in some patients with diabetes mellitus. The development of newer and more selective beta-blockers has overcome many of these problems. In addition, some of the newer agents have novel properties such as release of nitric oxide, which theoretically would make them more attractive in patients with diabetes mellitus. Overall, the adverse metabolic effects of beta-blockers do not appear to be important in clinical practice and these agents should no longer be contraindicated in patients with type 2 diabetes mellitus. Their proven cardiovascular benefits would seem to easily tip the balance in favour of their use.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Human_MeSH P_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 11324243
----K 5
----T Gender-specific issues in the treatment of migraine.
----A Migraine is approximately three times more common in women than in men. Women tend to have longer attacks and are more likely than men to experience aura with migraine, but both sexes can experience frequent and severe attacks. Treatment principles for migraine and guidelines for the use of prophylactic and abortive therapies are generally consistent between males and females. However, due to hormonal changes induced in the female during menstruation, oral contraceptive use, pregnancy, and menopause, gender-specific therapeutic strategies are often necessary when treating migraine in females.
----P Journal_Article Review Review__Tutorial 
----M M_Contraceptives__Oral_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Menopause_MeSH S_physiology_MeSH Menopause_physiology_MeSH M_Menstruation_MeSH S_physiology_MeSH Menstruation_physiology_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_epidemiology_MeSH Migraine_epidemiology_MeSH S_therapy_MeSH Migraine_therapy_MeSH M_Pregnancy_MeSH M_Prevalence_MeSH P_Sex_Characteristics_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH P_Women's_Health_MeSH 
****** 11323582
----K E
----T The effects of endoscopic variceal ligation and propranolol on portal hypertensive gastropathy: a prospective, controlled trial.
----A BACKGROUND: Endoscopic treatment of esophageal varices may accentuate portal hypertensive gastropathy. The impact of the combination of band ligation and propranolol on this condition remains unknown. METHODS: Patients with history of variceal bleeding were randomized to receive band ligation alone (control group, 40 patients) or a combination of band ligation and propranolol (propranolol group, 37 patients). Serial endoscopic evaluation of gastropathy was performed. Gastropathy was classified into 3 grades and scored as 0, 1, or 2. RESULTS: Before endoscopic treatment, 17% of the control group and 22% of the propranolol group had gastropathy (p = 0.78). The occurrence of gastropathy after endoscopic treatment was significantly higher in the control group than in the propranolol group (p = 0.002). Serial endoscopic follow-up revealed that the mean gastropathy score was significantly higher in the control group than in the propranolol group (p < 0.05). In patients with gastropathy the gastropathy score reached a peak at 6 months after endoscopic treatment in both the control and propranolol groups (85% vs. 48%, respectively). After variceal obliteration, accentuation of gastropathy was significant in the control group (p < 0.01) but not in the propranolol group. Gastropathy was less likely to develop in patients who developed gastric varices. Esophageal variceal recurrence was not related to the development of gastropathy after variceal obliteration with banding. Only one patient in the control group bled from gastropathy. CONCLUSION: Band ligation of esophageal varices may accentuate gastropathy, which in this study was partly relieved by propranolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Combined_Modality_Therapy_MeSH P_Endoscopy__Gastrointestinal_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_complications_MeSH Gastrointestinal_Hemorrhage_complications_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Ligation_MeSH S_methods_MeSH Ligation_methods_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Stomach_Diseases_MeSH S_etiology_MeSH Stomach_Diseases_etiology_MeSH S_pathology_MeSH Stomach_Diseases_pathology_MeSH S_therapy_MeSH Stomach_Diseases_therapy_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11322860
----K 3
----T Development and therapeutic indications of orally-active non-peptide vasopressin receptor antagonists.
----A Vasopressin (AVP) is a cyclic nonapeptide hormone that exhibits many physiological effects including free water reabsorption, vasoconstriction, cellular proliferation and adrenocorticotrophic hormone (ACTH) secretion. In a healthy organism, AVP plays an important role in the homeostasis of fluid osmolality and volume status. However, in several diseases or conditions such as the syndrome of inappropriate secretion of AVP (SIADH), congestive heart failure, arterial hypertension, liver cirrhosis, nephrotic syndrome, dysmenorrhoea and ocular hypertension, AVP may play an important role in their pathophysiology. Recently, orally-active non-peptide AVP receptor antagonists were developed by random screening of chemical entities and optimisation of lead compounds. These include agents specific for the V(1)-vascular and V(2)-renal AVP receptor subtypes. Dual V(1)/V(2) AVP receptor antagonists are also being studied. Some of these non-peptide receptor antagonists have been studied extensively, while others are currently under investigation. Potential therapeutic indications for AVP receptor antagonists comprise: 1) The blockade of V(1)-vascular AVP receptors in arterial hypertension, congestive heart failure, Raynaud's syndrome, peripheral vascular disease and dysmenorrhea. 2) The blockade of V(2)-renal AVP receptors in the syndrome of inappropriate secretion of vasopressin, congestive hart failure, liver cirrhosis, nephrotic syndrome and any state of excessive retention of free water and subsequent dilutional hyponatraemia. 3) The blockade of V(3)-pituitary AVP receptors in ACTH-secreting tumours. This review examines the pharmacology of orally-active non-peptide AVP receptor antagonists and their clinical applications.
----P Journal_Article 
----M M_Administration__Oral_MeSH M_Animals_MeSH M_Diabetes_Insipidus_MeSH S_drug_therapy_MeSH Diabetes_Insipidus_drug_therapy_MeSH M_Dysmenorrhea_MeSH S_drug_therapy_MeSH Dysmenorrhea_drug_therapy_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hyponatremia_MeSH S_drug_therapy_MeSH Hyponatremia_drug_therapy_MeSH M_Receptors__Vasopressin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Vasopressin_antagonists_&_inhibitors_MeSH 
****** 11333166
----K E
----T Effect of beta-blockade on autonomic modulation of heart rate and neurohormonal profile in decompensated heart failure.
----A BACKGROUND: One of the putative mechanisms for the salutary effects of beta-blockers in patients with congestive heart failure (CHF) is their ability to improve autonomic dysfunction. However, patients with profound neurohumoral abnormalities derive little survival benefit from beta-blockers. The purpose of the current study was to evaluate the effect of beta-blockers on heart rate variability (HRV) in decompensated CHF. METHODS: Time and frequency domain HRV indices were obtained from 24-hour Holter recordings and compared to assess the role of beta-blockade in 199 patients (mean age 60 +/- 14 years) with decompensated CHF. Neurohormonal differences were assessed by measuring norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6 in a subset of 64 patients. RESULTS: All HRV indices were markedly suppressed but were substantially higher in patients who were on beta-blockers. Time domain measures of parasympathetic cardiac activity, the percentage of R-R intervals with > 50 ms variation (4.9 +/- 0.6 vs 7.7 +/- 1.2%, P = 0.006) and the square root of mean squared differences of successive R-R intervals (22.7 +/- 2.0 vs 31.6 +/- 4.1 ms, P = 0.004), were higher in the beta-blocker group. Spectral analysis revealed that the total power and the ultra-low frequency power were significantly higher in patients on beta-blockers (82% and 59%, respectively). The high frequency power, a spectral index of parasympathetic modulation, was 41% higher in the beta-blocker group (121 +/- 25 vs 171 +/- 27 ms(2), P = 0.02). Norepinephrine and interleukin-6 levels were substantially lower in patients on beta-blockers (28% and 61%, respectively). However, these differences did not reach statistical significance. CONCLUSIONS: Beta-blockers improve the impaired cardiac autonomic regulation during high sympathetic stress of decompensated CHF. This effect may play an important role in protecting the myocardium and preventing arrhythmias during transient increases in sympathetic activity.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Disease_Progression_MeSH M_Electrocardiography__Ambulatory_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH S_drug_effects_MeSH Endothelin-1_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_immunology_MeSH Heart_Failure__Congestive_immunology_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Interleukin-6_MeSH S_blood_MeSH Interleukin-6_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neurotransmitters_MeSH S_blood_MeSH Neurotransmitters_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Prospective_Studies_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Treatment_Outcome_MeSH M_Tumor_Necrosis_Factor_MeSH S_drug_effects_MeSH Tumor_Necrosis_Factor_drug_effects_MeSH S_metabolism_MeSH Tumor_Necrosis_Factor_metabolism_MeSH 
****** 11334653
----K I
----T CAPRICORN: a story of alpha allocation and beta-blockers in left ventricular dysfunction post-MI.
----A Beta-blocker therapy is beneficial both after myocardial infarction and in mild, moderate and severe chronic heart failure. Recent sub-group analysis of the Goteborg Metoprolol Trial and the AIRE study confirm that patients receiving beta-blockers in the setting of post-MI heart failure fare better than patients not receiving this therapy. For all these reasons the CAPRICORN trial of carvedilol in post-MI LV dysfunction was an important and eagerly awaited trial. The results were presented for the first time at The American College of Cardiology on March 20 2001. CAPRICORN randomised 984 patients to placebo and 975 to carvedilol between 3 and 21 days (mean 10) after a confirmed MI. Patients had to have evidence of a left ventricular ejection fraction 40% or less. All patients had received ACEI therapy for at least 48 hours prior to randomisation. The mean ejection fraction of the patients recruited was 32.7% in the placebo group and 32.9% in the carvedilol group. Follow-up was for a mean of 15 months (maximum 2.7 years). All cause mortality was 15.3% (151 deaths) in the placebo group and 11.9% (116 deaths) in the carvedilol group, giving a hazard ratio of 0.77 (0.60-0.98) and a significance of p = 0.031. And yet this agent will probably not be given a licence for this indication in the European Union and the USA. The reason is one of trial design and statistical declarations. Some way into the trial the Steering Committee decided to change the primary end-point form all-cause mortality to two co-primary end-points and to allocate their alpha power of 0.05 unevenly between the combined end-points of all cause mortality and cardiovascular hospitalisation (alpha 0.045) and all cause mortality (alpha 0.005). In the end neither was achieved, one because of the large number of non-specific hospitalisations for chest pain and the mortality effect because it was allocated a punitive and unachievable target of p < 0.005. The trial is thus officially neutral despite showing convincing clinical benefit. Clearly arcane matters of statistical plans do matter and steering committees should think very carefully before changing the primary end-points of major trials.
----P Clinical_Trial Editorial Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Approval_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH 
****** 11345386
----K E
----T Influence of carvedilol on hospitalizations in heart failure: incidence, resource utilization and costs. U.S. Carvedilol Heart Failure Study Group.
----A BACKGROUND: Carvedilol reduces disease progression in heart failure, but to our knowledge, its effects on hospitalizations and costs have not been evaluated. OBJECTIVES: We examined the effects on hospitalization frequency and costs in the U.S. Carvedilol Heart Failure Trials Program. This program consisted of four concurrent, multicenter, double-blind, placebo-controlled studies involving 1,094 patients with New York Heart Association class II to IV heart failure, which treated patients with placebo or carvedilol for up to 15 months (median, 6.5 months). METHODS: Detailed resource utilization data were collected for all hospitalizations occurring between randomization and the end of follow-up. In-patient care costs were estimated based on observed levels of resource use. RESULTS: Compared with placebo, carvedilol reduced the risk of hospitalization for any reason by 29% (p = 0.009), cardiovascular hospitalizations by 28% (p = 0.034) and heart failure hospitalizations by 38% (p = 0.041). Carvedilol also decreased the mean number of hospitalizations per patient (for cardiovascular reasons 30% [p = 0.02], for heart failure 53% [p = 0.03]). Among hospitalized patients, carvedilol reduced severity of illness during hospital admission, as reflected by shorter length of stay and less frequent use of intensive care. For heart failure hospital admissions, carvedilol decreased mean length of stay by 37% (p = 0.03) and mean number of intensive care unit/coronary care unit days by 83% (p = 0.001), with similar effects on cardiovascular admissions. As a result, estimated inpatient care costs with carvedilol were 57% lower for cardiovascular admissions (p = 0.016) and 81% lower for heart failure admissions (p = 0.022). CONCLUSIONS: Carvedilol added to angiotensin-converting enzyme inhibition reduces hospitalization risk as well as severity of illness and resource utilization during admission in patients with chronic heart failure.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Follow-Up_Studies_MeSH M_Health_Resources_MeSH S_economics_MeSH Health_Resources_economics_MeSH S_utilization_MeSH Health_Resources_utilization_MeSH M_Health_Services_Research_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Hospital_Costs_MeSH S_statistics_&_numerical_data_MeSH Hospital_Costs_statistics_&_numerical_data_MeSH M_Hospitalization_MeSH S_economics_MeSH Hospitalization_economics_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Incidence_MeSH M_Intensive_Care_Units_MeSH S_economics_MeSH Intensive_Care_Units_economics_MeSH S_utilization_MeSH Intensive_Care_Units_utilization_MeSH M_Length_of_Stay_MeSH S_economics_MeSH Length_of_Stay_economics_MeSH S_statistics_&_numerical_data_MeSH Length_of_Stay_statistics_&_numerical_data_MeSH M_Multicenter_Studies_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Regression_Analysis_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_United_States_MeSH 
****** 11386263
----K I
----T Effect of carvedilol on survival in severe chronic heart failure.
----A BACKGROUND: Beta-blocking agents reduce the risk of hospitalization and death in patients with mild-to-moderate heart failure, but little is known about their effects in severe heart failure. METHODS: We evaluated 2289 patients who had symptoms of heart failure at rest or on minimal exertion, who were clinically euvolemic, and who had an ejection fraction of less than 25 percent. In a double-blind fashion, we randomly assigned 1133 patients to placebo and 1156 patients to treatment with carvedilol for a mean period of 10.4 months, during which standard therapy for heart failure was continued. Patients who required intensive care, had marked fluid retention, or were receiving intravenous vasodilators or positive inotropic drugs were excluded. RESULTS: There were 190 deaths in the placebo group and 130 deaths in the carvedilol group. This difference reflected a 35 percent decrease in the risk of death with carvedilol (95 percent confidence interval, 19 to 48 percent; P=0.00013, unadjusted; P=0.0014, adjusted for interim analyses). A total of 507 patients died or were hospitalized in the placebo group, as compared with 425 in the carvedilol group. This difference reflected a 24 percent decrease in the combined risk of death or hospitalization with carvedilol (95 percent confidence interval, 13 to 33 percent; P<0.001). The favorable effects on both end points were seen consistently in all the subgroups we examined, including patients with a history of recent or recurrent cardiac decompensation. Fewer patients in the carvedilol group than in the placebo group withdrew because of adverse effects or for other reasons (P=0.02). CONCLUSIONS: The previously reported benefits of carvedilol with regard to morbidity and mortality in patients with mild-to-moderate heart failure were also apparent in the patients with severe heart failure who were evaluated in this trial.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Risk_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 11386264
----K I
----T A trial of the beta-blocker bucindolol in patients with advanced chronic heart failure.
----A BACKGROUND: Although beta-adrenergic-receptor antagonists reduce morbidity and mortality in patients with mild-to-moderate chronic heart failure, their effect on survival in patients with more advanced heart failure is unknown. METHODS: A total of 2708 patients with heart failure designated as New York Heart Association (NYHA) functional class III (in 92 percent of the patients) or IV (in 8 percent) and a left ventricular ejection fraction of 35 percent or lower were randomly assigned to double-blind treatment with either bucindolol (1354 patients) or placebo (1354 patients) and followed for the primary end point of death from any cause. RESULTS: The data and safety monitoring board recommended stopping the trial after the seventh interim analysis. At that time, there was no significant difference in mortality between the two groups (unadjusted P=0.16). The results presented here are based on complete follow-up at the time of study termination (average, 2.0 years). There were a total of 449 deaths in the placebo group (33 percent) and 411 deaths in the bucindolol group (30 percent; adjusted P=0.13). The risk of the secondary end point of death from cardiovascular causes was lower in the bucindolol group (hazard ratio, 0.86; 95 percent confidence interval, 0.74 to 0.99), as was the risk of heart transplantation or death (hazard ratio, 0.87; 95 percent confidence interval, 0.77 to 0.99). CONCLUSIONS: In a demographically diverse group of patients with NYHA class III and IV heart failure, bucindolol resulted in no significant overall survival benefit.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Transplantation_MeSH S_statistics_&_numerical_data_MeSH Heart_Transplantation_statistics_&_numerical_data_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Proportional_Hazards_Models_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH 
****** 11357013
----K I
----T Overview of the results of recent beta blocker trials.
----A Results of the studies published or reported within the last 2 years provide convincing evidence that beta-blockers can decrease mortality in patients with chronic symptomatic heart failure because of left ventricular systolic dysfunction. The Cardiac Insufficiency Bisoprolol Study (CIBIS)-II and Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) trials showed a 34% reduction in all-cause death with bisoprolol and metoprolol therapy in patients with class II-III heart failure. Data from Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS), with a 35% mortality reduction, extended this benefit to class IV patients treated with carvedilol who do not require intravenous diuretics or positive inotropes. Ongoing beta-blocker studies address new topics, such as treatment of older patients, in whom diastolic heart failure may be more common, and direct comparison of different drugs. Although the use of beta-blockers for heart failure tends to increase, implementation of the knowledge from the trials in clinical practice still remains a challenge.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11356434
----K I
----T Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial.
----A BACKGROUND: The beneficial effects of beta-blockers on long-term outcome after acute myocardial infarction were shown before the introduction of thrombolysis and angiotensin-converting-enzyme (ACE) inhibitors. Generally, the patients recruited to these trials were at low risk: few had heart failure, and none had measurements of left-ventricular function taken. We investigated the long-term efficacy of carvedilol on morbidity and mortality in patients with left-ventricular dysfunction after acute myocardial infarction treated according to current evidence-based practice. METHODS: In a multicentre, randomised, placebo-controlled trial, 1959 patients with a proven acute myocardial infarction and a left-ventricular ejection fraction of </=40% were randomly assigned 6.25 mg carvedilol (n=975) or placebo (n=984). Study medication was progressively increased to a maximum of 25 mg twice daily during the next 4-6 weeks, and patients were followed up until the requisite number of primary endpoints had occurred. The primary endpoint was all-cause mortality or hospital admission for cardiovascular problems. Analysis was by intention to treat. FINDINGS: Although there was no difference between the carvedilol and placebo groups in the number of patients with the primary endpoint (340 [35%] vs 367 [37%], hazard ratio 0.92 [95% CI 0.80-1.07]), all-cause mortality alone was lower in the carvedilol group than in the placebo group (116 [12%] vs 151 [15%], 0.77 [0.60-0.98], p=0.03). Cardiovascular mortality, non-fatal myocardial infarctions, and all-cause mortality or non-fatal myocardial infarction were also lower on carvedilol than on placebo. INTERPRETATION: In patients treated long-term after an acute myocardial infarction complicated by left-ventricular systolic dysfunction, carvedilol reduced the frequency of all-cause and cardiovascular mortality, and recurrent, non-fatal myocardial infarctions. These beneficial effects are additional to those of evidence-based treatments for acute myocardial infarction including ACE inhibitors.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH 
****** 11368286
----K E
----T Levosimendan.
----A Levosimendan, a pyridazinone-dinitrile derivative, is a calcium sensitiser with additional action on adenosine triphosphate (ATP)-sensitive potassium channels. It is used intravenously (IV) for the treatment of decompensated cardiac failure. At therapeutic doses, levosimendan exhibits enhanced contractility with no increase in oxygen demands. It also produces antistunning effects without increasing myocardial intracellular calcium concentrations or prolonging myocardial relaxation. Levosimendan also causes coronary and systemic vasodilation. In patients with decompensated congestive heart failure (CHF), IV levosimendan significantly reduced the incidence of worsening CHF or death. IV levosimendan significantly increased cardiac output or cardiac index and decreased filling pressure in the acute treatment of stable or decompensated CHF in large, double-blind, randomised trials and after cardiac surgery in smaller trials. Levosimendan is well tolerated, with the most common adverse events (headache, hypotension, nausea) being secondary to vasodilation. It has not been shown to be arrhythmogenic. Levosimendan has shown no clinically important pharmacokinetic interactions with captopril, felodipine, beta-blockers, digoxin, warfarin, isosorbide-5-mononitrate, carvedilol, alcohol (ethanol) or itraconazole.
----P Journal_Article Review Review__Tutorial 
----M M_Biological_Availability_MeSH P_Cardiotonic_Agents_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH S_metabolism_MeSH Cardiotonic_Agents_metabolism_MeSH S_pharmacokinetics_MeSH Cardiotonic_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Half-Life_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH P_Hydrazones_MeSH S_adverse_effects_MeSH Hydrazones_adverse_effects_MeSH S_metabolism_MeSH Hydrazones_metabolism_MeSH S_pharmacokinetics_MeSH Hydrazones_pharmacokinetics_MeSH S_pharmacology_MeSH Hydrazones_pharmacology_MeSH S_therapeutic_use_MeSH Hydrazones_therapeutic_use_MeSH M_Protein_Binding_MeSH P_Pyridazines_MeSH S_adverse_effects_MeSH Pyridazines_adverse_effects_MeSH S_metabolism_MeSH Pyridazines_metabolism_MeSH S_pharmacokinetics_MeSH Pyridazines_pharmacokinetics_MeSH S_pharmacology_MeSH Pyridazines_pharmacology_MeSH S_therapeutic_use_MeSH Pyridazines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11376302
----K E
----T Comparative effects of carvedilol and metoprolol on left ventricular ejection fraction in heart failure: results of a meta-analysis.
----A BACKGROUND: Both metoprolol and carvedilol improve cardiac function and prolong survival in patients with heart failure. Carvedilol has broader antiadrenergic effects than metoprolol, but it is not clear whether this characteristic is associated with greater benefits on cardiac function during long-term treatment. STUDY DESIGN: We performed a meta-analysis of all 19 randomized controlled trials of carvedilol or metoprolol that measured left ventricular ejection fraction before and after an average of 8.3 +/- 0.1 months of treatment in 2184 patients with chronic heart failure. The mean daily doses were 58 +/- 1 mg of carvedilol and the equivalent of 162 +/- 1 mg of extended-release metoprolol. In the 15 placebo-controlled trials, the mean ejection fraction increased more in the trials of carvedilol than in the trials of metoprolol (placebo-corrected increases of +0.065 and +0.038, respectively), P = .0002. In the 4 active-controlled trials that compared metoprolol directly with carvedilol, the mean ejection fraction also increased more in the carvedilol groups than in the metoprolol groups (+0.084 on carvedilol and +0.057 on metoprolol, respectively), P = .009. The difference in favor of carvedilol in the active-controlled trials was nearly identical to the difference observed in the placebo-controlled trials and was apparent in patients with and without coronary artery disease. CONCLUSION: Long-term treatment with carvedilol produces greater effects on left ventricular ejection fraction than metoprolol when both drugs are prescribed in doses similar to those that have been shown to prolong life.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11378004
----K E
----T Carvedilol increases plasma vascular endothelial growth factor (VEGF) in patients with chronic heart failure.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_drug_effects_MeSH Atrial_Natriuretic_Factor_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelial_Growth_Factors_MeSH S_blood_MeSH Endothelial_Growth_Factors_blood_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Lymphokines_MeSH S_blood_MeSH Lymphokines_blood_MeSH S_drug_effects_MeSH Lymphokines_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Endothelial_Growth_Factor_A_MeSH M_Vascular_Endothelial_Growth_Factors_MeSH 
****** 11378005
----K E
----T Influence of carvedilol on the benefits of physical training in patients with moderate chronic heart failure.
----A AIMS: To evaluate prospectively the impact of carvedilol on a short-term physical training program in stable patients with moderate chronic heart failure (CHF), and to analyze parameters predictive of improvement after training. METHODS AND RESULTS: Thirty-eight patients with CHF were referred for cardiac rehabilitation. Etiology was ischemic in 26 patients, dilated in 12 patients and left ventricular ejection fraction was <35%. Patients were classified into three groups: group 1 (n=14)=ACE inhibitors, diuretics and digitalis; group 2 (n=11)=idem group 1+cardioselective beta-blocker; group 3 (n=13)=idem group 1+carvedilol. Exercise tests with VO2 measurement were performed before and after a 4-week exercise training program. Patients with carvedilol experienced a 16.6% increase in peak VO2 which was similar to the 13.9% increase in the group with cardioselective beta-blocker and to the 18.5% in the group without beta-blocker. Moreover non-ischemic etiology of CHF was the only parameter predictive of improvement after training (P=0.02). CONCLUSION: Addition of carvedilol did not alter benefits of a short-term physical training program in patients with moderate CHF. No baseline characteristic except for etiology of CHF was predictive of a response to training.
----P Journal_Article 
----M M_Acebutolol_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_rehabilitation_MeSH Heart_Failure__Congestive_rehabilitation_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH S_physiology_MeSH Oxygen_Consumption_physiology_MeSH M_Physical_Therapy_Techniques_MeSH M_Predictive_Value_of_Tests_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH 
****** 11378006
----K E
----T Differing beta-blocking effects of carvedilol and metoprolol.
----A BACKGROUND: Metoprolol is a beta(1)-selective beta-adrenergic antagonist while carvedilol is a non-selective beta-blocker with additional blockades of alpha(1)-adrenoceptors. Administration of metoprolol has been shown to cause up-regulation of beta-adrenoceptor density and to decrease nocturnal melatonin release, whereas carvedilol lacks these typical effects of beta-blocking drugs. AIMS: To compare beta-blocking effects of metoprolol and carvedilol when applied orally in healthy subjects. Methods: We investigated the effects of single oral doses of clinically recommended amounts of metoprolol (50, 100 and 200 mg) and carvedilol (25, 50 and 100 mg) to those of a placebo in a randomised, double-blind, cross-over study in 12 healthy male volunteers. Two hours after oral administration of the drugs heart rate and blood pressure were measured at rest, after 10 min of exercise, and after 15 min of recovery. RESULTS: Metoprolol tended to decrease heart rate during exercise (-21%, -25% and -24%) to a greater extent than carvedilol (-16%, -16% and -18%). At rest, increasing doses of metoprolol caused decreasing heart rates (62, 60 and 58 beats/min) whereas increasing doses of carvedilol caused increasing heart rates (62, 66 and 69 beats/min), 50 and 100 mg carvedilol failed to differ significantly from the placebo (71 beats/min). CONCLUSIONS: We conclude that clinically recommended doses of carvedilol cause a clinically relevant beta-blockade in humans predominantly during exercise where it appears to be slightly (although not significantly) less effective than metoprolol. On the other hand, the effects of carvedilol on heart rate at rest appear rather weak, particularly in subjects with a low sympathetic tone. This might be caused by a reflex increase on sympathetic drive secondary to peripheral vasodilation resulting from the alpha-blocking effects of the drug. These results might be helpful in explaining why carvedilol, in contrast to metoprolol, may fail to cause up-regulation of beta-adrenoceptor density and does not decrease nocturnal melatonin release. This, in turn, may be a reason for the weak side-effects of carvedilol resulting from the beta-blockade. In addition, our data might be of interest in the interpretation of the forthcoming results of the COMET trial, although it has to be emphasised that they were derived from healthy subjects and, therefore, cannot be directly extrapolated to patients with heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Reference_Values_MeSH 
****** 11378007
----K I
----T Systematic review of the impact of beta blockers on mortality and hospital admissions in heart failure.
----A Heart failure is a common condition that carries a high burden of mortality and morbidity. Several randomised trials have evaluated the effects of beta blockers in heart failure. This paper gives a systematic overview of published randomised trials of beta blockers in heart failure using standard methods. In all, 22 randomised controlled trials were identified with a total of 10480 patients, and an average of 11 months of treatment. The average age was 61 years and 4% were female. Most studies excluded patients with severe heart failure. Death rates in patients randomised to receive beta blockers compared to controls were 458/5657 (8.0%) and 635/4951 (12.8%) respectively, odds ratio 0.63, 95% CI 0.55-0.72, P<0.00001. Similar reductions were observed for hospital admissions for worsening heart failure (11.3 vs. 17.1%, respectively, odds ratio 0.63) and for the composite outcome of death or heart-failure hospital admission (19.4 vs. 26.9%, respectively, odds ratio 0.66). These results show that beta blockers reduce the risk of mortality or the need for heart-failure hospital admission by approximately one third. Absolute reductions of 5-6% in event rates were observed over approximately 1 year of treatment period. These important benefits should be implemented as a priority, since treatment with beta blockers is inexpensive and heart failure carries a high risk of death and disability. Further information on the effect of beta blockers in elderly patients and women would be helpful.
----P Clinical_Trial Journal_Article Meta-Analysis Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Double-Blind_Method_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH P_Patient_Admission_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11378009
----K E
----T A cost-effectiveness analysis of bisoprolol for heart failure.
----A Aims: This study considers the cost-effectiveness of bisoprolol in heart failure patients as an adjunctive therapy to usual treatment. Methods and results: A cost-effectiveness model was constructed using data available from the CIBIS I & II trials and other secondary sources. Differences in patient survival rates were calculated for bisoprolol (n=1327) and placebo groups (n=1320) extrapolating data over a 5-year period, under limited and extended benefits scenarios to calculate life years gained (LYG). Hospitalisation rates were calculated using data from both CIBIS trials. Costs were considered under two different patient management protocols for treatment initiation - shared care by outpatient clinics and GPs and initiation by a nurse working in the community. Discounted LYG were calculated to be 0.228 under the limited benefits scenario and 0.368 under the extended benefits scenario. Under the extended benefits scenario shared care resulted in a cost of pound268 per LYG or pound412 per LYG for community initiation. Under the limited benefits scenario the costs were a pound135 saving and pound69, respectively. Conclusion: This analysis has shown bisoprolol to be an economically attractive therapy in comparison with other treatments. It is hoped that its adoption by clinicians will be rapid, despite the labour intensive and time consuming up-titration process involved in its initiation.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_economics_MeSH Carbazoles_economics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Human_MeSH M_Propanolamines_MeSH S_economics_MeSH Propanolamines_economics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 11378011
----K E
----T The cardiac insufficiency talinolol study (CITAS) study design.
----A Beta-blockers without partial agonist activity are now considered to be strategic therapy for patients with chronic heart failure, but many issues remain to be clarified. The objective of the double-blind, randomized, placebo-controlled cardiac insufficiency talinolol study (CITAS) is to assess efficacy and safety of talinolol - a selective beta-1 adrenoreceptor blocker - in patients with ischemic and non-ischemic heart failure. The primary end-point refers to the influence of talinolol on exercise capacity, evaluated by 6-min walking-test. Secondary end-points consist of left ventricular function, cardiovascular and all-cause mortality, hospitalizations, quality of life, combined clinical end-points and adverse events. There were enrolled 294 patients with stable heart failure in NYHA class II-IV, LVEF <40%, receiving diuretics, ACE-inhibitors and optionally nitrates and digoxin. Talinolol was titrated up to 100 mg/day (one arm) or to 150 mg/d (the other arm), starting with 12.5 mg daily. Enrollment began in November 1997 and the last visit will be in December 2000.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Research_Design_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH 
****** 11378012
----K I
----T Clinical Trials Update: CAPRICORN, COPERNICUS, MIRACLE, STAF, RITZ-2, RECOVER and RENAISSANCE and cachexia and cholesterol in heart failure. Highlights of the Scientific Sessions of the American College of Cardiology, 2001.
----A This is a synopsis of presentations made at the American College of Cardiology (ACC) in 2001 summarising recent research developments relating to heart failure. Clinical studies of particular interest to physicians with an interest in heart failure and its prevention are reviewed. The COPERNICUS trial lends further support to the use of the beta-blocker, carvedilol, in severe heart failure and the CAPRICORN trial to its use in patients with post-infarction left ventricular systolic dysfunction. The MIRACLE study reinforces the evidence from three smaller trials that cardiac resynchronisation therapy is an effective treatment for the relief of symptoms in patients with severe heart failure and cardiac dyssynchrony. The STAF trial casts further doubt on the wisdom of cardioversion as a routine strategy for the management of chronic atrial fibrillation. The RITZ-2 trial suggests that an intravenous, non-selective endothelin antagonist is effective in improving haemodynamics and symptoms and possibly in reducing morbidity in severe heart failure. Observational studies in heart failure suggest that a moderate excess of body fat and elevated blood cholesterol may be desirable in patients with heart failure, challenging the current non-evidenced-based vogue for cholesterol lowering therapy in heart failure. The RENAISSANCE and RECOVER outcome studies of etanercept, a tumour necrosis factor (TNF) receptor analogue that blocks the effect of TNF, were stopped because of lack of evidence of benefit shortly after the ACC.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH M_Cachexia_MeSH S_complications_MeSH Cachexia_complications_MeSH S_drug_therapy_MeSH Cachexia_drug_therapy_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Carboxylic_Acids_MeSH S_therapeutic_use_MeSH Carboxylic_Acids_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Cytokines_MeSH S_antagonists_&_inhibitors_MeSH Cytokines_antagonists_&_inhibitors_MeSH M_Endothelins_MeSH S_antagonists_&_inhibitors_MeSH Endothelins_antagonists_&_inhibitors_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Indans_MeSH S_therapeutic_use_MeSH Indans_therapeutic_use_MeSH M_Injections__Intravenous_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Pyridines_MeSH S_administration_&_dosage_MeSH Pyridines_administration_&_dosage_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH M_United_States_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 11386927
----K E
----T Effect of ramipril vs amlodipine on renal outcomes in hypertensive nephrosclerosis: a randomized controlled trial.
----A CONTEXT: Incidence of end-stage renal disease due to hypertension has increased in recent decades, but the optimal strategy for treatment of hypertension to prevent renal failure is unknown, especially among African Americans. OBJECTIVE: To compare the effects of an angiotensin-converting enzyme (ACE) inhibitor (ramipril), a dihydropyridine calcium channel blocker (amlodipine), and a beta-blocker (metoprolol) on hypertensive renal disease progression. DESIGN, SETTING, AND PARTICIPANTS: Interim analysis of a randomized, double-blind, 3 x 2 factorial trial conducted in 1094 African Americans aged 18 to 70 years with hypertensive renal disease (glomerular filtration rate [GFR] of 20-65 mL/min per 1.73 m(2)) enrolled between February 1995 and September 1998. This report compares the ramipril and amlodipine groups following discontinuation of the amlodipine intervention in September 2000. INTERVENTIONS: Participants were randomly assigned to receive amlodipine, 5 to 10 mg/d (n = 217), ramipril, 2.5 to 10 mg/d (n = 436), or metoprolol, 50 to 200 mg/d (n = 441), with other agents added to achieve 1 of 2 blood pressure goals. MAIN OUTCOME MEASURES: The primary outcome measure was the rate of change in GFR; the main secondary outcome was a composite index of the clinical end points of reduction in GFR of more than 50% or 25 mL/min per 1.73 m(2), end-stage renal disease, or death. RESULTS: Among participants with a urinary protein to creatinine ratio of >0.22 (corresponding approximately to proteinuria of more than 300 mg/d), the ramipril group had a 36% (2.02 [SE, 0.74] mL/min per 1.73 m(2)/y) slower mean decline in GFR over 3 years (P =.006) and a 48% reduced risk of the clinical end points vs the amlodipine group (95% confidence interval [CI], 20%-66%). In the entire cohort, there was no significant difference in mean GFR decline from baseline to 3 years between treatment groups (P =.38). However, compared with the amlodipine group, after adjustment for baseline covariates the ramipril group had a 38% reduced risk of clinical end points (95% CI, 13%-56%), a 36% slower mean decline in GFR after 3 months (P =.002), and less proteinuria (P<.001). CONCLUSION: Ramipril, compared with amlodipine, retards renal disease progression in patients with hypertensive renal disease and proteinuria and may offer benefit to patients without proteinuria.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_African_Americans_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nephrosclerosis_MeSH S_complications_MeSH Nephrosclerosis_complications_MeSH S_drug_therapy_MeSH Nephrosclerosis_drug_therapy_MeSH M_Proportional_Hazards_Models_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11395222
----K E
----T Benefits of antihypertensive drug treatment in elderly patients with isolated systolic hypertension.
----A Isolated systolic hypertension affects over 15% of all people older than 60 years. In the elderly, systolic hypertension is a major modifiable cardiovascular risk factor. Systolic blood pressure is associated with higher risk of an adverse outcome, whereas diastolic blood pressure is inversely correlated with total mortality, independent of systolic blood pressure, highlighting the role of pulse pressure as risk factor. Three placebo-controlled outcome trials on antihypertensive drug treatment in older patients with isolated systolic hypertension have been published: the Systolic Hypertension in the Elderly Program (SHEP), the Systolic Hypertension in Europe (Syst-Eur) Trial and the Systolic Hypertension in China (Syst-China) Trial. These three trials demonstrated the benefit of antihypertensive drug treatment. A meta-analysis was performed by pooling the patients from these three trials with a subset of patients with isolated systolic hypertension from five other trials in the elderly. Antihypertensive treatment based on a calcium-channel blocker may provide additional benefits in diabetic patients and in the prevention of dementia and renal dysfunction. The pooled results of 15693 older patients with isolated systolic hypertension prove that antihypertensive drug treatment is justified if on repeated clinic measurements systolic blood pressure is 160 mmHg or higher.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Systole_MeSH 
****** 11396760
----K E
----T Endoscopic sclerosis versus cyanoacrylate endoscopic injection for the first episode of variceal bleeding: a prospective, controlled, and randomized study in Child-Pugh class C patients.
----A BACKGROUND AND STUDY AIMS: Despite the recognized efficacy of sclerotherapy and elastic band ligation in controlling variceal hemorrhage, the results of endoscopic treatment in Child-Pugh class C patients remain poor. The aim of this prospective, controlled, and randomized study was to compare conventional sclerotherapy with injection of the tissue adhesive N-butyl-2-cyanoacrylate in controlling the first episode of rupturing of esophageal varices. PATIENTS AND METHODS: From January 1994 to June 1997, 36 consecutive Child-Pugh class C cirrhotic patients were admitted with an initial episode of esophageal variceal bleeding. They were randomly assigned to receive sclerotherapy with a 3% ethanolamine oleate solution (group 1, 18 patients) or injection of tissue adhesive (group 2, 18 patients). Episodes of recurrent bleeding were managed after the randomization procedure. After bleeding had been controlled, patients in both groups received weekly sessions of conventional sclerotherapy to eradicate any remaining esophageal veins. RESULTS: The patients in the two treatment groups had similar characteristics on entry into the study. More than 80% of the patients were admitted with moderate or severe hemorrhage. Approximately half of them presented with active bleeding during the index endoscopy. Early recurrent bleeding was observed in ten of the 18 patients in group 1 (55.6%) and in two of the 18 in group 2 (11.1%; P = 0.01). The hospital mortality rates were 72.2% in group I and 33.3% in group II (P = 0.04). CONCLUSION: These findings support the view that cyanoacrylate injection is superior to conventional sclerosis for controlling esophageal variceal bleeding in Child-Pugh class C patients. It is also highly probable that the better bleeding control achieved using the cyanoacrylate tissue adhesive treatment led to a lower hospital mortality rate.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Cyanoacrylates_MeSH S_administration_&_dosage_MeSH Cyanoacrylates_administration_&_dosage_MeSH S_therapeutic_use_MeSH Cyanoacrylates_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH P_Esophagoscopy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Sclerosing_Solutions_MeSH S_therapeutic_use_MeSH Sclerosing_Solutions_therapeutic_use_MeSH P_Sclerotherapy_MeSH 
****** 11399339
----K E
----T Effect of beta-blockade on heart rate variability in decompensated heart failure.
----A BACKGROUND: One of the putative mechanisms for the salutary effects of beta-blockers in patients with congestive heart failure is their ability to improve autonomic dysfunction. However, patients with profound neurohumoral abnormalities derive little survival benefit from beta-blockers. The purpose of the current study was to evaluate the effect of beta-blockers on heart rate variability in decompensated heart failure. METHODS: Time and frequency domain heart rate variability indices were obtained from 24-h Holter recordings and compared to assess the role of beta-blockade in 199 patients (mean age 60+/-14 years [range 21 to 87]) with decompensated heart failure (New York Heart Association functional class III [66%] and IV [34%]). RESULTS: All heart rate variability indices were markedly suppressed but were substantially higher in patients who were on beta-blockers. Time domain measures of parasympathetic cardiac activity, the percentage of RR intervals with >50 ms variation (4.9+/-0.6 vs. 7.7+/-1.2%, P=0.006) and the square root of mean squared differences of successive RR intervals (22.7+/-2.0 vs. 31.6+/-4.1 ms, P=0.004), were higher in the beta-blocker group. Spectral analysis revealed that the total power and the ultra low frequency power were significantly higher in patients on beta-blockers (82% and 59%, respectively). The high frequency power, a spectral index of parasympathetic modulation, was 41% higher in the beta-blocker group (121+/-25 vs. 171+/-27 ms(2), P=0.02). Multiple linear regression, adjusted for clinical parameters and drug therapies, revealed a strong positive relationship between beta-blockade and higher values of time and frequency domain measures. The mean number of ventricular tachycardia episodes were significantly lower in patients on beta-blocker therapy (3.6+/-1.5 vs. 19.0+/-5.3, P=0.04). CONCLUSIONS: beta-blockers improve the impaired cardiac autonomic regulation during high sympathetic stress of decompensated heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11401110
----K E
----T The effect of correction of mild anemia in severe, resistant congestive heart failure using subcutaneous erythropoietin and intravenous iron: a randomized controlled study.
----A OBJECTIVES: This is a randomized controlled study of anemic patients with severe congestive heart failure (CHF) to assess the effect of correction of the anemia on cardiac and renal function and hospitalization. BACKGROUND: Although mild anemia occurs frequently in patients with CHF, there is very little information about the effect of correcting it with erythropoietin (EPO) and intravenous iron. METHODS: Thirty-two patients with moderate to severe CHF (New York Heart Association [NYHA] class III to IV) who had a left ventricular ejection fraction (LVEF) of < or =40% despite maximally tolerated doses of CHF medications and whose hemoglobin (Hb) levels were persistently between 10.0 and 11.5 g% were randomized into two groups. Group A (16 patients) received subcutaneous EPO and IV iron to increase the level of Hb to at least 12.5 g%. In Group B (16 patients) the anemia was not treated. The doses of all the CHF medications were maintained at the maximally tolerated levels except for oral and intravenous (IV) furosemide, whose doses were increased or decreased according to the clinical need. RESULTS: Over a mean of 8.2+/-2.6 months, four patients in Group B and none in Group A died of CHF-related illnesses. The mean NYHA class improved by 42.1% in A and worsened by 11.4% in B. The LVEF increased by 5.5% in A and decreased by 5.4% in B. The serum creatinine did not change in A and increased by 28.6% in B. The need for oral and IV furosemide decreased by 51.3% and 91.3% respectively in A and increased by 28.5% and 28.0% respectively in B. The number of days spent in hospital compared with the same period of time before entering the study decreased by 79.0% in A and increased by 57.6% in B. CONCLUSIONS: When anemia in CHF is treated with EPO and IV iron, a marked improvement in cardiac and patient function is seen, associated with less hospitalization and renal impairment and less need for diuretics.
----P Case_Reports Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Anemia_MeSH S_complications_MeSH Anemia_complications_MeSH S_drug_therapy_MeSH Anemia_drug_therapy_MeSH M_Erythropoietin_MeSH S_administration_&_dosage_MeSH Erythropoietin_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Injections__Subcutaneous_MeSH M_Iron_MeSH S_administration_&_dosage_MeSH Iron_administration_&_dosage_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH 
****** 11401111
----K I
----T Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: prognostic utility and prediction of benefit from carvedilol in chronic ischemic left ventricular dysfunction. Australia-New Zealand Heart Failure Group.
----A OBJECTIVES: We sought to assess plasma concentrations of the amino (N)-terminal portion of pro-brain natriuretic peptide (N-BNP) and adrenomedullin for prediction of adverse outcomes and responses to treatment in 297 patients with ischemic left ventricular (LV) dysfunction who were randomly assigned to receive carvedilol or placebo. BACKGROUND: Although neurohormonal status has known prognostic significance in heart failure, the predictive power of either N-BNP or adrenomedullin in chronic ischemic LV dysfunction has not been previously reported. METHODS: Plasma N-BNP and adrenomedullin were measured in 297 patients with chronic ischemic (LV) dysfunction before randomization to carvedilol or placebo, added to established treatment with a converting enzyme inhibitor and loop diuretic (with or without digoxin). The patients' clinical outcomes, induding mortality and heart failure events, were recorded for 18 months. RESULTS: Above-median N-BNP and adrenomedullin levels conferred increased risks (all p < 0.001) of mortality (risk ratios [95% confidence intervals]: 4.67 [2-10.9] and 3.92 [1.76-8.7], respectively) and hospital admission with heart failure (4.7 [2.2-10.3] and 2.4 [1.3-4.5], respectively). Both of these predicted death or heart failure independent of age, New York Heart Association functional class, LV ejection fraction, previous myocardial infarction or previous admission with heart failure. Carvedilol reduced the risk of death or heart failure in patients with above-median levels of N-BNP or adrenomedullin, or both, to rates not significantly different from those observed in patients with levels below the median value. CONCLUSIONS: In patients with established ischemic LV dysfunction, plasma N-BNP and adrenomedullin are independent predictors of mortality and heart failure. Carvedilol reduced mortality and heart failure in patients with higher pre-treatment plasma N-BNP and adrenomedullin.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Nerve_Tissue_Proteins_MeSH S_blood_MeSH Nerve_Tissue_Proteins_blood_MeSH M_Peptide_Fragments_MeSH S_blood_MeSH Peptide_Fragments_blood_MeSH M_Peptides_MeSH S_blood_MeSH Peptides_blood_MeSH M_Prognosis_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11401736
----K I
----T Beta-blockers to reduce mortality in patients with systolic dysfunction: a meta-analysis.
----A OBJECTIVE: The researchers reviewed published clinical trials and performed a meta-analysis to assess if therapy with adrenergic beta-antagonists (beta-blockers) reduces the risk of mortality in patients with systolic dysfunction. STUDY DESIGN: A systematic review was performed with meta-analysis where appropriate. Clinical trials were reviewed with respect to the quality of the research methods, including patient population and end points. Two independent reviewers calculated relative risk, relative risk reduction, absolute risk reduction, and number needed to treat for the total mortality end point reported in each trial. A meta-analysis was performed. DATA SOURCES: The study team searched pertinent indexing services and references from published articles for relevant literature. The selected clinical trials were randomized, double-blinded, and controlled, and included patients with systolic heart failure. Mortality was assessed as a primary or secondary end point. OUTCOMES MEASURED: The primary outcome was mortality. RESULTS: Statistically and clinically significant improvement, including a statistically significant reduction in mortality, has been noted in patients receiving therapy with either bisoprolol, carvedilol, or metoprolol. Pooled analysis revealed a statistically significant reduction in the risk of total mortality (odds ratio [OR]MH=0.66; 95% confidence interval [CI], 0.58-0.75) and sudden death (ORMH=0.61; 95% CI, 0.5-0.75) for patients receiving beta-blocker therapy. CONCLUSIONS: All patients with New York Heart Association class II and III heart failure should receive beta-blocker therapy with bisoprolol, carvedilol, or metoprolol. Additional clinical trials are ongoing and will provide further data on which patients receive the greatest benefit from therapy and which beta-blocker may be preferred.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Research_Design_MeSH S_standards_MeSH Research_Design_standards_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH P_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH 
****** 11403364
----K E
----T Rationale, design, methods and baseline demography of participants of the Anglo-Scandinavian Cardiac Outcomes Trial. ASCOT investigators.
----A OBJECTIVE: To test the primary hypothesis that a newer antihypertensive treatment regimen (calcium channel blocker +/- an angiotensin converting enzyme inhibitor) is more effective than an older regimen (beta-blocker +/- a diuretic) in the primary prevention of coronary heart disease (CHD). To test a second primary hypothesis that a statin compared with placebo will further protect against CHD endpoints in hypertensive subjects with a total cholesterol < or = 6.5 mmol/l. DESIGN: Prospective, randomized, open, blinded endpoint trial with a double-blinded 2 x 2 factorial component. SETTING: Patients were recruited mainly from general practices. PATIENTS: Men and women aged 40-79 were eligible if their blood pressure was > or = 160 mmHg systolic or > or = 100 mmHg diastolic (untreated) or > or = 140 mmHg systolic or > or = 90 mmHg diastolic (treated) at randomization. INTERVENTIONS: Patients received either amlodipine (5/ 10 mg) +/- perindopril (4/8 mg) or atenolol (50/ 100 mg) +/- bendroflumethiazide (1.25/2.5 mg) +K+ with further therapy as required to reach a blood pressure of < or = 140 mmHg systolic and 90 mmHg diastolic. Patients with a total cholesterol of < or = 6.5 mmol/l were further randomized to receive either atorvastatin 10 mg or placebo daily. MAIN OUTCOME MEASURE: Non-fatal myocardial infarction (MI) and fatal coronary heart disease (CHD). RESULTS: 19 342 men and women were initially randomized, of these 10297 were also randomized into the lipid-lowering limb. All patients had three or more additional cardiovascular risk factors. CONCLUSIONS: The study has 80% power (at the 5% level) to detect a relative difference of 20% in CHD endpoints between the calcium channel blocker-based regimen and the beta-blocker-based regimen. The lipid-lowering limb of the study has 90% power at the 1% level to detect a relative difference of 30% in CHD endpoints between groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Anticholesteremic_Agents_MeSH S_administration_&_dosage_MeSH Anticholesteremic_Agents_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Clinical_Protocols_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Scandinavia_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11403367
----K E
----T Regression of left ventricular hypertrophy in human hypertension with irbesartan.
----A BACKGROUND: The Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA). OBJECTIVE: Angiotensin II induces myocardial hypertrophy. We hypothesized that blockade of angiotensin II subtype 1 (AT1) receptors by the AT1-receptor antagonist irbesartan would reduce left ventricular mass (as measured by echocardiography) more than conventional treatment with a beta blocker. DESIGN AND METHODS: This double-blind study randomized 115 hypertensive men and women with left ventricular hypertrophy to receive either irbesartan 150 mg q.d. or atenolol 50 mg q.d. for 48 weeks. If diastolic blood pressure remained above 90 mmHg, doses were doubled, and additional medications (hydrochlorothiazide and felodipine) were prescribed as needed. Echocardiography was performed at weeks 0, 12, 24 and 48. RESULTS: Baseline mean blood pressure was 162/ 104 mmHg, and mean left ventricular mass index was 157 g/m2 for men and 133 g/m2 for women. Systolic and diastolic blood pressure reductions were similar in both treatment groups. Both irbesartan (P < 0.001) and atenolol (P< 0.001) progressively reduced left ventricular mass index, e.g. by 26 and 14 g/m2 (16 and 9%), respectively, at week 48, with a greater reduction in the irbesartan group (P = 0.024). The proportion of patients who attained a normalized left ventricular mass (i.e. < or = 131 g/m2 for men and < or = 100 g/m2 for women) tended to be greater with irbesartan (47 versus 32%, P = 0.108). CONCLUSIONS: Left ventricular mass was reduced more in the irbesartan group than in the atenolol group. These results suggest that blocking the action of angiotensin II at AT1-receptors may be an important mechanism, beyond that of lowering blood pressure, in the regulation of left ventricular mass and geometry in patients with hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 11402910
----K 1
----T [Change from ACE inhibitor, Ca-antagonist or beta-blocker to candesartan cilexetil: better efficacy and tolerance. SWITCH study (German study segment)]
----A BACKGROUND AND OBJECTIVE: Lack of efficacy in the treatment of hypertension with only one drug presents a problem in general practice and often requires switching to another type of drug, because higher dosage of currently used antihypertensives increases the frequency of side effects. Angiotensin II antagonists are well tolerated and there is no evidence of dose-related increase in side effects. This study in 574 hypertensives under therapy with ACE inhibitors, beta-blockers or calcium channel blockers was undertaken to determine whether direct switching to the Angiotensin II-antagonist candesartan cilexetil at its maximal dose of 16 mg is as effective and tolerable as starting therapy with candesartan cilexetil 8 mg followed by up-titration to 16 mg after 4 weeks. PATIENTS AND METHODS: 258 men (mean age 57 +/- 11 years) and 316 women (58 +/- 12) with essential hypertension (blood pressure < 180/95 mm Hg) under ambulatory therapy with ACE-inhibitors, beta-blockers or calcium channel blockers with inadequate efficacy or tolerability were switched to monotherapy with candesartan cilexetil. Half of the patients were treated with 8 mg for 4 weeks (n = 284), the other half received 16 mg (n = 290). Both groups then were treated with candesartan cilexetil, 16 mg, for further 4 weeks. Choice of treatment was doubly blinded and randomised. RESULTS: After 4 weeks significant blood pressure reduction was observed in both treatment groups (p < 0.0001 for each pretreatment group). A tendency for more adequate blood pressure reduction under initial therapy with candesartan cilexetil 16 mg was observed. There was a small further blood pressure reduction in both treatment groups after 8 weeks. In comparison with the previous medications the proportion of patients with blood pressure reduction < 90 mm Hg diastolic was doubled in both treatment arms after 4 weeks: after initial dose of candesartan cilexetil 8 mg from 36.7% to 78.8%, after initial dose of candesartan cilexetil 16 mg from 43.9% to 81.1%. Clinically relevant side effects were not observed. CONCLUSION: Switching of antihypertensive monotherapy with ACE inhibitors, beta-blockers or calcium channel blockers to candesartan cilexetil 8 mg or 16 mg under ambulatory conditions is safe and equally well tolerated and effectively reduces blood pressure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_adverse_effects_MeSH Benzimidazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 11409070
----K I
----T [Adrenergic beta inhibitors in heart insufficiency: which and when?]
----A After briefly reviewing the alterations of sympathetic nervous system in congestive heart failure and the possible ways of its pharmacological management, we review the present data regarding the use of blocking drugs in major trials (USCP, CIBIS and MERIT-HF). beta blocking drugs have a top and unquestionable role in the therapy of congestive heart failure; we conclude with a few practical rules about their use in this syndrome.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_English_Abstract_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiology_MeSH Sympathetic_Nervous_System_physiology_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 11410575
----K E
----T Angiotensin receptor blockers for chronic heart failure and acute myocardial infarction.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Angiotensin_II_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Models__Cardiovascular_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 11413085
----K E
----T Differential effects of nifedipine and co-amilozide on the progression of early carotid wall changes.
----A BACKGROUND: Common carotid artery intima-media thickness (IMT) progression was compared between 4 years of treatment with nifedipine and diuretic. METHODS AND RESULTS: This study, ancillary to the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT), involved nifedipine 30 mg or co-amilozide (hydrochlorothiazide 25 mg and amiloride 2.5 mg) with optional subsequent titration. Among 439 randomized hypertensive patients, 324 had >/=1 year of follow-up (intent-to-treat group), and 242 completed follow-up (until-end-of-study group). Ultrasonography was performed at baseline, 4 months later, and then every year. Central computerized reading provided far-wall IMT, diameter, and cross-sectional area IMT (CSA-IMT). The primary outcome was IMT progression rate (slope of IMT-time regression). Secondary outcomes were changes from baseline (Delta) in IMT, diameter, and CSA-IMT. In the until-end-of-study population, between-treatment differences existed in IMT progression rate (P=0.002), Delta IMT (P=0.001), and Delta CSA-IMT (P=0.006), because IMT progressed on co-amilozide but not on nifedipine. In the intent-to-treat population, treatment differences existed in Delta IMT (P=0.004) and Delta CSA-IMT (P=0.04) but not in IMT progression rate (P=0.09). Patients with >/=2, 3, or 4 years of follow-up showed treatment differences in IMT progression rate (P=0.04, 0.004, 0.007, respectively), Delta IMT (P=0.005, 0.001, 0.005), and Delta CSA-IMT (P=0.025, 0.013, 0.015). Diameter decreased more on co-amilozide than on nifedipine in the intent-to-treat population (P<0.05), whereas blood pressure decreased similarly on both treatments. CONCLUSIONS: A difference in early carotid wall changes is shown between 2 equally effective antihypertensive treatments.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amiloride_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carotid_Artery__Common_MeSH S_drug_effects_MeSH Carotid_Artery__Common_drug_effects_MeSH S_pathology_MeSH Carotid_Artery__Common_pathology_MeSH S_ultrasonography_MeSH Carotid_Artery__Common_ultrasonography_MeSH M_Carotid_Stenosis_MeSH S_complications_MeSH Carotid_Stenosis_complications_MeSH S_diagnosis_MeSH Carotid_Stenosis_diagnosis_MeSH S_pathology_MeSH Carotid_Stenosis_pathology_MeSH M_Comparative_Study_MeSH M_Disease_Progression_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Combinations_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_France_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11419108
----K E
----T [Comparison of preventive effect of "new" and "old" antihypertensive agents]
----A BACKGROUND: Until recently no morbidity-mortality study had examined the effects of newer drugs like angiotensin-converting enzyme inhibitors, calcium-antagonists and alpha-blockers compared to "old" but well-proven thiazide diuretics and beta-blockers in the treatment of essential hypertension. MATERIAL AND METHODS: The prospective and randomized clinical trials CAPPP, STOP-2, NORDIL, INSIGHT and one arm of ALLHAT, with a total of approximately 58,000 middle-aged or elderly hypertensive patients have been assessed. RESULTS: The primary outcome, composite cardiovascular (CV) death, cerebral stroke and myocardial infarction, in one study with heart failure, or composite fatal coronary heart disease and myocardial infarction, was equal in all trials. INTERPRETATION: According to current evidence, prevention of cardiovascular disease in hypertension is the same irrespective of the class of drug.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11423055
----K E
----T Comparison of the occurrence of ventricular arrhythmias in patients with acutely decompensated congestive heart failure receiving dobutamine versus nesiritide therapy.
----A Ventricular arrhythmias are common in patients with congestive heart failure (CHF) and may be exacerbated by positive inotropic therapy. Because human B-type natriuretic peptide (nesiritide), an arterial and venodilator, inhibits sympathetic activity, it may decrease the incidence of arrhythmias. Our investigation compares the arrhythmogenicity of dobutamine with nesiritide. A total of 305 patients with decompensated CHF requiring intravenous vasoactive therapy were randomized to receive standard therapy (n = 102) or nesiritide (0.015 microg/kg/min [n = 103] or 0.030 microg/kg/min [n = 100]) to gain additional data on the relative safety and efficacy of nesiritide compared with standard parenteral care. Dobutamine was chosen as the standard care agent in 58 subjects. During study drug infusion, all patients had continuous clinical hemodynamic and electrocardiographic monitoring. The dobutamine and nesiritide groups were similar with respect to baseline use of antiarrhythmic agents, including beta blockers. Serious arrhythmias and the incidence of cardiac arrest were more common in patients who received dobutamine than in those taking nesiritide: sustained ventricular tachycardia, 4 (7%) versus 2 (1%), respectively (p = 0.014); nonsustained ventricular tachycardia, 10 (17%) versus 23 (11%), respectively (p = 0.029); cardiac arrest, 3 (5%) versus 0, respectively (p = 0.011). We conclude that among patients with decompensated CHF for whom dobutamine is selected as standard therapy, the incidence of serious ventricular arrhythmias and cardiac arrest is significantly greater than the incidence of these events in patients randomized to nesiritide.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atrial_Natriuretic_Factor_MeSH S_therapeutic_use_MeSH Atrial_Natriuretic_Factor_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dobutamine_MeSH S_therapeutic_use_MeSH Dobutamine_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Natriuretic_Peptide__Brain_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Ventricular_MeSH S_epidemiology_MeSH Tachycardia__Ventricular_epidemiology_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Treatment_Outcome_MeSH 
****** 11423717
----K E
----T Comparison of adenosine and exercise stress test for quantitative perfusion imaging in patients on beta-blocker therapy.
----A Beta-blocker therapy is used to decrease myocardial ischemia during exercise but may cause suboptimal diagnostic performance in exercise stress testing. The aim of the present study was to compare results of quantitative technetium-99-sestamibi single photon emission tomography (SPECT), following exercise stress test or pharmacological stress test with adenosine. We chose adenosine as comparison, since betablockers may not interfere with adenosine induced vasodilatation and therefore possibly may not interfere with its diagnostic performance. Sixteen patients with angiographically documented coronary disease (5 single-vessel, 6 two-vessel and 5 three-vessel disease), who were chronically treated with beta-blockers, performed SPECT imaging at rest, following bicycle exercise and following adenosine infusion in random order. The SPECT data were analyzed visually and quantitatively, using dedicated computer software (CEqual). According to both visual and quantitative SPECT analysis, adenosine was superior to show reversibility. Higher reversibility extent (50 +/- 15 vs. 26 +/- 12 pixels, p < 0.01) and more intense reversibility severity (110 +/- 29 vs. 49 +/- 23 sum of SDs, p < 0.05) were observed during adenosine than exercise. Conclusions: Less myocardial perfusion abnormalities during exercise than during adenosine stress in patients treated with beta-blockers may indicate less ischemia but also an impaired diagnostic performance. Thus adenosine stress test should be preferred to optimize the diagnostic sensitivity in patients during beta-blocker treatment.
----P Case_Reports Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adenosine_MeSH S_diagnostic_use_MeSH Adenosine_diagnostic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radionuclide_imaging_MeSH Coronary_Disease_radionuclide_imaging_MeSH M_Female_MeSH P_Heart_Function_Tests_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tomography__Emission-Computed__Single-Photon_MeSH M_Vasodilator_Agents_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 11422094
----K I
----T A comparative study of oral acetylsalicyclic acid and metoprolol for the prophylactic treatment of migraine. A randomized, controlled, double-blind, parallel group phase III study.
----A This study was a multinational, multicentre, double-blind, active controlled phase III trial designed to investigate efficacy and safety of 300 mg acetylsalicyclic acid (ASA) (n = 135) vs. 200 mg metoprolol (n = 135) in the prophylaxis of migraine. In total 270 (51 male and 219 female) patients, aged 18-65 years, suffering between two and six migraine attacks per month were recruited. The main objective was to show equivalence with respect to efficacy, defined as a 50% reduction in the rate of migraine attacks. A run-in phase was carried out with placebo for 4 weeks, followed by a 16-week drug phase. In both treatment groups the median frequency of migraine attacks improved during the study period, from three to two in the ASA group and from three to one in the metoprolol group; 45.2% of all metoprolol patients were responders compared with 29.6% with ASA. Medication-related adverse events were less frequent in the ASA group (37) than in the metoprolol group (73). The findings from this trial show that metoprolol is superior to ASA for migraine prophylaxis but has more side-effects. Acetylsalicylic acid is better tolerated than metoprolol. Using a strict responder criterion ASA showed a responder rate comparable with the placebo rate in the literature.
----P Clinical_Trial Clinical_Trial__Phase_III Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11416689
----K E
----T Working group report on high blood pressure in pregnancy.
----A This report updates the 1990 National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy and focuses on classification, pathophysiology, and management of the hypertensive disorders of pregnancy. Using evidence-based medicine and consensus, this report updates contemporary approaches to hypertension control during pregnancy by expanding on recommendations made in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). The recommendations to use K5 for determining diastolic pressure and to eliminate edema as a criterion for diagnosing pre-eclampsia are discussed. In addition, the use of blood pressure increases of 30 mm Hg systolic or 15 mm Hg diastolic as a diagnostic criterion has not been recommended, as available evidence shows that women in this group are not likely to suffer increased adverse outcomes. Management considerations are made between chronic hypertension that is present before pregnancy and those occurring as part of the pregnancy-specific condition preeclampsia, as well as management considerations in women with comorbid conditions. A discussion of the pharmacologic treatment of hypertension in pregnancy includes recommendations for specific agents. The use of low-dose aspirin, calcium, or other dietary supplements in the prevention of pre-eclampsia is described, and expanded sections on counseling women for future pregnancies and recommendations for future research are included. Once again we thank Dr. Ray Gifford, Jr., and his committee for volunteering their time to produce this important report. We hope it helps the busy clinician prevent and manage a very important problem.
----P Guideline Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Counseling_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Diseases_MeSH S_complications_MeSH Kidney_Diseases_complications_MeSH M_Lactation_MeSH S_physiology_MeSH Lactation_physiology_MeSH M_Pre-Eclampsia_MeSH S_physiopathology_MeSH Pre-Eclampsia_physiopathology_MeSH S_prevention_&_control_MeSH Pre-Eclampsia_prevention_&_control_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH S_physiopathology_MeSH Pregnancy_Complications__Cardiovascular_physiopathology_MeSH M_Puerperium_MeSH S_physiology_MeSH Puerperium_physiology_MeSH 
****** 11416704
----K 3
----T Current concepts of pharmacotherapy in hypertension--ophthalmically administered beta blockers and their cardiopulmonary effects.
----A Early clinical studies revealed that timolol and other topical beta blockers were effective in reducing intra-ocular pressure, without the side effects associated with other antiglaucoma agents. However, because persons with cardiovascular or respiratory diseases were generally excluded from many of these early studies, the risk of serious cardiovascular and respiratory side effects was seriously underestimated. Once these drugs were made available to the general population, reports of systemic side effects began to proliferate. Very quickly, adverse effects from topical beta blockade became "old news." Despite this recognition, many treating physicians remained unaware of the potential for systemic beta blockade from topically applied beta blockers. A significant portion of a topically administered dose of a beta blocker can be absorbed and thereby affect systemic beta blockade. Sensitivity to systemic beta blockade can be quite dramatic in certain highly susceptible patients, particularly those with either cardiac or pulmonary abnormalities. Careful review of patients' medications will generally lessen, but not completely eliminate, the risk of undesired complications attributable to topical beta blockade.
----P Journal_Article Review Review__Tutorial 
----M M_Administration__Topical_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lung_MeSH S_drug_effects_MeSH Lung_drug_effects_MeSH M_Ophthalmic_Solutions_MeSH S_administration_&_dosage_MeSH Ophthalmic_Solutions_administration_&_dosage_MeSH 
****** 11426017
----K E
----T Effects of the American College of Rheumatology systemic sclerosis trial guidelines on the nature of systemic sclerosis patients entering a clinical trial.
----A OBJECTIVES: To compare the systemic sclerosis (SSc) patients entered into the d-penicillamine trial with SSc patients entered into previous controlled SSc trials. It was hypothesized that the d-penicillamine trial patients, who conformed to the American College of Rheumatology (ACR) guidelines for clinical trials in SSc were different from patients entered into previous trials. METHODS: Patients entering a double-blind, randomized trial of low- vs high-dose d-penicillamine were described carefully and completely. Their characteristics were then compared with previously published data on SSc and its treatment. RESULTS: One hundred and thirty-four patients had early [mean duration 9.5 (s.d. 4.2) months], diffuse [skin score 21 (8)] disease. Organ involvement in the patients was as follows: pulmonary 54%, cardiac 20%, joints 38%, muscular 20%. Thirty-three per cent had mild proteinuria and 13% were hypertensive when first seen. Compared with patients in most previous studies, these SSc patients had earlier disease and uniformly had diffuse disease. They had less muscular involvement, less dyspnoea, less abnormal pulmonary function and less cardiac and less renal involvement than patients in earlier studies. CONCLUSIONS: The use of the new ACR guidelines for SSc trials may change the nature of patient populations entering future studies.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Demography_MeSH M_Female_MeSH M_Guidelines_MeSH M_Human_MeSH M_Literature_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Patient_Selection_MeSH M_Randomized_Controlled_Trials_MeSH S_standards_MeSH Randomized_Controlled_Trials_standards_MeSH M_Scleroderma__Systemic_MeSH S_physiopathology_MeSH Scleroderma__Systemic_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11428837
----K E
----T Reduced costs with bisoprolol treatment for heart failure: an economic analysis of the second Cardiac Insufficiency Bisoprolol Study (CIBIS-II).
----A BACKGROUND: Beta-blockers, used as an adjunctive to diuretics, digoxin and angiotensin converting enzyme inhibitors, improve survival in chronic heart failure. We report a prospectively planned economic analysis of the cost of adjunctive beta-blocker therapy in the second Cardiac Insufficiency BIsoprolol Study (CIBIS II). METHODS: Resource utilization data (drug therapy, number of hospital admissions, length of hospital stay, ward type) were collected prospectively in all patients in CIBIS II. These data were used to determine the additional direct costs incurred, and savings made, with bisoprolol therapy. As well as the cost of the drug, additional costs related to bisoprolol therapy were added to cover the supervision of treatment initiation and titration (four outpatient clinic/office visits). Per diem (hospital bed day) costings were carried out for France, Germany and the U.K. Diagnosis related group costings were performed for France and the U.K. Our analyses took the perspective of a third party payer in France and Germany and the National Health Service in the U.K. RESULTS: Overall, fewer patients were hospitalized in the bisoprolol group, there were fewer hospital admissions per patient hospitalized, fewer hospital admissions overall, fewer days spent in hospital and fewer days spent in the most expensive type of ward. As a consequence the cost of care in the bisoprolol group was 5-10% less in all three countries, in the per diem analysis, even taking into account the cost of bisoprolol and the extra initiation/up-titration visits. The cost per patient treated in the placebo and bisoprolol groups was FF35 009 vs FF31 762 in France, DM11 563 vs DM10 784 in Germany and pound4987 vs pound4722 in the U.K. The diagnosis related group analysis gave similar results. INTERPRETATION: Not only did bisoprolol increase survival and reduce hospital admissions in CIBIS II, it also cut the cost of care in so doing. This 'win-win' situation of positive health benefits associated with cost savings is favourable from the point of view of both the patient and health care systems. These findings add further support for the use of beta-blockers in chronic heart failure.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH S_economics_MeSH Chemotherapy__Adjuvant_economics_MeSH M_Cost-Benefit_Analysis_MeSH M_France_MeSH S_epidemiology_MeSH France_epidemiology_MeSH M_Germany_MeSH S_epidemiology_MeSH Germany_epidemiology_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Prospective_Studies_MeSH M_Quality-Adjusted_Life_Years_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11430394
----K I
----T A prospective comparison of four antihypertensive agents in daily clinical practice.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Mass_Index_MeSH M_Comparative_Study_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nisoldipine_MeSH S_therapeutic_use_MeSH Nisoldipine_therapeutic_use_MeSH M_Prevalence_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11430179
----K 5
----T Hypertension.
----A This article reviews some of the salient points in the management of hypertension as recommended by the "Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure." New developments since publication of this 1997 report are also discussed.
----P Journal_Article Review Review__Tutorial 
----M M_Algorithms_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_therapy_MeSH Hypertension_therapy_MeSH 
****** 11434453
----K E
----T Barnidipine.
----A Bamidipine is an antihypertensive drug belonging to the dihydropyridine (DHP) group of calcium antagonists. It is available in a modified-release formulation which has a gradual onset of action and is effective in a single daily oral dose of 10 to 20 mg. Bamidipine has selective action against cardiovascular calcium antagonist receptors and its antihypertensive action is related to the reduction of peripheral vascular resistance secondary to its vasodilatory action. The clinical antihypertensive efficacy of barnidipine is similar to that of other DHP calcium antagonists such as nitrendipine and amlodipine, and antihypertensives belonging to other drug classes such as atenolol and enalapril. Barnidipine has been found to be as efficacious and well tolerated as hydrochlorothiazide in the management of hypertension in elderly patients. Barnidipine is generally well tolerated. As with other DHP calcium antagonists, vasodilator adverse events such as headache, flushing and peripheral oedema account for most of the adverse events reported with its use and are usually transient. Oedema is less frequent than with amlodipine and nitrendipine. Its use is not associated with reflex tachycardia.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Animals_MeSH M_Area_Under_Curve_MeSH M_Biological_Availability_MeSH P_Calcium_Channel_Blockers_MeSH S_metabolism_MeSH Calcium_Channel_Blockers_metabolism_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH P_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Intestinal_Absorption_MeSH M_Multicenter_Studies_MeSH P_Nifedipine_MeSH S_analogs_&_derivatives_MeSH Nifedipine_analogs_&_derivatives_MeSH S_metabolism_MeSH Nifedipine_metabolism_MeSH S_pharmacokinetics_MeSH Nifedipine_pharmacokinetics_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11433884
----K 1
----T Use of propranolol in heart failure patients: safety, tolerability, and effects on left ventricular function.
----A INTRODUCTION AND OBJECTIVES: Beta-blockers have been shown to improve prognosis in patients with heart failure (HF). Propranolol, which is a low-cost drug, has not been fully studied in this setting. We sought to determine the safety, tolerability and effects on left ventricular function observed with the use of propranolol in HF patients, in functional class II-IV of the New York Heart Association. POPULATION AND METHODS: Prospective study in which 20 outpatients (10 male, mean age 56 +/- 12 years, ranging from 20 to 70) were included. Mean left ventricular ejection fraction (EF) was 28%. Safety, tolerability and effects on electrocardiographic and echocardiographic variables were analyzed. Patients were evaluated in three steps: a) Step I--optimization on conventional drugs and assessment of baseline parameters; b) Step II--start of propranolol (10-20 mg/day), increasing the dose weekly to achieve a heart rate of 60 bpm, or a maximum daily dose of 120 mg; c) Step III--reappraisal of the parameters analyzed in step I, after 3 months of propranolol treatment. RESULTS: On average, after treatment with propranolol, EF increased by 52% (p = 0.0003), E wave deceleration time was prolonged by 62% (p = 0.001) and effective ventricular filling time increased by 38.5% (p = 0.0005). Two patients developed mild congestion which was controlled by increasing diuretic doses, with no need to interrupt the protocol. Four patients had bradycardia-related symptoms, controlled by reducing digoxin doses. Nine subjects developed hyperkalemia, reversed by interrupting or reducing spironolactone. CONCLUSION: Propranolol was safe and well tolerated, and had beneficial effects on ventricular function in HF patients. Its impact on mortality requires further study.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11435332
----K E
----T Trends in acute coronary heart disease mortality, morbidity, and medical care from 1985 through 1997: the Minnesota heart survey.
----A BACKGROUND: Coronary heart disease (CHD) mortality continued to decline from 1985 to 1997. METHODS AND RESULTS: We tabulated CHD deaths (ICD-9 codes 410 through 414) in the Minneapolis/St Paul, Minnesota, area. For 1985, 1990, and 1995, trained nurses abstracted the hospital records of patients 30 to 74 years old with a discharge diagnosis of acute CHD (ICD-9 codes 410 or 411). Acute myocardial infarction (AMI) events were validated and followed for 3-year all-cause mortality. Between 1985 and 1997, age-adjusted CHD mortality rates in Minneapolis/St Paul fell 47% and 51% in men and women, respectively; the comparable declines in US whites were 34% and 29%. In-hospital mortality declined faster than out-of-hospital mortality. The rate of AMI (ICD-9 code 410) hospital discharges declined almost 20% between 1985 and 1995, whereas the discharge rate for unstable angina (ICD-9 code 411) increased substantially. The incidence of hospitalized definite AMI declined approximately 10%, whereas recurrence rates fell 20% to 30%. Three-year case fatality rates after hospitalized AMI decreased consistently by 31% and 41% in men and women, respectively. In-hospital administration of thrombolytic therapy, emergency angioplasty, ACE inhibitors, beta-blockers, heparin, and aspirin increased greatly. CONCLUSIONS: Declining out-of-hospital death rates, declining incidence and recurrence of AMI in the population, and marked improvements in the survival of AMI patients all contributed to the 1985 to 1997 decline of CHD mortality in the Minneapolis/St Paul metropolitan area. The effects of early and late medical care seem to have had the greatest contribution to rates during this time period.
----P Journal_Article 
----M M_Acute_Disease_MeSH M_Adult_MeSH M_Age_Distribution_MeSH M_Aged_MeSH M_Comorbidity_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_European_Continental_Ancestry_Group_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH P_Health_Surveys_MeSH M_Hospital_Mortality_MeSH S_trends_MeSH Hospital_Mortality_trends_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Minnesota_MeSH S_epidemiology_MeSH Minnesota_epidemiology_MeSH M_Morbidity_MeSH S_trends_MeSH Morbidity_trends_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH M_Recurrence_MeSH M_Sex_Distribution_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH S_trends_MeSH Survival_Rate_trends_MeSH 
****** 11435335
----K E
----T Randomized, placebo-controlled study for immunosuppressive treatment of inflammatory dilated cardiomyopathy: two-year follow-up results.
----A BACKGROUND: Previous studies have shown disappointing results for immunosuppressive treatment in patients with dilated cardiomyopathy. Therefore, we studied the effectiveness of such therapy in patients with HLA upregulation on biopsy. METHODS AND RESULTS: Of 202 patients with dilated cardiomyopathy, 84 patients with increased HLA expression were randomized to receive either immunosuppression or placebo for 3 months; they were then followed for 2 years. After 2 years, there were no significant differences in the primary end point (a composite of death, heart transplantation, and hospital readmission) between the 2 study groups (22.8% for the immunosuppression group and 20.5% for the placebo). The secondary efficacy end point included changes in ejection fraction, end-diastolic diameter, end-diastolic volume, end-systolic volume and NYHA class; left ventricular ejection fraction increased significantly in the immunosuppression group compared with the placebo group (95% CI, 4.20 to 13.12; P<0.001) after 3 months of follow-up. The early favorable effects of immunosuppressive therapy on left ventricular volume, left ventricular diastolic dimension, and New York Heart Association class were also present. This improvement was maintained in the immunosuppression group at 2 years (ejection fraction: 95% CI, 6.94 to 19.04; P<0.001). In addition, on the basis of the protocol-specified definition of improvement, 71.8% patients in the immunosuppression group versus 20.9% patients in the placebo group met the criteria of improvement after 3 months (P<0.001). At the end of the follow-up period, 71.4% patients from the immunosuppression group versus 30.8% patients from the placebo group were improved (P=0.001). CONCLUSIONS: These data demonstrate a long-term benefit of immunosuppressive therapy in patients with dilated cardiomyopathy and HLA upregulation on biopsy specimens. Thus, restoration of immunosuppressive therapy for such patients should be considered.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Azathioprine_MeSH S_adverse_effects_MeSH Azathioprine_adverse_effects_MeSH S_therapeutic_use_MeSH Azathioprine_therapeutic_use_MeSH M_Biopsy_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_immunology_MeSH Cardiomyopathy__Congestive_immunology_MeSH S_pathology_MeSH Cardiomyopathy__Congestive_pathology_MeSH M_Chronic_Disease_MeSH M_Drug_Therapy__Combination_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_HLA_Antigens_MeSH S_biosynthesis_MeSH HLA_Antigens_biosynthesis_MeSH M_Human_MeSH M_Hypertension_MeSH S_chemically_induced_MeSH Hypertension_chemically_induced_MeSH M_Immunosuppressive_Agents_MeSH S_adverse_effects_MeSH Immunosuppressive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH M_Male_MeSH M_Myocarditis_MeSH S_complications_MeSH Myocarditis_complications_MeSH S_drug_therapy_MeSH Myocarditis_drug_therapy_MeSH S_immunology_MeSH Myocarditis_immunology_MeSH S_pathology_MeSH Myocarditis_pathology_MeSH M_Myocardium_MeSH S_immunology_MeSH Myocardium_immunology_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Prednisone_MeSH S_adverse_effects_MeSH Prednisone_adverse_effects_MeSH S_therapeutic_use_MeSH Prednisone_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11435337
----K E
----T Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial.
----A BACKGROUND: This clinical investigation was performed to compare the effects of permanent dual-chamber cardiac pacing with pharmacological therapy in patients with recurrent vasovagal syncope. METHODS AND RESULTS: Patients from 14 centers were randomized to receive either a DDD pacemaker provided with rate-drop response function or the beta-blocker atenolol at the dosage of 100 mg once a day. Inclusion criteria were age >35 years, >/=3 syncopal spells in the preceding 2 years, and positive response to tilt table testing with syncope occurring in association with relative bradycardia. The primary outcome was the first recurrence of syncope after randomization. Enrollment was started in December 1997, and the first formal interim analysis was performed on July 30, 2000. By that time, 93 patients (38 men and 55 women; mean age, 58.1+/-14.3 years) had been enrolled and randomized, although follow-up data were available for all patients (46 patients in the pacemaker arm, 47 patients in the pharmacological arm). The interim analysis showed a significant effect in favor of permanent cardiac pacing (recurrence of syncope in 2 patients [4.3%] after a median of 390 days) compared with medical treatment (recurrence of syncope in 12 patients [25.5%] after a median of 135 days; OR, 0.133; 95% CI, 0.028 to 0.632; P=0.004). Consequently, enrollment and follow-up were terminated. CONCLUSIONS: DDD pacing with rate-drop response function is more effective than beta-blockade for the prevention of syncopal recurrences in highly symptomatic vasovagal fainters with relative bradycardia during tilt-induced syncope.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH P_Defibrillators__Implantable_MeSH M_Disease-Free_Survival_MeSH M_Electrocardiography_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Function_Tests_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Syncope__Vasovagal_MeSH S_diagnosis_MeSH Syncope__Vasovagal_diagnosis_MeSH S_prevention_&_control_MeSH Syncope__Vasovagal_prevention_&_control_MeSH M_Tilt-Table_Test_MeSH M_Treatment_Outcome_MeSH 
****** 11435745
----K E
----T Factor analysis, including antihypertensive medication, of the outcome of pregnancy in pregnancy-associated hypertension.
----A AIM: To study the influence of different maternal factors, including antihypertensive medication, on the outcome of pregnancy in primi- and multiparas with pregnancy-associated hypertension. METHODS: A retrospective, multiple-variate analysis was undertaken of the influence of several maternal factors, including antihypertensive medication, on fetal death and Apgar scores and the correlation between the medication and the number of caesarean sections in 127 episodes of pregnancy-associated hypertension was studied for the whole group as well as for primi- and multiparas separately. Of the multiparas, 40.8% had a history of preeclampsia, 19.7% of chronic hypertension and 9.2% of diabetes mellitus. Antihypertensive treatment aimed at achieving a blood pressure of 140/90 mm Hg. Forty-one patients (32.3%) received intravenous hydralazine, 25 (19.7%) received nifedipine per os and 44 (34.6%) received labetalol per os. RESULTS: The maximum systolic and diastolic blood pressure in the patients given intravenous hydralazine, nifedipine per os or labetalol per os did not differ, whereas in the multiparas, the number of patients who reached the target blood pressure while using labetalol was higher than with the two other medications, especially in comparison with intravenous hydralazine. For the primiparas, the time of delivery was the only factor with a significant impact on the Apgar scores. In the multiparas, there was an additional negative influence of the use of intravenous hydralazine. This was not seen in the patients using nifedipine and labetalol. CONCLUSIONS: The results suggest that in multiparas, intravenous hydralazine is possibly associated with more fetal distress when compared to primiparas.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Apgar_Score_MeSH M_Cesarean_Section_MeSH S_statistics_&_numerical_data_MeSH Cesarean_Section_statistics_&_numerical_data_MeSH M_Comorbidity_MeSH M_Disease_Susceptibility_MeSH M_Female_MeSH M_Fetal_Death_MeSH S_epidemiology_MeSH Fetal_Death_epidemiology_MeSH M_Gestosis__EPH_MeSH S_drug_therapy_MeSH Gestosis__EPH_drug_therapy_MeSH S_epidemiology_MeSH Gestosis__EPH_epidemiology_MeSH M_Human_MeSH M_Hydralazine_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Infant__Newborn_MeSH M_Labetalol_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Multivariate_Analysis_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Parity_MeSH M_Pre-Eclampsia_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH S_epidemiology_MeSH Pre-Eclampsia_epidemiology_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH S_epidemiology_MeSH Pregnancy_Complications__Cardiovascular_epidemiology_MeSH M_Pregnancy_Outcome_MeSH M_Pregnancy_in_Diabetics_MeSH S_epidemiology_MeSH Pregnancy_in_Diabetics_epidemiology_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 11441320
----K E
----T Age-related differences in the use of cardiac medications in patients with coronary artery disease.
----A BACKGROUND: Benefits of aspirin and beta-blocker use in patients with coronary artery disease and angiotensin-converting enzyme (ACE) inhibitors in those with left ventricular systolic dysfunction are well documented in all age groups. OBJECTIVE: To investigate whether aspirin, beta-blockers, and ACE inhibitors are equally used in geriatric (> or =65 years) versus younger (<65 years) patients with coronary artery disease. SETTING: University-affiliated major academic hospital. METHODS: Records of 402 patients with coronary artery disease were analyzed for use of aspirin, beta-blockers, and ACE inhibitors. One hundred thirty patients with contraindications to use of these agents were excluded. RESULTS: Of 272 study patients, 85% were using aspirin and 71% beta-blockers. Among the patients with left ventricular systolic dysfunction, 79% were using ACE inhibitors. One hundred forty-seven patients were of geriatric age, whereas 125 were of younger age. No significant difference in the use of aspirin (82% versus 89%, P = 0.10), beta-blockers (71% versus 70%, P = 0.85), or ACE inhibitors (86% versus 69%, P = 0.13) was found between geriatric and younger patients. This lack of difference in use of cardiac medications between geriatric and younger patients persisted on gender-based subgroup analysis. On decade-of-age-based analysis, aspirin use was not equally distributed among all the decades of age (P < 0.005), but beta-blocker use was. CONCLUSION: Results of this study demonstrate equal use of aspirin, beta-blockers, and ACE inhibitors in geriatric versus younger patients with coronary artery disease. Aspirin use was not equally distributed among all the decades of age.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Aspirin_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH M_Cross-Sectional_Studies_MeSH M_Drug_Utilization_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH 
****** 11444579
----K E
----T Patient-reported adherence to guidelines of the Sixth Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
----A OBJECTIVES: To compare antihypertensive drug compliance with treatment guidelines established by the Sixth Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI), and to identify patient adherence to antihypertensive drugs and factors affecting prescribing patterns. METHODS: Patients filling antihypertensive drug prescriptions in metropolitan New York area pharmacies were enrolled. Pharmacy externs collected patient-reported demographics, medical and drug histories, and blood pressure measurements. Compliance with JNC VI guidelines was assessed. RESULTS: Eight hundred twenty-one patients from 102 pharmacies participated. Blood pressure was controlled in 61% of patients at the time of the study. The most prescribed class of antihypertensive agents was angiotensin-converting enzyme inhibitors, followed by diuretics and beta-blockers. Over the study period, compliance with JNC VI guidelines decreased significantly from 85% to 64% (p<0.05). Thirty-seven percent of patients reported consistent adherence to their antihypertensive regimens. Patients' education level was the only factor found to correlate positively with the appropriateness of antihypertensive agents prescribed. CONCLUSION: Compliance with JNC VI guidelines decreased over time, and patient adherence to drug therapy was suboptimal. Continuing-education efforts to reinforce optimal blood pressure management are necessary.
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_psychology_MeSH Hypertension_psychology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH P_Practice_Guidelines_MeSH M_Prospective_Studies_MeSH M_Questionnaires_MeSH 
****** 11453892
----K E
----T Influence of beta-adrenoceptor antagonists on the pharmacokinetics of rizatriptan, a 5-HT1B/1D agonist: differential effects of propranolol, nadolol and metoprolol.
----A AIMS: Patients with migraine may receive the 5-HT1B/1D agonist, rizatriptan (5 or 10 mg), to control acute attacks. Patients with frequent attacks may also receive propranolol or other beta-adrenoceptor antagonists for migraine prophylaxis. The present studies investigated the potential for pharmacokinetic or pharmacodynamic interaction between beta-adrenoceptor blockers and rizatriptan. METHODS: Four double-blind, placebo-controlled, randomized crossover investigations were performed in a total of 51 healthy subjects. A single 10 mg dose of rizatriptan was administered after 7 days' administration of propranolol (60 and 120 mg twice daily), nadolol (80 mg twice daily), metoprolol (100 mg twice daily) or placebo. Rizatriptan pharmacokinetics were assessed. In vitro incubations of rizatriptan and sumatriptan with various beta-adrenoceptor blockers were performed in human S9 fraction. Production of the indole-acetic acid-MAO-A metabolite of each triptan was measured. RESULTS: Administration of rizatriptan during propranolol treatment (120 mg twice daily for 7.5 days) increased the AUC(0, infinity) for rizatriptan by approximately 67% and the Cmax by approximately 75%. A reduction in the dose of propranolol (60 mg twice daily) and/or the incorporation of a delay (1 or 2 h) between propranolol and rizatriptan administration did not produce a statistically significant change in the effect of propranolol on rizatriptan pharmacokinetics. Administration of rizatriptan together with nadolol (80 mg twice daily) or metoprolol (100 mg twice daily) for 7 days did not significantly alter the pharmacokinetics of rizatriptan. No untoward adverse experiences attributable to the pharmacokinetic interaction between propranolol and rizatriptan were observed, and no subjects developed serious clinical, laboratory, or other significant adverse experiences during coadministration of rizatriptan with any of the beta-adrenoceptor blockers. In vitro incubations showed that propranolol, but not other beta-adrenoceptor blockers significantly inhibited the production of the indole-acetic acid metabolite of rizatriptan and sumatriptan. CONCLUSIONS: These results suggest that propranolol increases plasma concentrations of rizatriptan by inhibiting monoamine oxidase-A. When prescribing rizatriptan to migraine patients receiving propranolol for prophylaxis, the 5 mg dose of rizatriptan is recommended. Administration with other beta-adrenoceptor blockers does not require consideration of a dose adjustment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Biological_Availability_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_In_Vitro_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_pharmacology_MeSH Nadolol_pharmacology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Receptor__Serotonin__5-HT1B_MeSH M_Receptor__Serotonin__5-HT1D_MeSH M_Receptors__Serotonin_MeSH S_metabolism_MeSH Receptors__Serotonin_metabolism_MeSH M_Serotonin_Agonists_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH M_Triazoles_MeSH S_pharmacokinetics_MeSH Triazoles_pharmacokinetics_MeSH 
****** 11461738
----K E
----T Propranolol treatment of congestive heart failure in infants with congenital heart disease: The CHF-PRO-INFANT Trial. Congestive heart failure in infants treated with propanol.
----A AIM: Infants with congenital heart disease and left-to-right shunts may develop significant clinical symptoms of congestive heart failure in spite of therapy with digoxin and diuretics. We investigated the effects of beta-blockade in infants with severe heart failure. METHODS AND RESULTS: We performed a prospective, randomized, open monocenter trial in infants treated with digoxin and diuretics (n=10) in comparison to 10 infants receiving additional beta-blocker therapy. After 17 days on average beta-blocker treated infants (propranolol:1,6 mg/kg/day) improved significantly with respect to Ross heart failure score (3.3+/-2.3 vs. 8.3+/-1.9, P=0.002), lower renin levels (338+/-236 vs. 704+/-490 microU/l, P=0.008) and lower mean heart rates in Holter ECG (118+/-10 vs. 142+/-11 beats/min, P<0.001). While digoxin and diuretic treated infants had unchanged mean heart rate (149+/-8 vs. 148+/-10 beats/min), less decrease of symptoms (Ross Score: 8.5+/-1.7 vs. 6.8+/-2.3, P=0.02) but a significant increase of renin levels (139+/-102 vs. 938+/-607 microU/l, P=0.001). CONCLUSION: Additional propranolol treatment but not digoxin and diuretics alone can effectively reduce clinical symptoms of heart failure in infants with congenital heart disease, who suffer from increased neurohormonal activation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Heart_Defects__Congenital_MeSH S_complications_MeSH Heart_Defects__Congenital_complications_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Septal_Defects_MeSH S_complications_MeSH Heart_Septal_Defects_complications_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Hormones_MeSH S_blood_MeSH Hormones_blood_MeSH M_Human_MeSH M_Infant_MeSH M_Infant__Newborn_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Statistics__Nonparametric_MeSH 
****** 11465647
----K I
----T Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH.
----A Left ventricular hypertrophy (LVH) in hypertensive subjects is associated with an increased prevalence of ventricular arrhythmias. To evaluate the effect of antihypertensive treatment on cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), we studied 46 hypertensive patients with LVH, divided into four groups randomly treated with enalapril, hydrochlorothiazide (HCTZ), atenolol, or verapamil (SR-V) for 6 months. Office blood pressure and office heart rate values were recorded, in basal conditions, after 1 and 6 months of treatment, and all patients underwent echocardiography, electrocardiographic Holter monitoring, and stress testing. All drugs significantly lowered blood pressure, whereas left ventricular mass index was reduced by atenolol, enalapril, and SR-V, but not by HCTZ. Treatment induced a significant reduction in the number of patients with supraventricular arrhythmias (35 v 15, P < .034, and 28 v 8, excluding patients treated with HCTZ, P < .008). The number of patients with ventricular arrhythmias was also reduced (32 v 16 considering all groups, P < .08, and 24 v 9, excluding patients treated with HCTZ, P < .04). The number of TEMI during Holter monitoring significantly decreased from 47 to 23 (P = .043) in all patients, and from 39 to 14 (P = .013) excluding patients treated with HCTZ. In all groups, irrespective of treatment, a reduction of blood pressure, heart rate, and systolic blood pressure/heart rate product measured by exercise stress test was observed. The present study shows that in hypertensive patients with LVH, antihypertensive treatment with atenolol, enalapril and SR-V reduces LVH and decreases the prevalence of CA and TEMI. Treatment with HCTZ during the 6-month study did not alter LVH and did not appear to reduce CA and TEMI.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Electrocardiography__Ambulatory_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH 
****** 11465655
----K E
----T Antihypertensive effect of alpha- and beta-adrenergic blockade in obese and lean hypertensive subjects.
----A The purpose of this study was to determine the contribution of the adrenergic system in mediating hypertension in obese and lean patients. Thirteen obese, hypertensive patients with a body mass index (BMI) > or =28 kg/m2 (obese) and nine lean patients with a BMI < or =25 kg/m2 (lean) were recruited. After a 1-week washout period, participants underwent daytime ambulatory blood pressure monitoring (ABPM). Participants were then treated with the alpha-adrenergic antagonist doxazosin, titrating to 4 mg QHS in 1 week. In the next week, the beta-adrenergic antagonist atenolol was added at an initial dose of 25 mg/day and titrated to 50 mg/day within 1 week. One month after the addition of atenolol, all patients underwent a second ABPM session. There were no differences between the obese and lean subjects in baseline systolic (SBP), diastolic (DBP), or mean arterial pressures (MAP) measured by office recording or ABPM. However, obese subjects had higher heart rates than lean subjects (87.5+/-2.4 v 76.8+/-4.9 beats/min). After 1 month of treatment with the adrenergic blockers, obese patients had a significantly lower SBP (130.0+/-2.5 v 138.9+/-2.1 mm Hg, P = .02) and MAP (99.6+/-2.3 v 107.0+/-1.5 mm Hg, P = .02) than lean patients. Obese patients also tended to have a lower DBP than lean patients (84.3+/-2.5 v 90.9+/-1.6 mm Hg, P = .057), but there was no significant difference in heart rate after 1 month of adrenergic blockade. These results indicate that blood pressure is more sensitive to adrenergic blockade in obese than in lean hypertensive patients and suggest that increased sympathetic activity may be an important factor in the maintenance of hypertension in obesity.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Comparative_Study_MeSH M_Doxazosin_MeSH S_administration_&_dosage_MeSH Doxazosin_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH M_Prospective_Studies_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH 
****** 11465878
----K E
----T Perindopril/indapamide 2/0.625 mg/day: a review of its place in the management of hypertension.
----A The fixed low-dose combination of the ACE inhibitor perindopril and the non-thiazide diuretic indapamide has been evaluated in the management of patients with mild to moderate hypertension. Combination therapy aims to improve overall therapeutic efficacy while minimising adverse effects. In well-designed multicentre clinical trials, perindopril/indapamide at doses ranging from 2/0.625 to 8/2.5 mg/day was significantly more effective than placebo in achieving adequate blood pressure (BP) control. A similar reduction in supine BP was observed when combined perindopril/indapamide 2/0.625 mg/day was compared with losartan 50 mg/day or atenolol 50 mg/day. Similar reductions in 24-hour ambulatory BP were also seen with perindopril/indapamide 2/0.625 mg/day and irbesartan 150 mg/day. However, response and normalisation rates were significantly higher with combination therapy than with losartan or irbesartan monotherapy. Combined perindopril/indapamide 2/0.625 mg/day therapy effectively reduced BP in elderly patients aged 65 to 85 years to a significantly greater extent than either atenolol 50 mg/day or placebo. Supine BP was also normalised in approximately two-thirds of patients in a small noncomparative trial in patients with hypertension and renal impairment. Low-dose perindopril/indapamide 2/0.625 mg/day was well tolerated in clinical trials; the most common adverse events were headache and cough. Hypokalaemia, associated with the use of diuretics, occurred with a higher incidence with combined perindopril/indapamide 2/0.625 mg/day therapy than with either atenolol 50 mg/day or placebo. Perindopril/indapamide 2/0.625 mg/day has shown efficacy in well designed comparative trials with atenolol, losartan and irbesartan including elderly patients and patients with renal impairment. Studies comparing this dosage of perindopril/ indapamide with other combination therapies would be beneficial in allowing the place of perindopril/indapamide to be more accurately determined. The fixed-low dose combination of perindopril/indapamide provides a promising and well tolerated treatment option in the management of patients with mild to moderate hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Disease_Models__Animal_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_chemically_induced_MeSH Hypertrophy__Left_Ventricular_chemically_induced_MeSH M_Hypokalemia_MeSH S_chemically_induced_MeSH Hypokalemia_chemically_induced_MeSH M_Indapamide_MeSH S_administration_&_dosage_MeSH Indapamide_administration_&_dosage_MeSH S_adverse_effects_MeSH Indapamide_adverse_effects_MeSH S_pharmacokinetics_MeSH Indapamide_pharmacokinetics_MeSH S_pharmacology_MeSH Indapamide_pharmacology_MeSH M_Kidney_Diseases_MeSH S_chemically_induced_MeSH Kidney_Diseases_chemically_induced_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH S_adverse_effects_MeSH Perindopril_adverse_effects_MeSH S_pharmacokinetics_MeSH Perindopril_pharmacokinetics_MeSH S_pharmacology_MeSH Perindopril_pharmacology_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11466259
----K 4
----T Meta-analysis of randomised controlled trials comparing latanoprost with timolol in the treatment of patients with open angle glaucoma or ocular hypertension.
----A AIM: To evaluate the comparative efficacy and tolerance of latanoprost versus timolol through a meta-analysis of randomised controlled trials (RCTs). METHODS: Systematic retrieval of RCTs of latanoprost versus timolol to allow pooling of results from head to head comparison studies. Quality of trials was assessed based on randomisation, masking, and withdrawal. Sensitivity analyses were used to estimate the effects of quality of study on outcomes. The data sources were Medline, Embase, Scientific Citation Index, Merck Glaucoma, and Pharmacia and Upjohn ophthalmology databases. There were 1256 patients with open angle glaucoma or ocular hypertension reported in 11 trials of latanoprost versus timolol. The main outcome measures were (i) percentage intraocular pressure (IOP) reduction for efficacy; (ii) relative risk, risk difference, and number needed to harm for side effects such as hyperaemia, conjunctivitis, increased pigmentation, hypotension, and bradycardia expressed as dichotomous outcomes; and (iii) reduction in systemic blood pressure and heart rate as side effects. RESULTS: Both 0.005% latanoprost once daily and 0.5% timolol twice daily reduced IOP. The percentage reductions in IOP from baseline (mean (SE)) produced by latanoprost and timolol were 30.2 (2.3) and 26.9 (3.4) at 3 months. The difference in IOP reduction between the two treatments were 5.0 (95% confidence intervals 2.8, 7.3). However, latanoprost caused iris pigmentation in more patients than timolol (relative risk = 8.01, 95% confidence intervals 1.87, 34.30). The 2 year risk with latanoprost reached 18% (51/277). Hyperaemia was also more often observed with latanoprost (relative risk =2.20, 95% confidence intervals 1.33, 3.64). Timolol caused a significant reduction in heart rate of 4 beats/minute (95% confidence interval 2, 6). CONCLUSION: This meta-analysis suggests that latanoprost is more effective than timolol in lowering IOP. However, it often causes iris pigmentation. While current evidence suggests that this pigmentation is benign, careful lifetime evaluation of patients is still justified.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Iris_Diseases_MeSH S_chemically_induced_MeSH Iris_Diseases_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Pigmentation_Disorders_MeSH S_chemically_induced_MeSH Pigmentation_Disorders_chemically_induced_MeSH M_Prostaglandins_F__Synthetic_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Single-Blind_Method_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11465967
----K I
----T Antihypertensive therapy and the risk of malignancies.
----A AIMS: To assess the relationship between antihypertensive therapy and malignancy. METHODS AND RESULTS: A MEDLINE search for English-language articles published between January 1966 and August 1999 identified 29 prospective studies that reported cancer incidence or mortality and 28 case-control studies that reported specific drug use in cancer patients and controls. The association between rauwolfia derivatives and breast cancer was analysed in 5852 cases and 9776 controls, yielding an odds ratio (OR) of 1.25 (95% CI, 1.09-1.44). The association between diuretics and renal cell carcinoma was analysed in 4389 cases and 6566 controls, yielding a pooled OR of 1.54 (95% CI, 1.41-1.68). The association between atenolol and cancer death was analysed pooling three randomized controlled studies, including 1879 treated patients and 3078 non-treated patients, yielding a pooled OR of 1.36 (95% CI, 1.02-1.82); however, data from non-randomized studies did not confirm the latter. The association between calcium antagonists and malignancy was analysed pooling five randomized controlled studies, including 5451 treated patients and 5207 untreated ones, yielding a pooled OR of 0.78 (CI, 0.60-1.00). A meta-analysis of an additional five longitudinal studies, including 9087 treated patients and 15 559 non-treated patients, yielded a pooled OR of 1.04 (CI, 0.91-1.19). The association between ACE inhibitors and malignancy was analysed pooling two randomized controlled trials involving 1585 treated patients and 1567 non-treated patients, yielding a pooled OR of 1.57 (95% CI, 0.97-2.57); however, non-randomized studies showed no association or a decreased risk for malignancy with ACE inhibitors. CONCLUSIONS: With the exception of diuretics and renal cell carcinoma, the association between antihypertensive drugs and malignancy was either low grade (rauwolfia), uncertain (atenolol), absent (ACE inhibitors), or absent with a yet to be investigated inverse association (calcium antagonists). Ongoing long-term prospective studies with cardiovascular drugs should carefully monitor the risk of malignancy.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Breast_Neoplasms_MeSH S_chemically_induced_MeSH Breast_Neoplasms_chemically_induced_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Carcinoma__Renal_Cell_MeSH S_chemically_induced_MeSH Carcinoma__Renal_Cell_chemically_induced_MeSH M_Case-Control_Studies_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Kidney_Neoplasms_MeSH S_chemically_induced_MeSH Kidney_Neoplasms_chemically_induced_MeSH M_Longitudinal_Studies_MeSH M_Neoplasms_MeSH S_chemically_induced_MeSH Neoplasms_chemically_induced_MeSH S_mortality_MeSH Neoplasms_mortality_MeSH M_Odds_Ratio_MeSH M_Randomized_Controlled_Trials_MeSH M_Reserpine_MeSH S_adverse_effects_MeSH Reserpine_adverse_effects_MeSH 
****** 11465968
----K E
----T Bisoprolol reduces cardiac death and myocardial infarction in high-risk patients as long as 2 years after successful major vascular surgery.
----A AIM: To assess the long-term cardioprotective effect of bisoprolol in a randomized high-risk population after successful major vascular surgery. High-risk patients were defined by the presence of one or more cardiac risk factor(s) and a dobutamine echocardiography test positive for ischaemia. METHODS: 1351 patients were screened prior to surgery, 846 patients had one or more risk factor(s), and 173 of these patients also had ischaemia during dobutamine echocardiography. One hundred and twelve patients could be randomized for additional bisoprolol therapy or standard care. Eleven patients died in the peri-operative period (up to 1 month after surgery). Randomized patients continued bisoprolol or standard care after surgery. During follow-up of 101 survivors (median 22 months, range 11-30) cardiac death or myocardial infarction was noted. No patient was lost during follow-up.Results The incidence of cardiac events during follow-up in the bisoprolol group was 12% vs 32% in the standard care group (P=0.025). Cardiac death occurred in 15 patients, nine patients in the standard care and in six in the bisoprolol group; myocardial infarction occurred in six patients, five in the standard care and one in the bisoprolol group. The odds ratio for cardiac death or myocardial infarction after surgery in high-risk patients with additional bisoprolol therapy was 0.30 (0.11-0.83). CONCLUSIONS: Bisoprolol significantly reduced long-term cardiac death and myocardial infarction in high-risk patients after successful major cardiac vascular surgery.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aorta__Abdominal_MeSH S_surgery_MeSH Aorta__Abdominal_surgery_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Dobutamine_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Echocardiography_MeSH M_Femoral_Artery_MeSH S_surgery_MeSH Femoral_Artery_surgery_MeSH M_Follow-Up_Studies_MeSH M_Heart_Diseases_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH S_prevention_&_control_MeSH Heart_Diseases_prevention_&_control_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_ultrasonography_MeSH Myocardial_Ischemia_ultrasonography_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Time_Factors_MeSH P_Vascular_Surgical_Procedures_MeSH 
****** 11467761
----K E
----T The Captopril Prevention Project, further analyses on left ventricular hypertrophy and diabetes.
----A 
----P Comment Editorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11467759
----K E
----T Regression of left ventricular mass with captopril and metoprolol, and the effects on glucose and lipid metabolism.
----A OBJECTIVE: Angiotensin II and insulin have been suggested to promote the development of hypertensive left ventricular (LV) hypertrophy. We compared the effects of captopril and metoprolol on the regression of LV mass and the relation to insulin sensitivity. DESIGN: 51 previously untreated non-diabetic hypertensive patients (mean age 51 +/- 8 years, body mass index, BMI 25.9 +/- 3.2 kg/m2, office blood pressure, 158/102 mmHg) were randomized to captopril or metoprolol; a low-dose diuretic and/or a calcium cannel antagonist were added, if needed. INTERVENTIONS: LV mass index (LVMI; by echocardiography) and 24-h ambulatory blood pressure were examined at baseline, 6 and 12 months. At baseline and 12 months, insulin sensitivity index (MI) was calculated by a hyperinsulinemic-euglycemic insulin clamp technique. RESULTS: Blood pressures were reduced similarly in both groups. LVMI (115 +/- 21 g/m2 at baseline) was reduced in both groups (p < 0.01), but more with captopril than with metoprolol (e.g. -16 vs -7 g/m2, i.e. -13 vs -6%, at 12 months, p < 0.01). MI decreased by 6% with captopril (p = 0.05) and by 23% with metoprolol (p < 0.01), with no difference between the groups. Changes in LVMI were not related to changes in MI in the two groups, or when all patients were analyzed together. High-density lipoprotein (HDL)-cholesterol decreased (p < 0.05) by both drugs, with small effects on low-density lipoprotein (LDL), and triglycerides increased by 30% with metoprolol (p < 0.01). CONCLUSION: Blockade of the renin-angiotensin-aldosterone system has a role beyond that of blood pressure reduction in the regression of LV mass. There was no relationship between regression of LV mass and improvement in insulin sensitivity. We could not confirm a beneficial effect of ACE inhibition on insulin sensitivity. Thus, our results do not support the importance of insulin in the control of LV geometry.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Comparative_Study_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_blood_MeSH Hypertrophy__Left_Ventricular_blood_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Insulin_MeSH S_administration_&_dosage_MeSH Insulin_administration_&_dosage_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Insulin_Resistance_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11468019
----K I
----T Beta-blocker treatment in heart failure.
----A Heart failure treatment has markedly changed during the last few decades, with demonstration of benefit of afterload reduction by vasodilator therapy and introduction of the concept of the deleterious consequences of the neuro-hormonal compensatory stimulation. Blockade of beta-adrenergic receptors, initially contra-indicated in heart failure, provide a marked reduction of mortality and morbidity in combination with diuretics and angiotensin-converting enzyme inhibitors, as demonstrated in many clinical trials. We performed a review of all clinical trials that compare beta-blockers vs. placebo in chronic heart failure. Beta-blockers with different pharmacological profiles have been tested, mainly metoprolol, bisoprolol, bucindolol and carvedilol. With progressive dose increment, tolerance of such treatment was generally good, left ventricular function improved, hospitalisations for heart failure were less frequent and mortality was reduced. The meta-analysis of the 16 randomised trials, with at least one death in each treatment group, provides a 24% relative risk reduction for such hospitalisations (95% CI=19%-29%) and 22% reduction for mortality (95% CI=16%-28%). Heterogeneity of beta-blocker effect for mortality was found and related to the non-significant benefit obtained in the BEST trial with bucindolol. When such a trial is excluded, the effect model analysis shows that relative risk reduction (beta-blocker induced benefit) is constant whatever the severity of the disease. The mechanism of beta-blocker induced benefit remains unclear, but is at least partly related to left ventricular function improvement and prevention of severe ventricular arrhythmias. In conclusion, beta-blocker treatment has become an established therapy for heart failure, in combination with diuretics and ACE inhibitors. Complementary informations will be needed to clarify the mechanism of benefit and to define the best therapeutic strategy according to the individual characteristics of patients with heart failure.
----P Journal_Article Meta-Analysis Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH 
****** 11470011
----K E
----T The INSIGHT and NORDIL trials: Are calcium antagonists equivalent to established drug therapies for cardiovascular protection?
----A Calcium channel blockers have come into worldwide use for treating hypertension and other circulatory disorders. In recent years, results of several observational studies have suggested that these drugs may not be as safe or effective as other available therapies, such as diuretics and beta-blockers, in the prevention of cardiovascular events. The Nordic Diltiazem (NORDIL) and the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) studies were the first two randomized interventional trials in hypertensive patients that directly compared the effects of therapy based on calcium antagonists with those of diuretic and beta-blocker-based treatment on major cardiovascular endpoints. Both studies found that the effectiveness of calcium antagonist therapy was similar to that of diuretic and beta-blocker therapy for preventing the composite primary endpoint of fatal and nonfatal stroke, myocardial infarction, and other cardiovascular death. The two studies shared several nonsignificant trends for cause-specific events, including greater stroke prevention and lesser coronary event prevention in the calcium antagonist groups compared with the diuretic and beta-blocker groups. There is not yet sufficient evidence to prove whether cause-specific differences exist. Results of the NORDIL and INSIGHT studies support incorporating calcium antagonist-based therapy as an additional safe and effective approach for preventing blood pressure-related illness and death.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 11470017
----K I
----T Prospectively designed overviews of recent trials comparing antihypertensive regimens based on different drug classes.
----A Randomized trials have provided clear evidence of the beneficial effects of many different blood pressure-lowering regimens compared with placebo. The comparative effects of antihypertensive regimens based on different drug classes are less well established. The Blood Pressure Lowering Treatment Trialists' Collaboration conducted a series of prospectively designed overviews of randomized trials that compared the effects of different drug classes on major cause-specific outcomes. These overviews found no differences between the effects of regimens based on angiotensin converting enzyme inhibitors and those based on diuretics or b-blockers. There was limited evidence of small differences between regimens based on calcium antagonists and those based on diuretics or beta-blockers. The overviews of regimens based on calcium antagonists compared with those based on angiotensin converting enzyme inhibitors recorded too few events to provide reliable findings. Over the next few years, the findings of ongoing trials and future cycles of overview analyses conducted by the Collaboration should substantially add to these data.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Meta-Analysis_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11472461
----K E
----T An economic evaluation of atenolol vs. captopril in patients with Type 2 diabetes (UKPDS 54).
----A AIMS: To compare the net cost of a tight blood pressure control policy with an angiotensin converting enzyme inhibitor (captopril) or beta blocker (atenolol) in patients with Type 2 diabetes. DESIGN: A cost-effectiveness analysis based on outcomes and resources used in a randomized controlled trial and assumptions regarding the use of these therapies in a general practice setting. SETTING: Twenty United Kingdom Prospective Diabetes Study Hospital-based clinics in England, Scotland and Northern Ireland. SUBJECTS: Hypertensive patients (n = 758) with Type 2 diabetes (mean age 56 years, mean blood pressure 159/94 mmHg), 400 of whom were allocated to the angiotensin converting enzyme inhibitor captopril and 358 to the beta blocker atenolol. MAIN OUTCOME MEASURES: Life expectancy and mean cost per patient. RESULTS: There was no statistically significant difference in life expectancy between groups. The cost per patient over the trial period was 6485 UK pounds in the captopril group, compared with 5550 UK pounds in the atenolol group, an average cost difference of 935 UK pounds (95% confidence interval 188 UK pounds, 1682 UK pounds). This 14% reduction arose partly because of lower drug prices, and also because of significantly fewer and shorter hospitalizations in the atenolol group, and despite higher antidiabetic drug costs in the atenolol group. CONCLUSIONS: Treatment of hypertensive patients with Type 2 diabetes using atenolol or captopril was equally effective. However, total costs were significantly lower in the atenolol group. Diabet. Med. 18, 438-444 (2001)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_economics_MeSH Atenolol_economics_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Captopril_MeSH S_economics_MeSH Captopril_economics_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Cost-Benefit_Analysis_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_economics_MeSH Diabetes_Mellitus__Type_II_economics_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Family_Practice_MeSH S_economics_MeSH Family_Practice_economics_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_analysis_MeSH Hemoglobin_A__Glycosylated_analysis_MeSH M_Hospitalization_MeSH S_economics_MeSH Hospitalization_economics_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Hypoglycemic_Agents_MeSH S_economics_MeSH Hypoglycemic_Agents_economics_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11477813
----K 1
----T [Clinical study of purified xuefu capsule in treating angina pectoris]
----A OBJECTIVE: To study the effect of purified Xuefu Capsule (PXFC) in treating angina pectoris (AP). METHODS: Fifty-seven patients with AP were randomly divided into two groups. Group A (30 cases) was treated with PXFC and western medicine, and group B(27 cases) with western medicine (isosorbide dinitrate, diltiazem or atenolol) alone. RESULTS: The total effective rates and ECG ST-T changes of AP were 93.3% and 63.3% respectively in group A. These results were all superior to those of group B (P < 0.05). Moreover, in group A the level of plasma endothelin (ET-1) decreased from 85.09 +/- 37.56 ng/L to 61.19 +/- 4.02 ng/L, and that of calcitonin gene related peptide (CGRP) increased from 58.64 +/- 19.30 ng/L to 88.87 +/- 20.41 ng/L. Comparing with group B, these changes were statistically different (P < 0.01). CONCLUSIONS: The effects of adding PXFC on conventional treatment with western medicine were better than those of western medicine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcitonin_Gene-Related_Peptide_MeSH S_blood_MeSH Calcitonin_Gene-Related_Peptide_blood_MeSH M_Capsules_MeSH M_Drug_Therapy__Combination_MeSH M_Drugs__Chinese_Herbal_MeSH S_therapeutic_use_MeSH Drugs__Chinese_Herbal_therapeutic_use_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11479245
----K E
----T Nebivolol reverses endothelial dysfunction in essential hypertension: a randomized, double-blind, crossover study.
----A BACKGROUND: Vascular endothelial dysfunction may predict future atherosclerosis. Hence, an antihypertensive agent that reverses endothelial dysfunction and lowers blood pressure might improve the prognosis of patients with hypertension. We hypothesized that nebivolol, a vasodilating beta-blocker, could improve endothelial dysfunction. We tested this hypothesis by comparing the effects of nebivolol and atenolol on endothelial function. METHODS AND RESULTS: Twelve hypertensive patients with a mean ambulatory blood pressure of 154+/-7/97+/-10 mm Hg were randomized after a 2-week placebo run-in period (baseline) in a double-blind, crossover fashion to 8-week treatment periods with either 5 mg of nebivolol with 2.5 mg of bendrofluazide or 50 mg of atenolol with 2.5 mg of bendrofluazide. Forearm venous occlusion plethysmography and intra-arterial infusions of acetylcholine and N(G)-monomethyl-L-arginine (L-NMMA) were used to assess stimulated and basal endothelium-dependent nitric oxide release, respectively. Sodium nitroprusside was used as an endothelium-independent control. Nebivolol/bendrofluazide and atenolol/bendrofluazide each lowered the clinic blood pressure to the same extent (132+/-7/82+/-6 and 132+/-9/83+/-8 mm Hg, respectively; P<0.001 from baseline). The vasodilatory response to acetylcholine was significantly increased with nebivolol/bendrofluazide (maximum percentage change in forearm blood flow [mean+/-SEM], 435+/-27%, P<0.001) but not with atenolol/bendrofluazide. Similarly, the endothelium-dependent vasoconstrictive response to L-NMMA was significantly improved only with nebivolol treatment (percentage change in forearm blood flow, -54+/-5%; P<0.001). The response to sodium nitroprusside was not different between treatments, suggesting that the endothelium-independent pathway was unaffected. CONCLUSIONS: Nebivolol/bendrofluazide increased both stimulated and basal endothelial nitric oxide release, whereas for the same degree of blood pressure control, atenolol/bendrofluazide had no effect on nitric oxide bioactivity. Thus, nebivolol may offer additional vascular protection in treating hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroprusside_MeSH S_pharmacology_MeSH Nitroprusside_pharmacology_MeSH M_Vasoconstriction_MeSH S_drug_effects_MeSH Vasoconstriction_drug_effects_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH M_omega-N-Methylarginine_MeSH S_pharmacology_MeSH omega-N-Methylarginine_pharmacology_MeSH 
****** 11482924
----K E
----T Maintenance of sinus rhythm after electrical cardioversion of persistent atrial fibrillation; sotalol vs bisoprolol.
----A AIMS: The purpose of the study was to compare the efficacy and safety of sotalol and bisoprolol in the maintenance of sinus rhythm after electrical cardioversion of atrial fibrillation. METHODS: Patients (n=128) were randomized to sotalol (80 mg b.i.d.) or bisoprolol (5 mg x day(-1)). Patients with contraindications to beta-blockers, class III antiarrhythmic drugs or prior treatment with use of study medication for prevention of atrial fibrillation were excluded. Follow-up clinical evaluation was performed 1 day and 1 month after cardioversion and thereafter at 3-month intervals. RESULTS: There were no group differences in baseline clinical characteristics. After a follow-up of 12 months, 59% of all patients were still in sinus rhythm. The fraction remaining in sinus rhythm was calculated for the two groups by Kaplan--Meier analysis. During follow-up, 41% of patients on sotalol and 42% on bisoprolol developed atrial fibrillation (ns). In two patients (3.1%) on sotalol, life-threatening proarrhythmias (torsade de pointes tachycardias) occurred, whereas none were found in the bisoprolol group. Symptomatic bradycardias occurred in two patients on sotalol and three on bisoprolol. CONCLUSION: This study demonstrates that sotalol (160 mg x day(-1)) and bisoprolol (5 mg x day(-1)) are equally effective in maintaining sinus rhythm. Because of the side effects of sotalol, bisoprolol seems to be advantageous for maintenance of sinus rhythm after cardioversion of atrial fibrillation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Electric_Countershock_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Recurrence_MeSH M_Sotalol_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11485131
----K E
----T Cost-effectiveness results from the US Carvedilol Heart Failure Trials Program.
----A OBJECTIVE: To evaluate the cost-effectiveness of carvedilol, a beta-blocker that is approved for use in the US for the treatment of heart failure, based on data from Phase III clinical trials. METHODS: We conducted an economic evaluation alongside the US Carvedilol Heart Failure Trials Program, which consisted of four concurrent, randomized, double-blind, placebo-controlled clinical trials; the mean duration of follow-up across these four trials was 6.5 months (the program was terminated prematurely based on a finding of a 65% mortality benefit). Using data from these trials, we examined the cost-effectiveness of carvedilol in terms of the estimated cost per death averted among patients randomized to such therapy versus those receiving placebo. Attention was focused on the cost of carvediol therapy plus the cost of cardiovascular-related inpatient care. Costs of care were estimated by combining infomation on healthcare utilization from the clinical trials with secondary sources of cost data. RESULTS: Patients randomized to receive carvedilol had lower mean +/- SD estimated costs of cardiovascular-related inpatient care over 6.5 months compared with those receiving placebo ($1912 +/- $7595 vs. $4463 +/- $20,565, respectively). As mortality alsowas lower among carvedilol patients, the estimated cost per death averted was negative. The probability that carvedilol would both increase survival and decrease costs of cardiovascular-related care over a 6.5-month period was estimated to be 0.98. CONCLUSIONS: Data from the US Carvedilol Heart Failure Trials Program indicate that carvedilol reduces mortality in patients with heart failure; our study suggests that it also may be cost-saving over a period of approximately six months.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_economics_MeSH Carbazoles_economics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH P_Cost-Benefit_Analysis_MeSH P_Economics__Pharmaceutical_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Propanolamines_MeSH S_economics_MeSH Propanolamines_economics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_United_States_MeSH 
****** 11486156
----K E
----T Effect of beta-blockade on the premature ventricular beats/heart rate relation and heart rate variability in patients with coronary heart disease and severe ventricular arrhythmias.
----A We examined the effects of beta-blockers on the associations between heart rate and number of premature ventricular beats (PVBs) and on heart rate variability and myocardial ischemia in patients with coronary heart disease. After 2 weeks of run-in placebo treatment, 18 patients with coronary artery disease were randomized to a 7-day treatment with either propranolol (40 mg) three times a day or placebo. During run-in and after 7 days of treatment, patients underwent 24-hour Holter monitoring and exercise tests. We analyzed the 24-hour Holter recordings with customized software that computes the correlation between heart rate and occurrence of PVBs. We also computed spectral measures of heart rate variability on the same recordings. Propranolol caused a significant decrease in the log-transformed total number of PVBs recorded over 24 hours and during the day. The number of PVBs was much lower during the night than during the day both after placebo and after propranolol. There were no differences between the two treatments. During the day, there was a positive correlation between heart rate and the number of PVBs in all 18 patients. The mean correlation coefficients between heart rate and number of PVBs increased significantly after propranolol treatment both during the 24-hour monitoring (p < 0.05) and during the day (p < 0.05). The night-recorded correlation coefficients between heart rate and number of PVBs were not significantly different in the placebo versus propranolol group. Propranolol significantly increased the total power during the day. Placebo caused a significant decrease in the low-frequency band (LF) and a significant increase in the high-frequency band (HF) during the night compared with the day. During the day, propranolol significantly reduced LF power and increased HF power, with respect to placebo. After propranolol treatment, the values of LF and HF power during the day were comparable to those recorded at night. The LF/HF ratio decreased significantly after propranolol treatment with respect to placebo in the day and became similar to that recorded during sleep. Propranolol significantly reduced heart rate and systolic blood pressure at rest and at peak exercise and reduced signs of myocardial ischemia. Propranolol administration reduces PVBs in patients with coronary artery disease and severe ventricular arrhythmias possibly through an improvement of cardiac autonomic regulation and through anti-ischemic effects, antiarrhythmic effects, or both.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Ventricles_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH M_Vagus_Nerve_MeSH S_physiopathology_MeSH Vagus_Nerve_physiopathology_MeSH M_Ventricular_Premature_Complexes_MeSH S_drug_therapy_MeSH Ventricular_Premature_Complexes_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Premature_Complexes_physiopathology_MeSH 
****** 11487547
----K E
----T Randomized comparison of long-term losartan versus propranolol in lowering portal pressure in cirrhosis.
----A BACKGROUND & AIMS: It has been suggested that losartan, an angiotensin II (A-II) type 1 receptor blocker, may have a pronounced portal pressure reducing effect, far greater than that of propranolol. This randomized controlled trial compared the hemodynamic and renal effects of continued 6-week administration of losartan (n = 25) vs. propranolol (n = 15) in portal hypertensive patients with cirrhosis treated endoscopically after a variceal bleeding episode. METHODS: Hepatic venous pressure gradient (HVPG), systemic hemodynamics, renal function, and vasoactive factors were measured before and at 6 weeks of treatment. RESULTS: Losartan did not reduce HVPG (-2% +/- 12%, NS) but significantly decreased mean arterial pressure (MAP, -8% +/- 10%, P = 0.001). On the contrary, propranolol significantly reduced HVPG (-10% +/- 11%, P = 0.003) and cardiac output (-16% +/- 12%, P = 0.001) but did not modify MAP (2.5% +/- 10%, NS). Losartan increased A-II levels, reduced aldosterone, and decreased glomerular filtration rate (GFR) in Child B patients. Propranolol did not modify renal function. Adverse events related to therapy were mild and similar in both groups. CONCLUSIONS: Unlike propranolol, long-term losartan administration does not significantly reduce HVPG in patients with cirrhosis treated after a variceal bleeding episode, and it caused hypotension and reduced GFR in patients with moderate liver failure. Therefore, losartan is not an alternative to propranolol in preventing variceal rebleeding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Urea_Nitrogen_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Losartan_MeSH S_administration_&_dosage_MeSH Losartan_administration_&_dosage_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11489654
----K E
----T Impact of myocardial protection during coronary bypass surgery on patient outcome.
----A We have recently shown that continuous coronary perfusion with warm blood enriched with the ultra-short acting beta-blocker Esmolol (ES) improves functional and structural myocardial protection during coronary artery surgery as compared with conventional cardioplegia (CP). The purpose of the present study was to compare both myocardial protection techniques in terms of patient outcome. We retrospectively analyzed the charts of 150 consecutive patients subjected to coronary artery surgery using the ES-technique; 150 patients matched for age, gender, preoperative left ventricular function, history of renal failure, and history of neurological symptoms undergoing surgery with conventional CP during the same time period served as control group. There were no significant differences between both groups with respect to perioperative myocardial infarction rate, need for positive inotropic medication, need for mechanical circulatory support, duration of mechanical ventilation, duration of intensive care unit stay, time of mobilization, postoperative renal failure, cardiac arrhythmias, neurological symptoms, infections or in-hospital mortality. ES-patients were less frequently readmitted to the intensive care unit (ES: 3/150; 2.2% [95% confidence interval: 0-4.2%] vs. CP: 13/150; 8.7% [4.2-13.2%]; P=0.010) and total hospital stay was shorter (ES: 12.3+/-4.8 days [95% CI: 11.5-13.0] vs CP: 13.5+/-3.8 [12.9-14.1] days; P=0.0013), thus saving 159 patient days on the normal ward. Procedural costs were less for the ES-technique (US$ 60 per patient) as compared to the cardioplegia technique (US$ 120 per patient). These data suggest that myocardial protection using the ES-technique does not improve clinical outcome in patients subjected to routine coronary artery surgery, but may save costs.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Cardioplegic_Solutions_MeSH S_therapeutic_use_MeSH Cardioplegic_Solutions_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Female_MeSH M_Heart_Arrest__Induced_MeSH S_methods_MeSH Heart_Arrest__Induced_methods_MeSH M_Human_MeSH M_Length_of_Stay_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_surgery_MeSH Myocardial_Ischemia_surgery_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 11493129
----K E
----T Antihypertensive drug therapy in Saskatchewan: patterns of use and determinants in hypertension.
----A BACKGROUND: The benefits of continuous treatment of hypertension have been extensively documented in randomized controlled trials. However, clinical trials may not reflect actual drug use in the population. OBJECTIVE: To examine the distribution and determinants of patterns of use of antihypertensive agents in the first 5 years of hypertension treatment in Saskatchewan. METHODS: Patterns of use and modifications to therapy were derived from a careful examination of medication use in a cohort of 19 501 subjects aged 40 to 79 years, without recognized cardiac disease and initiating therapy with an angiotensin-converting enzyme inhibitor, a calcium antagonist, or a beta-blocker in Saskatchewan between 1990 and 1993. RESULTS: Angiotensin-converting enzyme inhibitors (37.4%), followed by calcium antagonists (27.5%) and beta-blockers (26.4%), were the most commonly prescribed agents to initiate treatment in our study population. Patients with diabetes were less likely to be dispensed a beta-blocker, as were younger and female patients. Previous visits to a cardiologist decreased the likelihood of receiving combination therapy or angiotensin-converting enzyme inhibitors but increased that of using calcium antagonists. Apart from dose adjustment, 89% of study subjects underwent at least 1 modification to their initial regimen, at a median time of 134 days. After 1 year, only 33.8% of patients were still using their initial drug. An early decrease in the proportion of patients continuing to receive initial therapy was noted, especially among beta-blocker users. CONCLUSIONS: Erratic drug-taking behaviors were observed in this Saskatchewan population. In addition, initial drug use does not seem to be in accordance with the stepped-care approach to hypertension therapy recommended in the Canadian guidelines.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prescriptions__Drug_MeSH S_statistics_&_numerical_data_MeSH Prescriptions__Drug_statistics_&_numerical_data_MeSH M_Saskatchewan_MeSH S_epidemiology_MeSH Saskatchewan_epidemiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11498655
----K E
----T The African American Study of Kidney Disease and Hypertension (AASK): new findings.
----A In September, 2000, the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health called an early halt to the amlodipine arm of the African American Study of Kidney Disease and Hypertension (AASK) trial after careful deliberation by an independent data and safety monitoring board. An interim analysis of the AASK at 3 years revealed a renoprotective effect of the angiotensin-converting enzyme inhibitor ramipril as compared to the dihydropyridine calcium channel blocker (DHP-CCB) amlodipine in patients with mild to moderate renal insufficiency. This differential effect was independent of the blood pressure (BP) levels reached and was evident in proteinuric patients and suggestive in patients with baseline proteinuria < 300 mg/d, but was not conclusive. The AASK trial data suggest that DHP-CCBs should be used cautiously in the presence of mild to moderate renal insufficiency. Judgment should be reserved for the use of other CCBs, such as verapamil or diltiazem, since these are fundamentally different CCBs with the potential for a different impact on hypertensive nephrosclerosis. The blinded observation period for AASK will be completed at the end of September, 2001, at which time additional, clinically useful information is expected to become available. (c)2001 Le Jacq Communications, Inc.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_African_Americans_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Diseases_MeSH S_drug_therapy_MeSH Kidney_Diseases_drug_therapy_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Time_Factors_MeSH 
****** 11499735
----K E
----T Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction.
----A OBJECTIVES: The study assessed the relative predictive potency of neurohumoral factors in patients with advanced left ventricular (LV) dysfunction during neurohumoral blocking therapy. BACKGROUND: The course of heart failure is characterized by progressive LV deterioration associated with an increase in cardiac (natriuretic peptides) and predominantly extracardiac (norepinephrine, big endothelin [big ET]) hormone plasma levels. METHODS: Plasma hormones were measured at baseline and months 3, 6, 12 and 24 in 91 patients with heart failure (left ventricular ejection fraction [LVEF] <25%) receiving 40 mg enalapril/day and double-blind atenolol (50 to 100 mg/day) or placebo. After the double-blind study phase, patients were followed up to four years. Stepwise multivariate regression analyses were performed with 10 variables (age, etiology, LVEF, symptom class, atenolol/placebo, norepinephrine, big ET, log aminoterminal atrial natriuretic peptide, log aminoterminal B-type natriuretic peptide [N-BNP] and log B-type natriuretic peptide [BNP]). During the study, the last values prior to patient death were used, and in survivors the last hormone level, New York Heart Association class and LVEF at month 24 were used. RESULTS: Thirty-one patients died from a cardiovascular cause during follow-up. At baseline, log BNP plasma level (x2 = 13.9, p = 0.0002), treatment allocation (x2 = 9.5, p = 0.002) and LVEF (x2 = 5.6, p = 0.017) were independently related to mortality. During the study, log BNP plasma level (x2 = 21.3, p = 0.0001) remained the strongest predictive marker, with LVEF (x2 = 11.2, p = 0.0008) log N-BNP plasma level (x2 = 8.9, p = 0.0027) and treatment allocation (x2 = 6.4, p = 0.0109) providing additional independent information. CONCLUSIONS: In patients with advanced LV dysfunction receiving high-dose angiotensin-converting enzyme inhibitors and beta-blocker therapy BNP and N-BNP plasma levels are both independently related to mortality. This observation highlights the importance of these hormones and implies that they will likely emerge as a very useful blood test for detection of the progression of heart failure, even in the face of neurohumoral blocking therapy.
----P Clinical_Trial Evaluation_Studies Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelin-1_MeSH M_Endothelins_MeSH S_blood_MeSH Endothelins_blood_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hormones_MeSH S_blood_MeSH Hormones_blood_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Placebos_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Protein_Precursors_MeSH S_blood_MeSH Protein_Precursors_blood_MeSH M_Random_Allocation_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11500582
----K E
----T Effectiveness of bi-atrial pacing for reducing atrial fibrillation after coronary artery bypass graft surgery.
----A Atrial fibrillation (AF) is common after cardiac surgery and adds significant cost and morbidity. The use of prophylactic pacing strategies to prevent post-operative AF has been controversial. We previously performed a pilot study which suggested that the combination of beta-blockers and bi-atrial pacing (BAP) may reduce AF after cardiac surgery.We prospectively randomized 118 patients to continuous BAP for up to 96 hours post-operatively versus standard therapy. All patients were treated with beta-blockers as tolerated. Patients were paced in the AAI mode at a rate of 100 pulses per minute. The primary endpoint of the study was the occurrence of sustained AF (>10 minutes).There was a significant reduction in the incidence of AF in the BAP group among patients undergoing coronary artery bypass graft surgery with or without aortic valve replacement (35 % vs. 19 % AF; OR=0.38, 95 % CI 0.15, 0.93; p <0.05). Including patients undergoing isolated aortic valve surgery (n=7), there remained a strong trend toward a reduction of AF with pacing (no atrial pacing [NAP] vs. BAP; 35 % vs. 21 % AF; OR=0.48, 95 % CI 0.21, 1.11; p=0.08). Patients age 70 or greater benefited most from pacing (NAP vs. BAP; 55 vs. 25 % AF; p<0.05), while those less than 70 years of age did not (17 vs. 18 % p=NS). There was a significant reduction in the amount of time spent in the intensive care unit among patients receiving BAP (50+/-40 vs. 37+/-25 h; p<0.05).BAP together with beta-blockade after coronary artery bypass graft surgery reduces the incidence of post-operative atrial AF. Elderly patients (age 70 or greater) appear to benefit most, and may be a group to whom this therapy should be targeted.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Cardiac_Pacing__Artificial_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH S_methods_MeSH Coronary_Artery_Bypass_methods_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Postoperative_Care_MeSH M_Probability_MeSH M_Prospective_Studies_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11547718
----K E
----T Endoscopic ligation compared with combined treatment with nadolol and isosorbide mononitrate to prevent recurrent variceal bleeding.
----A BACKGROUND: After an episode of acute bleeding from esophageal varices, patients are at high risk for recurrent bleeding and death. We compared two treatments to prevent recurrent bleeding--endoscopic ligation and combined medical therapy with nadolol and isosorbide mononitrate. METHODS: We randomly assigned 144 patients with cirrhosis who were hospitalized with esophageal variceal bleeding to receive treatment with endoscopic ligation (72 patients) or the combined medical therapy (72 patients). Sessions of ligation were repeated every two to three weeks until the varices were eradicated. The initial dose of nadolol was 80 mg orally once daily, with adjustment according to the resting heart rate; isosorbide mononitrate was given in increasing doses, beginning at 20 mg once a day at bed time and rising over the course of one week to 40 mg orally twice a day, unless side effects occurred. The primary end points were recurrent bleeding, complications, and death. RESULTS: The median follow-up period was 21 months. A total of 35 patients in the ligation group and 24 in the medication group had recurrent bleeding. The probability of recurrence was lower in the medication group, both for all episodes related to portal hypertension (P=0.04) and for recurrent variceal bleeding (P=0.04). There were major complications in nine patients treated with ligation (seven had bleeding esophageal ulcers and two had aspiration pneumonia) and two treated with medication (both had bradycardia and dyspnea) (P=0.05). Thirty patients in the ligation group died, as did 23 patients in the medication group (P=0.52). The probability of recurrent bleeding was lower for patients with a hemodynamic response to therapy, defined as a decrease in the hepatic venous pressure gradient of more than 20 percent from the base-line value or to less than 12 mm Hg (18 percent, vs. 54 percent in patients with no hemodynamic response at one year; P<0.001), and the probability of survival was higher (94 percent vs. 78 percent at one year, P=0.02). CONCLUSIONS: Combined therapy with nadolol and isosorbide mononitrate is more effective than endoscopic ligation for the prevention of recurrent bleeding and is associated with a lower rate of major complications. A hemodynamic response to treatment is associated with a better long-term prognosis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Actuarial_Analysis_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH P_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH S_surgery_MeSH Gastrointestinal_Hemorrhage_surgery_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Ligation_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_administration_&_dosage_MeSH Nadolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Nadolol_adverse_effects_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Postoperative_Complications_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11504165
----K 3
----T Comparison of the effect of perindopril and acebutolol on cerebral hemodynamics in hypertensive patients.
----A PURPOSE: The aim of the study was to compare effect of perindopril (4 mg once a day) versus acebutolol (400 mg once a day) on cerebral hemodynamics in hypertensive patients. METHODS: Thirty untreated patients with mild-to-moderate hypertension were studied. Drug influences on Doppler-derived parameters from the cerebral blood flow (CBF) velocity wave form were evaluated in a randomized, double blind, cross-over, placebo controlled study. The mean CBF velocity, pulsatility index (PI), cerebrovascular resistance and index of CBF were calculated from concomitant transcranial Doppler measurements and systemic blood pressure. RESULTS: Acebutolol and perindopril significantly decreased systolic, diastolic and mean blood pressure in relation to placebo. The mean value of CBF velocity increased to a comparable level after both drugs (54.9 +/- 9.1 cm/s on placebo vs 62.8 +/- 14.5 cm/s on perindopril p<0.01 and 61.4 +/- 9.2 cm/s on acebutolol, p<0.01). Also, the cerebrovascular resistance index decreased similarly after both drugs (2.26 +/- 0.35 on placebo vs 1.68 +/- 0.42 on perindopril p<0.01 and 1.7 +/- 0.36 on acebutolol p<0.01). The calculated CBF index increased significantly after each drug (25.23 +/- 7.99 on placebo vs 33.98 +/- 11.23 p<0.01 on perindopril and 30.90 +/- 8.04 on acebutolol p<0.01). However, perindopril augmented the CBF index more effectively than acebutolol (p<0.05). CONCLUSIONS: Among patients with mild-to-moderate hypertension both acebutolol and perindopril beneficially decreased cerebrovascular resistance and increased the CBF index in comparison with placebo. The increase of CBF index was greater after perindopril than acebutolol, which suggests a more significant improvement in cerebral perfusion by perindopril. The non-invasive transcranial Doppler ultrasonography method of CBF velocity measurement may contribute to choosing optimal antihypertensive therapies and to monitor their effect.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH S_physiology_MeSH Cerebrovascular_Circulation_physiology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Ultrasonography__Doppler__Transcranial_MeSH 
****** 11511429
----K E
----T Beneficial effect of carvedilol on heart rate response to exercise in digitalised patients with heart failure in atrial fibrillation due to idiopathic dilated cardiomyopathy.
----A Fourteen digitalised patients diagnosed with heart failure (NYHA Functional class II) with idiopathic dilated cardiomyopathy in chronic established atrial fibrillation were administered carvedilol in addition to their anti-heart failure medications in an attempt to improve their heart rate control. Fourteen matched patients who did not receive carvedilol acted as control subjects. Patients treated with carvedilol showed significantly reduced resting heart rates (10-36%), maximal heart rates on exercise (5-20%) and an increased exercise time (2-30%) on treadmill stress tests (all P=0.001). Ventricular ectopic activity was also diminished. This was associated with symptomatic improvement in effort intolerance and palpitations. NYHA functional class, left ventricular dimensions and ejection fractions did not improve during the study period of 3 months. Thus, addition of carvedilol to digoxin had a beneficial effect on exercise tolerance in patients with idiopathic dilated cardiomyopathy in atrial fibrillation by virtue of an improved heart rate control both at rest and on exercise. Carvedilol was well tolerated despite impaired myocardial function.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Comparative_Study_MeSH M_Digitalis_Glycosides_MeSH S_administration_&_dosage_MeSH Digitalis_Glycosides_administration_&_dosage_MeSH M_Exercise_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Function_Tests_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Reference_Values_MeSH M_Sensitivity_and_Specificity_MeSH M_Treatment_Outcome_MeSH 
****** 11511433
----K E
----T Effect of metoprolol CR/XL on exercise tolerance in chronic heart failure - a substudy to the MERIT-HF trial.
----A BACKGROUND: Beta-blockade usually causes a slight reduction in exercise capacity among healthy subjects, while more variable results have been observed in chronic heart failure (CHF), probably related to patients studied, methods and agent used. The effect of metoprolol controlled release/extended release (CR/XL) on peak oxygen uptake (peak VO(2)) in this patient population has not previously been investigated. AIMS: We examined the effect of long-term treatment with the selective beta(1)-receptor blocker metoprolol CR/XL once daily on exercise capacity in patients with CHF. METHODS: Ninety-four patients (70 males and 24 females; mean age 63.6+/-10.6 years) with chronic symptomatic heart failure in New York Heart Association (NYHA) functional class II-IV, and with ejection fraction <or=40%, stabilized on optimum standard therapy were randomized to metoprolol CR/XL or placebo in a double-blind trial. Exercise capacity was evaluated by peak VO(2) at baseline, after 3 months and at the end of study (mean follow-up 11.4+/-0.4 months). RESULTS: Compared with placebo metoprolol CR/XL produced a significant decrease in heart rate by 11 beats/min at rest and 18 beats/min at peak exercise. There was a tendency for a temporal decline in peak VO(2) after 3 months of therapy in both groups, but altogether peak VO(2) remained unchanged from baseline with no difference between the groups at 1 year. CONCLUSIONS: In patients with moderate to severe CHF, 11.4 months of beta(1)-blockade with metoprolol CR/XL had no effect on exercise capacity when compared with placebo or baseline.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Function_Tests_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH S_physiology_MeSH Oxygen_Consumption_physiology_MeSH M_Probability_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11511434
----K I
----T Results from post-hoc analyses of the CIBIS II trial: effect of bisoprolol in high-risk patient groups with chronic heart failure.
----A BACKGROUND: The beneficial effects of the beta-blocker bisoprolol on mortality and rate of hospitalisation as well as its safety in patients with chronic heart failure has been proven. However, its efficacy in patients in whom beta-blockers have traditionally been contraindicated or caution has been advised has not been clearly determined. Therefore, analyses in high-risk subgroups of patients taking part in CIBIS II have been performed to investigate the effect of bisoprolol in elderly patients, in patients with type 2 diabetes, with renal failure, NYHA functional class IV or concomitantly treated with digitalis, aldosterone antagonists or amiodarone. METHODS: High-risk subgroups of patients with chronic heart failure taking part in the CIBIS II study were retrospectively analysed with respect to mortality, hospitalisation, combined endpoint of cardiovascular mortality or hospitalisation for cardiovascular reasons and treatment withdrawal as well as cause of death and hospitalisation. Analysis is based on intention-to-treat. RESULTS: It was demonstrated that in spite of the expected increase in the overall risk of death and hospitalisation, patients who are diabetic, have renal impairment, NYHA class IV symptoms, are elderly, are taking either digitalis, amiodarone or aldosterone antagonists as co-medication benefit equally from beta-blockade with bisoprolol as patients without these complications or drugs. Benefit was shown for the primary endpoint all cause mortality, as well as for the secondary endpoints. CONCLUSIONS: Contrary to the hitherto prevailing doctrine of not using beta-blockers in high risk patient groups with chronic heart failure, retrospective analyses of the CIBIS II study justify the use of this drug class in patients regardless of age, NYHA functional class, the presence of diabetes, renal impairment or concomitant treatment with digitalis, amiodarone or aldosterone antagonists.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Age_Distribution_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH P_Cause_of_Death_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Female_MeSH M_Germany_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Kidney_Failure_MeSH S_complications_MeSH Kidney_Failure_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Reference_Values_MeSH M_Retrospective_Studies_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Sex_Distribution_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 11511435
----K E
----T The CARE-HF study (CArdiac REsynchronisation in Heart Failure study): rationale, design and end-points.
----A BACKGROUND: Cardiac resynchronisation is a promising new intervention for patients with heart failure, left ventricular systolic dysfunction and ventricular dyssynchrony. OBJECTIVE: The CARE-HF trial is designed to evaluate the long-term effects of cardiac (atrio-bi-ventricular) resynchronisation on the mortality and morbidity of patients with heart failure due to left ventricular systolic dysfunction already receiving diuretics and optimal medical therapy with ACE inhibitors and beta-blockers (where indicated and tolerated). METHODS AND RESULTS: Approximately 800 patients will be randomised to device therapy or control and followed for a minimum of 18 months. A pragmatic study design has been chosen that does not attempt to conceal allocation from investigators or patients because it is impossible to guarantee maintenance of blinding for the duration of the study. The end-points committee will adjudicate events in a blinded fashion. Since cardiac resynchronisation may alter other aspects of the management of the patient, as would occur in clinical practice, the study should be considered a comparison of strategies rather than simply of a device. The primary end-point is all-cause mortality or unplanned cardiovascular hospitalisation. The study should complete recruitment during 2002 and report in 2004.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH P_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH P_Heart-Assist_Devices_MeSH M_Human_MeSH M_Male_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Reference_Values_MeSH M_Sensitivity_and_Specificity_MeSH M_Severity_of_Illness_Index_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH S_therapy_MeSH Ventricular_Dysfunction__Left_therapy_MeSH 
****** 11511438
----K E
----T Ambulatory heart failure management in private practice in France.
----A Management of ambulatory heart failure was assessed in a group of 600 patients, mean age 73, 64% males, NYHA I: 9%; II: 52%; III: 33%; IV: 6%; followed up by a representative sample of private cardiologists. Fifty-two percent of patients had been previously hospitalised for worsening heart failure with a mean duration of stay of 13.1 days, for those hospitalised in the year preceding the survey (26%). First diagnosis of heart failure had been performed by a cardiologist (57%), a general practitioner (37%) or another category of physician (6%). Seventy percent of patients received three or more different classes of heart failure medications. Diuretics were prescribed to 71%, angiotensin converting enzyme inhibitors to 54% and digitalis to 35% of the population. Beta-blockers were given to only 14% of the patients. In patients aged over 80 years, only 45% received angiotensin converting enzyme inhibitors. CONCLUSION: This survey of ambulatory heart failure patients confirms that the disease is predominantly observed in elderly patients, and associated with prolonged and recurrent hospitalisations. The underuse of recommended therapeutic classes including angiotensin converting enzyme inhibitors and beta-blockers deserves further investigation.
----P Journal_Article 
----M M_Age_Distribution_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Ambulatory_Care_MeSH S_methods_MeSH Ambulatory_Care_methods_MeSH M_Cardiology_MeSH S_methods_MeSH Cardiology_methods_MeSH S_statistics_&_numerical_data_MeSH Cardiology_statistics_&_numerical_data_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_France_MeSH S_epidemiology_MeSH France_epidemiology_MeSH M_Health_Care_Surveys_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Private_Practice_MeSH S_statistics_&_numerical_data_MeSH Private_Practice_statistics_&_numerical_data_MeSH M_Risk_Factors_MeSH M_Sampling_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Sex_Distribution_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 11518845
----K E
----T Effect of calcium antagonist or beta blockade treatment on nitric oxide-dependent vasodilation and oxidative stress in essential hypertensive patients.
----A OBJECTIVES: Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Since calcium antagonists can improve endothelial function in hypertensive patients, we tested whether this beneficial effect could be related to restoration of NO availability by antioxidant activity. METHODS: In 10 healthy subjects and 20 essential hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (from 0.15-15 microg/100 ml per min), bradykinin (0.005-0.05 microg/100 ml per min), two endothelium-dependent vasodilators, and sodium nitroprusside (1-4 microg/100 ml forearm tissue per min), an endothelium independent vasodilator, in the absence and presence of NG-monomethyl-L-arginine (L-NMMA) (100 microg/100 ml forearm tissue per min), an NO synthase inhibitor. RESULTS: In controls, vasodilation to acetylcholine and bradykinin was inhibited by L-NMMA. In hypertensive patients, vasodilation to acetylcholine and bradykinin, but not to sodium nitroprusside, was blunted and resistant to L-NMMA. Hypertensive patients were randomized to a 12-week treatment with lacidipine (4-6 mg/daily) or atenolol (50-100 mg/daily) (n = 10 each group). Lacidipine but not atenolol increased the vasodilation to acetylcholine and bradykinin and restored the inhibiting effect of L-NMMA on endothelium-dependent vasodilation, without affecting the response to sodium nitroprusside. Moreover, lacidipine reduced circulating markers of oxidative stress including plasma and low-density lipoprotein (LDL) hydroperoxides, the susceptibility of LDL to Cu2+-induced oxidation and the reactive oxygen species generated from human umbilical vein endothelial cells after incubation with LDL derived from plasma of the patients. CONCLUSIONS: Lacidipine increases endothelium-dependent vasodilation by restoring NO availability, and this effect possibly is related to antioxidant activity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antioxidants_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biological_Availability_MeSH M_Biological_Markers_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Dihydropyridines_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitric_Oxide_MeSH S_blood_MeSH Nitric_Oxide_blood_MeSH S_physiology_MeSH Nitric_Oxide_physiology_MeSH M_Oxidative_Stress_MeSH S_drug_effects_MeSH Oxidative_Stress_drug_effects_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH S_physiology_MeSH Vasodilation_physiology_MeSH 
****** 11518851
----K E
----T Effects of nebivolol and atenolol on insulin sensitivity and haemodynamics in hypertensive patients.
----A OBJECTIVES: To compare the effects of nebivolol and atenolol in 25 ambulatory hypertensive patients with impaired glucose tolerance. DESIGN: Clinic and ambulatory blood pressure, insulin sensitivity (euglycemic-hyperinsulinemic clamp), glucose tolerance (intravenous glucose tolerance test), systemic and regional haemodynamics were measured after 4 weeks of placebo and after each 16-week treatment period in a double-blind, crossover fashion. RESULTS: Nebivolol and atenolol similarly reduced (P< 0.001) clinic and ambulatory blood pressure by approximately 15/10 mmHg, systolic and diastolic. Clinic and ambulatory heart rate was reduced to a greater extent (P < 0.01) by atenolol than nebivolol. Atenolol was associated with an approximately 20% reduction in insulin sensitivity (insulin-induced glucose disposal rate/mean insulin concentration ratio, P < 0.01) and an approximately 10% reduction in glucose disappearance rate (K-value, P < 0.05), whereas these variables were not significantly modified with nebivolol. Cardiac output was reduced similarly (P < 0.05) by both drugs at rest but forearm blood flow, forearm vascular resistance or total peripheral resistance were unaffected. A significant inverse correlation coefficient between cardiac output and insulin sensitivity was found at baseline, suggesting that a compensatory increase in systemic blood flow occurs in hypertensive patients with progressively more marked insulin resistance. This relationship was unaffected by nebivolol but was lost with atenolol. CONCLUSIONS: These results indicate that insulin sensitivity was not modified significantly by nebivolol, whereas it was reduced by atenolol, although blood pressure was decreased to the same extent by both drugs. Neither drug induced systemic or forearm vasodilatation but the inverse relationship between cardiac output and insulin sensitivity was preserved with nebivolol but not with atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Insulin_Resistance_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11520524
----K E
----T Relation between drug treatment and cancer in hypertensives in the Swedish Trial in Old Patients with Hypertension 2: a 5-year, prospective, randomised, controlled trial.
----A BACKGROUND: Is cancer related to hypertension and blood pressure? Do antihypertensive drugs promote cancer? Do antihypertensive drugs protect against cancer? We previously analysed the frequency of cardiovascular mortality and morbidity in elderly people who participated in the Swedish Trial in Old Patients with Hypertension 2 (STOP-Hypertension-2). We have also looked at the frequency of cancer in these patients. METHODS: We randomly assigned 6614 elderly patients with hypertension (mean age 76 years, median time of follow-up 5.3 years) to one of three treatment strategies: conventional drugs (diuretics or b-blockers), calcium antagonists, or ACE inhibitors. We matched the patients to the Swedish Cancer Registry and compared our findings with expected values based on age, sex, and calendar-year-specific reference frequencies for the general Swedish population. We also compared the number of cancers between the three treatment groups. FINDINGS: At baseline, 607 (9%) patients had previous malignant disease. Diagnoses were closely similar to the distribution of cancer types that might be seen in elderly patients. During follow-up, there were 625 new cases of cancer in 590 patients. The frequency of cancer did not differ significantly between the treatment strategies, including all cancers and those at individual sites. The standardised incidence ratios (SIRs) for all cancers were also close to unity: 0.92 (95% CI 0.80-1.06) for conventional drugs, 0.96 (0.83-1.10) for calcium antagonists, and 0.99 (0.86-1.13) for ACE inhibitors. INTERPRETATIONS: No difference in cancer risk was seen between patients randomly assigned to conventional drugs, calcium antagonists, or ACE inhibitors. Thus, the general message to the practising physician is that more attention should be given to getting the blood pressure down than to the risk of cancer.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Chi-Square_Distribution_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Incidence_MeSH M_Male_MeSH M_Neoplasms_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH S_etiology_MeSH Neoplasms_etiology_MeSH M_Poisson_Distribution_MeSH M_Prevalence_MeSH M_Prospective_Studies_MeSH M_Registries_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH 
****** 11526364
----K E
----T Effect of carvedilol on survival and hemodynamics in patients with atrial fibrillation and left ventricular dysfunction: retrospective analysis of the US Carvedilol Heart Failure Trials Program.
----A BACKGROUND: Atrial fibrillation (AF) is present in a significant number of patients with congestive heart failure (CHF) caused by left ventricular dysfunction and is associated with significant morbidity and increased mortality rates. Thus it is necessary to establish therapy to improve the outcome in this high-risk population. METHODS: We conducted a retrospective analysis of data from the US Carvedilol Heart Failure Trials Program and identified patients with AF at the time of enrollment. In these trials, 1094 patients with at least 3 months of heart failure symptoms and an ejection fraction < or = 0.35 were randomly assigned to receive carvedilol or placebo in a double-blind, stratified program according to performance on an exercise test. RESULTS: One hundred thirty-six patients with concomitant AF and CHF were identified during the screening visit (84 assigned to carvedilol and 52 to placebo). Therapy with carvedilol resulted in a significant improvement in left ventricular ejection fraction (from 23% to 33% with carvedilol and from 24% to 27% with placebo, P =.001). The physician global assessment improved in a greater number of patients treated with carvedilol than in those treated with placebo (71% vs 48%, P =.025). A trend toward a reduction in the combined end point of death or CHF hospitalization was also observed (19% in patients treated with placebo and 7% in patients on carvedilol; relative risk, 0.35; 95% confidence interval, 0.12, 1.02; P =.055). CONCLUSIONS: In patients with AF complicating CHF, carvedilol significantly improves left ventricular ejection fraction and physician global assessment and probably reduces the combined end point of CHF hospitalizations or death.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_pathology_MeSH Atrial_Fibrillation_pathology_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Mortality_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_pathology_MeSH Ventricular_Dysfunction__Left_pathology_MeSH M_Ventricular_Function__Left_MeSH 
****** 11526365
----K E
----T Challenges of subgroup analyses in multinational clinical trials: experiences from the MERIT-HF trial.
----A BACKGROUND: International placebo-controlled survival trials (Metoprolol Controlled-Release Randomised Intervention Trial in Heart Failure [MERIT-HF], Cardiac Insufficiency Bisoprolol Study [CIBIS-II], and Carvedilol Prospective Randomized Cumulative Survival trial [COPERNICUS]) evaluating the effects of b-blockade in patients with heart failure have all demonstrated highly significant positive effects on total mortality as well as total mortality plus all-cause hospitalization. Also, the analysis of the US Carvedilol Program indicated an effect on these end points. Although none of these trials are large enough to provide definitive results in any particular subgroup, it is natural for physicians to examine the consistency of results across various subgroups or risk groups. Our purpose was to examine both predefined and post hoc subgroups in the MERIT-HF trial to provide guidance as to whether any subgroup is at increased risk, despite an overall strongly positive effect, and to discuss the difficulties and limitations in conducting such subgroup analyses. METHODS: The study was conducted at 313 clinical sites in 16 randomization regions across 14 countries, with a total of 3991 patients. Total mortality (first primary end point) and total mortality plus all-cause hospitalization (second primary end point) were analyzed on a time to first event. The first secondary end point was total mortality plus hospitalization for heart failure. RESULTS: Overall, MERIT-HF demonstrated a hazard ratio of 0.66 for total mortality and 0.81 for mortality plus all-cause hospitalization. The hazard ratio of the first secondary end point of mortality plus hospitalization for heart failure was 0.69. The results were remarkably consistent for both primary outcomes and the first secondary outcome across all predefined subgroups as well as for nearly all post hoc subgroups. The results of the post hoc US subgroup showed a mortality hazard ratio of 1.05. However, the US results regarding both the second primary combined outcome of total mortality plus all-cause hospitalization and of the first secondary combined outcome of total mortality plus heart failure hospitalization were in concordance with the overall results of MERIT-HF. Tests of country by treatment interaction (14 countries) revealed a nonsignificant P value of.22 for total mortality. The mortality hazard ratio for US patients in New York Heart Association (NYHA) class III/IV was 0.80, and it was 2.24 for patients in NYHA class II, which is not consistent with causality by biologic gradient. We have not been able to identify any confounding factor in baseline characteristics, baseline treatment, or treatment during follow-up that could account for any treatment by country interaction. Thus we attribute the US subgroup mortality hazard ratio to be due to chance. CONCLUSIONS: Just as we must be extremely cautious in overinterpreting positive effects in subgroups, even those that are predefined, we must also be cautious in focusing on subgroups with an apparent neutral or negative trend. We should examine subgroups to obtain a general sense of consistency, which is clearly the case in MERIT-HF. We should expect some variation of the treatment effect around the overall estimate as we examine a large number of subgroups because of small sample size in subgroups and chance. Thus the best estimate of the treatment effect on total mortality for any subgroup is the estimate of the hazard ratio for the overall trial.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_International_Cooperation_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH P_Randomized_Controlled_Trials_MeSH M_Reproducibility_of_Results_MeSH M_Research_Design_MeSH M_Risk_Factors_MeSH M_Sample_Size_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 11526366
----K E
----T Carvedilol titration in patients with congestive heart failure receiving inotropic therapy.
----A BACKGROUND: Carvedilol has been shown to improve morbidity and mortality in patients with congestive heart failure (CHF). There are limited data of carvedilol use in patients on inotrope therapy. We present our experience with carvedilol titration in New York Heart Association (NYHA) class IIIb/IV patients stabilized on milrinone therapy, as a nonrandomized study with a parallel control group of patients never on inotropes. These patients achieved volume control and stabilization of their symptoms during the course of milrinone therapy. METHODS AND RESULTS: Seventeen patients in class IIIb/IV CHF (group 1) on intermittent intravenous milrinone therapy and 15 patients in class II/IIIa compensated CHF (group 2) on standard triple heart failure therapy were titrated on carvedilol. Success and adverse events during titration were compared between the 2 groups. Fifteen (88%) patients in group 1 and 14 (93%) patients in group 2 were successfully titrated on carvedilol over 8.1 +/- 1.8 weeks and 6.7 +/- 2.8 weeks, respectively. The target dose of carvedilol (25 or 50 mg twice daily) was achieved in 13 (87%) patients (group 1) and 14 (93%) patients (group 2). Seven (47%) patients in group 1 and 4 (28%) patients in group 2 had adverse events during carvedilol titration. Eight (53%) patients in group 1 were weaned off milrinone over a period of 8.4 weeks after carvedilol titration, whereas the rest of the patients had reduction in the frequency of infusion. Ten (63%) patients in group 1 improved by one or more functional classes. CONCLUSIONS: Patients in NYHA class IIIb/IV who are treated with inotropic therapy can be titrated on carvedilol after reaching a stable state while on milrinone and standard oral drugs. Most of these patients can be successfully weaned off of milrinone or have decreased frequency of infusions and demonstrate improved functional status. Prospective randomized trials are required to evaluate these observations made in a limited number of patients in class IIIb and IV CHF because the combination of milrinone and beta-blockers has never been adequately evaluated.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Milrinone_MeSH S_therapeutic_use_MeSH Milrinone_therapeutic_use_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Retrospective_Studies_MeSH 
****** 11527840
----K E
----T Does a fixed physician reminder system improve the care of patients with coronary artery disease? A randomized controlled trial.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_California_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH P_Decision_Support_Systems__Clinical_MeSH M_Female_MeSH M_Hospitals__Veterans_MeSH M_Human_MeSH M_Intervention_Studies_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH M_Physician's_Practice_Patterns_MeSH S_standards_MeSH Physician's_Practice_Patterns_standards_MeSH P_Reminder_Systems_MeSH M_Treatment_Outcome_MeSH 
****** 11543734
----K E
----T Factors affecting fluvoxamine antidepressant activity: influence of pindolol and 5-HTTLPR in delusional and nondelusional depression.
----A BACKGROUND: It has been recently reported that the short variant of the serotonin transporter (5-HTT) gene-linked functional polymorphic region (5-HTTLPR) influences the antidepressant response to certain selective serotonin reuptake inhibitors. The aim of the present study was to test this finding in a sample of major and bipolar depressives, with or without psychotic features. METHODS: One hundred fifty-five inpatients were treated with fluvoxamine 300 mg and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Allelic variation of 5-HTTLPR in each subject was determined using a polymerase chain reaction-based technique. RESULTS: 5-HTTLPR short variant was associated with a poor response to fluvoxamine treatment, independently from the recorded clinical variables. More specifically, the diagnosis, the presence of psychotic features, and the severity of depressive symptomatology did not influence this association. Conversely, pindolol augmentation may ameliorate the rate of response in 5-HTTLPR short variant subjects, thus reducing the difference in the response rate among the genotype variants. CONCLUSIONS: If confirmed, these results may improve patient care by helping the clinician to individualize treatment according to the patient's genetic 5-HTTLPR pattern.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antidepressive_Agents_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antidepressive_Agents_adverse_effects_MeSH M_Bipolar_Disorder_MeSH S_diagnosis_MeSH Bipolar_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Bipolar_Disorder_drug_therapy_MeSH S_genetics_MeSH Bipolar_Disorder_genetics_MeSH M_Carrier_Proteins_MeSH S_genetics_MeSH Carrier_Proteins_genetics_MeSH M_Comparative_Study_MeSH M_Delusions_MeSH S_diagnosis_MeSH Delusions_diagnosis_MeSH S_drug_therapy_MeSH Delusions_drug_therapy_MeSH S_genetics_MeSH Delusions_genetics_MeSH M_Depression__Involutional_MeSH S_diagnosis_MeSH Depression__Involutional_diagnosis_MeSH S_drug_therapy_MeSH Depression__Involutional_drug_therapy_MeSH S_genetics_MeSH Depression__Involutional_genetics_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fluvoxamine_MeSH S_administration_&_dosage_MeSH Fluvoxamine_administration_&_dosage_MeSH S_adverse_effects_MeSH Fluvoxamine_adverse_effects_MeSH M_Genotype_MeSH M_Human_MeSH M_Male_MeSH M_Membrane_Glycoproteins_MeSH S_genetics_MeSH Membrane_Glycoproteins_genetics_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH M_Polymorphism_(Genetics)_MeSH S_genetics_MeSH Polymorphism_(Genetics)_genetics_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_administration_&_dosage_MeSH Serotonin_Uptake_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Uptake_Inhibitors_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Variation_(Genetics)_MeSH 
****** 11565518
----K E
----T Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy.
----A BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal disease. Interruption of the renin-angiotensin system slows the progression of renal disease in patients with type 1 diabetes, but similar data are not available for patients with type 2, the most common form of diabetes. We assessed the role of the angiotensin-II-receptor antagonist losartan in patients with type 2 diabetes and nephropathy. METHODS: A total of 1513 patients were enrolled in this randomized, double-blind study comparing losartan (50 to 100 mg once daily) with placebo, both taken in addition to conventional antihypertensive treatment (calcium-channel antagonists, diuretics, alpha-blockers, beta-blockers, and centrally acting agents), for a mean of 3.4 years. The primary outcome was the composite of a doubling of the base-line serum creatinine concentration, end-stage renal disease, or death. Secondary end points included a composite of morbidity and mortality from cardiovascular causes, proteinuria, and the rate of progression of renal disease. RESULTS: A total of 327 patients in the losartan group reached the primary end point, as compared with 359 in the placebo group (risk reduction, 16 percent; P=0.02). Losartan reduced the incidence of a doubling of the serum creatinine concentration (risk reduction, 25 percent; P=0.006) and end-stage renal disease (risk reduction, 28 percent; P=0.002) but had no effect on the rate of death. The benefit exceeded that attributable to changes in blood pressure. The composite of morbidity and mortality from cardiovascular causes was similar in the two groups, although the rate of first hospitalization for heart failure was significantly lower with losartan (risk reduction, 32 percent; P=0.005). The level of proteinuria declined by 35 percent with losartan (P<0.001 for the comparison with placebo). CONCLUSIONS: Losartan conferred significant renal benefits in patients with type 2 diabetes and nephropathy, and it was generally well tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Creatine_MeSH S_blood_MeSH Creatine_blood_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Nephropathies_MeSH S_complications_MeSH Diabetic_Nephropathies_complications_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_prevention_&_control_MeSH Proteinuria_prevention_&_control_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11548874
----K E
----T Renin-angiotensin system is involved in the mechanism of increased serum asymmetric dimethylarginine in essential hypertension.
----A Endothelium-dependent/nitric oxide (NO)-mediated vasodilation is impaired in hypertensive individuals. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, is synthesized by many types of cells including vascular endothelial cells. The serum level of ADMA is elevated in patients with essential hypertension, but the mechanism for this increase is unknown. Therefore, the present study examined whether the renin-angiotensin system (RAS) is involved. Patients with essential hypertension [systolic blood pressure (BP) > 160 mmHg and/or diastolic BP > 95 mmHg] were randomized to an angiotensin-converting enzyme (ACE) inhibitor treatment group (perindopril, 4mg/day for 4 weeks, n = 7), an angiotensin II type 1 (AT1) receptor antagonist treatment group (losartan, 50 mg/day for 4 weeks, n = 7) or a beta-blocker treatment group (bisoprolol, 5 mg/day for 4 weeks, n = 7). Before and after the treatment, BP, serum concentration of ADMA and plasma concentration of von Willebrand factor (vWF, a biological marker of endothelial injury) were measured. Perindopril, losartan and bisoprolol decreased BP to a similar extent, and either perindopril or losartan, but not bisoprolol, significantly decreased serum ADMA and plasma vWF. These findings suggest that the RAS may contribute to the mechanism of increased serum ADMA as well as to the endothelial injury observed in hypertensive patients. The vasculoprotective actions of ACE inhibitors or AT1 receptor antagonists may be explained at least in part by amelioration of the endothelial injury through a decrease in the serum ADMA concentration.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Arginine_MeSH S_adverse_effects_MeSH Arginine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Arginine_analogs_&_derivatives_MeSH S_blood_MeSH Arginine_blood_MeSH S_drug_effects_MeSH Arginine_drug_effects_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_pathology_MeSH Endothelium__Vascular_pathology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Losartan_MeSH S_administration_&_dosage_MeSH Losartan_administration_&_dosage_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitric-Oxide_Synthase_MeSH S_antagonists_&_inhibitors_MeSH Nitric-Oxide_Synthase_antagonists_&_inhibitors_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH S_pharmacology_MeSH Perindopril_pharmacology_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_von_Willebrand_Factor_MeSH S_drug_effects_MeSH von_Willebrand_Factor_drug_effects_MeSH S_metabolism_MeSH von_Willebrand_Factor_metabolism_MeSH 
****** 11549204
----K E
----T Pharmacokinetic and dynamic interactions of the angiotensin-converting enzyme inhibitor imidapril with hydrochlorothiazide, bisoprolol and nilvadipine.
----A OBJECTIVE: The pharmacokinetic and dynamic interactions of the angiotensin-converting enzyme (ACE) inhibitor imidapril with other therapeutic principles used in hypertension and heart failure were evaluated. METHODS: In three separate, double-blind, placebo-controlled, four-way cross-over studies in healthy volunteers (n = 16 each), single oral doses of imidapril 10 mg (I), hydrochlorothiazide 12.5 mg (H), bisoprolol 5 mg (B) and nilvadipine 8 mg (N) were administered as monotherapies, and in IH, IB and IN combinations. Plasma concentrations of imidaprilat and H were followed up to 48 h, those of B and N up to 24 h and area under the concentration time curve (AUC), maximum plasma concentration (Cmax) and time to Cmax (tmax) were determined. Blood pressure (BP), heart rate (HR) and non-invasive haemodynamics [total peripheral resistance (TPR, N and H), systolic time intervals (STI, N and H), and plasma renin activity (PRA)] were assessed up to 24 h. RESULTS: There were no pharmacokinetic interactions between I plus H, B or N. Bioequivalence between single and combined administrations was verified for all investigational compounds [AUC point estimates (90% confidence interval CI): imidaprilat IH 109% (97.8, 122.8); IB 99.6% (91.2, 109.4); IN 105.7% (92.1, 121.3); H 96.6% (92.5, 100.8); B 103% (100.2, 105.8); N 98% (89, 108)]. The haemodynamic effects were mostly additive and without relevant pharmacodynamic interactions. I significantly reduced the BP by 5-8 mmHg, B by 4-8 mmHg and N by 4-6 mmHg. In addition, H induced a significant reduction of the preload as seen from STI, and B significantly reduced HR (-5 bpm). N induced a significant decrease in TPR (about 15% of baseline values) and showed corresponding changes in STI. PRA increased significantly following I alone (1.5-2.0 ng/ml/h), as well as combined with N (2.5 ng/ ml/h) or H (3.1 ng/ml/h). This increase was clearly blunted by the co-administration of B (0.6 ng/ml/h). CONCLUSIONS: The combination of imidapril with a diuretic, beta-adrenoceptor antagonist or calcium-channel blocker seems a reasonable and safe treatment option when striving for additive pharmacodynamic effects not accompanied by relevant pharmacokinetic interactions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Area_Under_Curve_MeSH M_Bisoprolol_MeSH S_pharmacokinetics_MeSH Bisoprolol_pharmacokinetics_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Thiazide_MeSH S_pharmacokinetics_MeSH Diuretics__Thiazide_pharmacokinetics_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_pharmacokinetics_MeSH Hydrochlorothiazide_pharmacokinetics_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH M_Imidazoles_MeSH S_pharmacokinetics_MeSH Imidazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Imidazoles_pharmacology_MeSH M_Male_MeSH M_Nifedipine_MeSH S_analogs_&_derivatives_MeSH Nifedipine_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Nifedipine_pharmacokinetics_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH 
****** 11551875
----K E
----T Effects of once-daily angiotensin-converting enzyme inhibition and calcium channel blockade-based antihypertensive treatment regimens on left ventricular hypertrophy and diastolic filling in hypertension: the prospective randomized enalapril study evaluating regression of ventricular enlargement (preserve) trial.
----A BACKGROUND: The Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) study was designed to test whether enalapril achieves greater left ventricular (LV) mass reduction than does a nifedipine gastrointestinal treatment system by a prognostically meaningful degree on a population basis (10 g/m(2)). METHODS AND RESULTS: An ethnically diverse population of 303 men and women with essential hypertension and increased LV mass at screening echocardiography were enrolled at clinical centers on 4 continents and studied by echocardiography at baseline and after 6- and 12-month randomized therapy. Clinical examination and blinded echocardiogram readings 48 weeks after study entry in an intention-to-treat analysis of 113 enalapril-treated and 122 nifedipine-treated patients revealed similar reductions in systolic/diastolic pressure (-22/12 versus -21/13 mm Hg) and LV mass index (-15 versus -17g/m(2), both P>0.20). No significant between-treatment difference was detected in population subsets defined by monotherapy treatment, sex, age, race, or severity of baseline hypertrophy. Similarly, there was no between-treatment difference in change in velocities of early diastolic or atrial phase transmitral blood flow. More enalapril-treated than nifedipine-treated patients required supplemental treatment with hydrochlorothiazide (59% versus 34%, P<0.001) but not atenolol (27% versus 22%, NS). CONCLUSIONS: Once-daily antihypertensive treatment with enalapril or long-acting nifedipine, plus adjunctive hydrochlorothiazide and atenolol when needed to control blood pressure, both had moderately beneficial and statistically indistinguishable effects on regression of LV hypertrophy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH S_physiology_MeSH Diastole_physiology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11551371
----K I
----T Meta-analyses of antihypertensive therapy: Are some of them misleading?
----A Meta-analysis has become a very popular tool to compare the efficacy of different antihypertensive regimens. Combining results from various outcome studies may provide evidence to guide the therapeutic approach even before results from large prospective studies are available. However, meta-analysis may be misleading if it is not done meticulously. Some meta-analyses that received broad news media coverage in the recent years were misleading. One analysis suggested that the use of short-acting nifedipine in moderate to high doses in patients with coronary disease increased mortality. This claim was refuted later by observational studies. Based on another meta-analysis, it was claimed that diuretics and beta-blockers are equally effective in reducing cardiovascular morbidity and mortality. Another more careful meta-analysis, omitting one study in which most patients were on combination therapy and not on beta-blocker monotherapy, showed the superiority of diuretic versus b-blocker treatment in the elderly. Calcium antagonists were recently blamed for increasing the rate of myocardial infarction and congestive heart failure in hypertensive patients, and therefore their use was not recommended as first-line therapy in hypertension. This recommendation was based on a meta-analysis subject to major drawbacks and was misleading. Another notion based on meta-analysis was that angiotensin converting enzyme inhibitors reduce left ventricular mass more than diuretics. This notion was refuted by three large randomized studies. A recent meta-analysis, which showed a similar blood pressure lowering effect for all angiotensin receptor blockers, was refuted by head-to-head studies. Thus, when performed correctly, meta-analysis can be an important tool, but when uncritically employed, it is prone to be misleading.
----P Journal_Article Meta-Analysis Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH 
****** 11558835
----K E
----T Telmisartan: a review of its use in hypertension.
----A Telmisartan is an angiotensin II receptor antagonist that is highly selective for type 1 angiotensin II receptors. It was significantly more effective than placebo in large (n >100), double-blind, randomised, multicentre clinical trials in patients with mild to moderate hypertension. Telmisartan 20 to 160 mg once daily produced mean reductions in supine trough systolic blood pressure and diastolic blood pressure of up to 15.5 and 10.5 mm Hg, respectively. Maximum blood pressure reduction occurred with a dosage of 40 to 80 mg/day. Telmisartan 40 to 120 mg/day was as effective as amlodipine 5 to 10 mg/day or atenolol 50 to 100 mg/day in dose-titration studies. Telmisartan 20 to 160 mg/day was generally similar in efficacy to enalapril 5 to 20 mg/day or lisinopril 10 to 40 mg/day in both titration-to-response and other studies. Hydrochlorothiazide was coadministered in most of the titration-to-response studies if patients remained hypertensive. Telmisartan 80 mg/day was more effective than submaximal dosages of losartan (50 mg/day) or valsartan (80 mg/day) and was as effective as a fixed-dose combination of losartan 50 mg plus hydrochlorothiazide 12.5 mg over the last 6 hours of the dosage interval and the whole 24-hour postdose interval. In patients with severe hypertension, telmisartan 80 to 160 mg/day was as effective as enalapril 20 to 40 mg/day (both agents could be titrated and combined sequentially with hydrochlorothiazide 25 mg and amlodipine 5 mg). The addition of hydrochlorothiazide to telmisartan was more effective than each agent alone at lowering blood pressure in patients with hypertension. Telmisartan was well tolerated in patients with mild to moderate hypertension and was significantly less likely to cause persistent, dry cough than lisinopril. Conclusion: Telmisartan is an effective antihypertensive agent with a tolerability profile similar to that of placebo. Comparative data have shown telmisartan to be as effective as other major classes of antihypertensive agents at lowering blood pressure. Compared with lisinopril, telmisartan is associated with a significantly lower incidence of dry, persistent cough. Therefore, telmisartan is a useful therapeutic option in the management of patients with hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin_II_MeSH S_pharmacology_MeSH Angiotensin_II_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Benzimidazoles_MeSH S_administration_&_dosage_MeSH Benzimidazoles_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Benzimidazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Benzimidazoles_pharmacology_MeSH M_Benzoates_MeSH S_administration_&_dosage_MeSH Benzoates_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Benzoates_pharmacokinetics_MeSH S_pharmacology_MeSH Benzoates_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Drug_Interactions_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Treatment_Outcome_MeSH 
****** 11558836
----K I
----T Hypertension in diabetes mellitus: role of beta-blockers.
----A 
----P Comment Letter 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Coronary_Arteriosclerosis_MeSH S_etiology_MeSH Coronary_Arteriosclerosis_etiology_MeSH S_prevention_&_control_MeSH Coronary_Arteriosclerosis_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH M_Weight_Gain_MeSH 
****** 11561225
----K E
----T Rehabilitation of patients with congestive heart failure with or without beta-blockade therapy.
----A BACKGROUND: Management of heart failure includes beta-blockade (betaB) therapy and cardiac rehabilitation. The aim of this study was to compare the exercise training response of patients with congestive heart failure (CHF) receiving betaB therapy with that of patients not receiving treatment. METHODS AND RESULTS: Thirty-four consecutive patients with CHF were included in a 4-week training program at their ventilatory threshold (VT); 6 patients received betaB treatment and 18 did not. The patients underwent a cardiopulmonary exercise test before and after training. Oxygen uptake (VO(2)) at peak exercise and at VT increased in both groups (P < or =.0001) without any significant differences between the groups. The same results were found after adjustment to ejection fraction and VO(2) at the start of the training program. There was no difference in VT improvement, measured as a percentage of utilization of maximal oxygen uptake, between the groups. After training, heart rate and ventilation decreased (P < or =.0001) at submaximal levels in both groups without significant differences between the groups. CONCLUSIONS: betaB therapy does not impair functional improvement induced by a rehabilitation program in patients with CHF. betaB therapy does not interfere with exercise training prescription if patient exercise evaluations are made at the time of therapeutic intake.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Exercise_Test_MeSH P_Exercise_Therapy_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_rehabilitation_MeSH Heart_Failure__Congestive_rehabilitation_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH M_Prospective_Studies_MeSH M_Pulmonary_Ventilation_MeSH M_Time_Factors_MeSH 
****** 11574896
----K E
----T Physician characteristics in relation to cardiovascular drugs commonly prescribed for hypertension in Nova Scotia.
----A BACKGROUND: Cardiovascular drugs are the most frequently prescribed class of drugs in Canada. Among them, drugs used to treat hypertension are the single largest component. Variability in how these drugs are prescribed should be based on the specific characteristics of patients. However, some evidence shows that physician characteristics can also play a substantial role in prescribing trends. Such variation is also associated with varying beneficial and adverse patient outcomes. PURPOSE: To determine whether prescribing patterns of drugs used to treat hypertension in elderly patients in Nova Scotia varied by physician characteristics. METHODS: A retrospective, population-based descriptive study was done using the Nova Scotia Pharmacare program data for the fiscal year 1995/96. The unit of analysis was the individual physician. All drugs indicated in the management of hypertension were included for the analysis. RESULTS: Of 1466 physicians included in the analysis, 1004 were family physicians (FPs) and/or general practitioners (GPs), 155 were internal medicine specialists and 307 were other specialists. Fifty-eight per cent of 103,193 eligible senior citizens received at least one of the study medications. FPs and/or GPs prescribed 95.9% of all the study drugs. Internists prescribed proportionately fewer angiotensin-converting enzyme inhibitors, thiazides and other diuretics compared with the FPs and/or GPs but more beta-blockers and calcium channel blockers. A large proportion of the FPs and/or GPs (55.3%) prescribed less than 10% of the total day's supply of drugs, whereas a small proportion of FPs and/or GPs (16.3%) prescribed 52.6% of all the study drugs. There was no variation in the distribution of the types of antihypertensives prescribed based on physician age, sex or volume of prescribing. A slight variation in prescribing was seen with location of practice. CONCLUSIONS: Patterns of prescribing cardiovascular drugs used to treat hypertension were remarkably unaffected by physician characteristics. This finding counters other evidence in the literature that has raised concerns over prescribing patterns of certain types of physicians. Prescribing patterns may vary for other drug classes, but for this group of antihypertensives, little variability was found.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Health_Services_for_the_Aged_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nova_Scotia_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11576319
----K E
----T Effective blood pressure treatment improves LDL-cholesterol susceptibility to oxidation in patients with essential hypertension.
----A OBJECTIVES: LDL-cholesterol particles from hypertensive patients exhibit enhanced susceptibility to in vitro oxidation, an abnormality thought to increase cardiovascular risk. We tested whether blood pressure (BP) normalization can reverse this abnormality. DESIGN: Double-blind, randomized pharmacological intervention trial. SETTING: Clinical research centre. Subjects. A total of 29 nondiabetic, normolipidaemic patients with essential hypertension (BP= 151 +/- 3/99 +/- 1 mmHg) and 11 normotensive controls (BP=125 +/- 3/85 +/- 1 mmHg) matched for gender, age, obesity, glucose tolerance and lipid profile. Intervention. Anti-hypertensive treatment for 3 months with a calcium-antagonist in randomized combination with either an ACE inhibitor or a beta-blocker. MAIN OUTCOME MEASURES: Lag phase of copper-induced LDL oxidation, cell-mediated (human umbilical vein endothelium) generation of malondialdehyde (MDA) by LDL and vitamin E content in LDL. RESULTS: At baseline in hypertensives versus controls, lag phase was shorter (89 +/- 3 vs. 107 +/- 6 min, P < 0.04), MDA generation was higher (5.8 +/- 0.1 vs. 5.1 +/- 0.2 nmol L(-1), P=0.002), and vitamin E was reduced (6.40 +/- 0.05 vs. 6.67 +/- 0.11 microg mg(-1), P=0.03). At 3 months, BP was normalized (124 +/- 3/81 +/- 1, P < 0.0001 vs. baseline, P=ns versus controls), lag phase was prolonged (to 98 +/- 3 min, P=0.0005), MDA generation was reduced (5.6 +/- 0.1 nmol L-1, P = 0.001), and vitamin E was increased (6.53 +/- 0.05 microg mg(-1), P=0.003), with no significant differences between the randomized groups. CONCLUSIONS: In nondiabetic, nonobese, normolipidaemic patients with essential hypertension, LDL susceptibility to copper- and cell-mediated oxidation is increased. BP normalization is associated with a significant improvement, but not a full reversal, of this abnormality.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_adverse_effects_MeSH Indoles_adverse_effects_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Malondialdehyde_MeSH S_blood_MeSH Malondialdehyde_blood_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Oxidative_Stress_MeSH S_drug_effects_MeSH Oxidative_Stress_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiobarbituric_Acid_Reactive_Substances_MeSH S_metabolism_MeSH Thiobarbituric_Acid_Reactive_Substances_metabolism_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 11579362
----K I
----T Reliability, validity, and responsiveness of the six-minute walk test in patients with heart failure.
----A BACKGROUND: Our purpose was to evaluate the reliability, validity, and responsiveness of the 6-minute walk test (6MWT) in patients with heart failure (HF) enrolled in the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) pilot study. METHODS: A total of 768 patients was enrolled in a multicenter randomized clinical trial evaluating the effect of candesartan, enalapril, and metoprolol on left ventricular ejection fraction (LVEF), 6MWT distance, neurohormones, and quality of life. The 6MWT was performed once at screening and twice at baseline, 18 weeks, and 43 weeks by a standardized method. RESULTS: Test-retest reliability at baseline (intraclass correlation coefficient [ICC] = 0.90), 18 weeks (ICC = 0.88), and 43 weeks (ICC = 0.91) was very good. Baseline 6MWT distance was weakly inversely correlated to the quality-of-life cumulative score (r = -0.26, P =.0001) and moderately inversely correlated to the New York Heart Association functional classification (NYHA-FC) (r = -0.43, P =.001). In the RESOLVD study, the 6MWT was not responsive to change when effect sizes and standardized response means were used. Disease-specific quality of life was responsive to change in patients treated with candesartan and enalapril and NYHA-FC was responsive to change in the candesartan and enalapril combination and for enalapril alone with small effect sizes. The 6MWT, NYHA-FC, and quality of life were not responsive to change during the metoprolol or placebo phase. CONCLUSIONS: The 6MWT is highly reproducible in patients with symptoms of HF. It is somewhat correlated to NYHA-FC and quality of life. Overall, quality of life was most responsive to change, whereas 6MWT and NYHA-FC were comparable but less responsive to change in the RESOLVD study.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_Test_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Female_MeSH M_Health_Status_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Reproducibility_of_Results_MeSH M_Sickness_Impact_Profile_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Walking_MeSH S_statistics_&_numerical_data_MeSH Walking_statistics_&_numerical_data_MeSH 
****** 11579363
----K E
----T Regression of left ventricular remodeling in chronic heart failure: Comparative and combined effects of captopril and carvedilol.
----A BACKGROUND: This study evaluated the independent and combined effects of captopril and carvedilol on left ventricular remodeling in chronic heart failure. Although angiotensin-converting enzyme inhibitors and b-blockers are known to attenuate the remodeling process in chronic heart failure, a direct comparison of these agents has not been performed. METHODS: We investigated 57 patients with mild to moderate chronic heart failure (48 ischemic, 9 nonischemic) who were randomized in a double-blind fashion to treatment with carvedilol or captopril at maximum doses of 25 mg twice daily for 3 months, followed by 3 months of combined treatment. Serial echocardiography, right heart catheterization, and treadmill exercise testing were performed at baseline, 3 months, and 6 months. After exclusions, 49 patients were evaluated during monotherapy and 48 during combination therapy. RESULTS: Carvedilol monotherapy produced significant reductions in end-systolic volume, leading to a greater median increase in ejection fraction compared with captopril monotherapy (4.7% vs 1.5%, respectively; P <.05). Each drug caused similar reductions in left ventricular mass, chamber sphericity, and pulmonary artery wedge pressure during monotherapy and combined treatment. Adjunctive treatment with carvedilol produced a trend toward a greater increase in ejection fraction (4.3% vs 2.7%, respectively; P not significant) and significantly greater reductions in the wall thickening score index than with captopril (0.25 vs 0.08, respectively; P =.04). CONCLUSIONS: Although angiotensin-converting enzyme inhibitor therapy did not alter left ventricular volume, treatment with carvedilol was associated with reductions in chamber volume; both drugs reduced left ventricular mass and sphericity. These beneficial effects on remodeling may help to explain the relative prognostic benefits of these therapies.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 11581535
----K 5
----T Anesthetic considerations in patients with cardiac arrhythmias, pacemakers, and AICDs.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Anesthesia_MeSH S_adverse_effects_MeSH Anesthesia_adverse_effects_MeSH S_methods_MeSH Anesthesia_methods_MeSH M_Arrhythmia_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH M_Cardiovascular_Physiology_MeSH P_Defibrillators__Implantable_MeSH M_Human_MeSH P_Pacemaker__Artificial_MeSH M_Surgical_Procedures__Operative_MeSH 
****** 11583861
----K I
----T Metoprolol controlled release/extended release in patients with severe heart failure: analysis of the experience in the MERIT-HF study.
----A OBJECTIVES: This study analyzed the effect of the beta(1)-selective beta-blocker metoprolol succinate controlled release/extended release (CR/XL) once daily on mortality, hospitalizations and tolerability in patients with severe heart failure.BACKGROUND: There continues to be resistance to the incorporation of beta-blockers into clinical care, largely due to concerns about their benefit in patients with more severe heart failure.METHOD: SA subgroup of patients from Metoprolol CR/XL Randomized Intervention Trial in chronic Heart Failure (MERIT-HF) in New York Heart Association (NYHA) functional class III/IV with left ventricular ejection fraction < 0.25 were identified (n = 795). The analysis was by intention-to-treat.RESULTS: The mean ejection fraction at baseline was 0.19, and the yearly placebo mortality during follow-up was 19.1%. Treatment with metoprolol CR/XL compared to placebo resulted in significant reductions in all predefined mortality end points including: total mortality, 45 versus 72 deaths (risk reduction 39%; 95% confidence interval 11% to 58%; p = 0.0086); sudden death, 22 vs. 39 deaths (45% [7% to 67%]; p = 0.024); and death due to worsening heart failure, 13 vs. 28 deaths (55% [13% to 77%]; p = 0.015). Metoprolol CR/XL also reduced the number of hospitalizations for worsening heart failure by 45% compared with placebo (p < 0.0001). The NYHA functional class improved in the metoprolol CR/XL group compared with placebo (p = 0.0031). Metoprolol CR/XL was well tolerated, with 31% fewer patients withdrawn from study medicine (all causes) compared with placebo (p = 0.027).CONCLUSIONS: This subgroup analysis of the MERIT-HF study shows that patients with severe heart failure receive a similar mortality benefit and a similar reduction in hospitalizations for worsening heart failure with metoprolol CR/XL treatment as those patients included in the total study.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Delayed-Action_Preparations_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11583862
----K E
----T Prospective crossover comparison of carvedilol and metoprolol in patients with chronic heart failure.
----A OBJECTIVES: This study investigates the effects of a change of beta-adrenergic blocking agent treatment from metoprolol to carvedilol and vice versa in patients with heart failure (HF).BACKGROUND: Beta-blockers improve ventricular function and prolong survival in patients with HF. It has recently been suggested that carvedilol has more pronounced effects on left ventricular ejection fraction (LVEF) compared with metoprolol. It is uncertain whether a change from one beta-blocker to the other is safe and leads to any change of left ventricular function.METHODS: Forty-four patients with HF due to ischemic (n = 17) or idiopathic cardiomyopathy (n = 27) that had responded well to long-term treatment with either metoprolol (n = 20) or carvedilol (n = 24) were switched to an equivalent dose of the respective other beta-blocker. Before and six months after crossover of treatment, echocardiography, radionuclide ventriculography and dobutamine stress echocardiography were performed.RESULTS: Six months after crossover of beta-blocker treatment, LVEF had further improved with both carvedilol and metoprolol (carvedilol: 32 +/- 3% to 36 +/- 4%; metoprolol: 27 +/- 4% to 30 +/- 5%; both p < 0.05 vs. baseline), without interindividual differences. There were no changes in either New York Heart Association functional class or any other hemodynamic parameters at rest. Dobutamine stress echocardiography revealed a more pronounced increase of heart rate after dobutamine infusion in metoprolol- compared with carvedilol-treated patients. After dobutamine infusion, LVEF increased in the carvedilol- but not in the metoprolol-treated group.CONCLUSIONS: When switching treatment from one beta-blocker to the other, improvement of LVEF in patients with HF is maintained. Despite similar long-term effects on hemodynamics at rest, beta-adrenergic responsiveness is different in both treatments.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH P_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11583866
----K E
----T Use of risk stratification to identify patients with unstable angina likeliest to benefit from an invasive versus conservative management strategy.
----A OBJECTIVES: This study was designed to determine whether patient characteristics collected at presentation can identify which patients benefit from immediate coronary angiography and revascularization. BACKGROUND: Risk stratification may offer a method for identifying which patients with unstable angina or non-Q-wave myocardial infarction (NQMI) are likeliest to benefit from invasive management strategies. METHODS: The analysis was based on data from a randomized controlled trial that enrolled 1,473 patients presenting with unstable angina or NQMI who were randomly assigned to an early invasive or early conservative (medical) management strategy. We constructed a risk-stratification score for each patient based on adjusted odds ratios for clinical variables likely to predict adverse outcomes. We stratified all trial subjects by their risk scores and studied the rates of death or myocardial infarction (MI) of the early invasive management strategy in each stratum. RESULTS: The final multivariate model included older age, ST segment depression on presentation, history of complicated angina before presentation, and elevation in baseline creatine kinase-MB fraction. Although patients with a higher risk score had an increased rate of death or MI within 42 days and 365 days (p < 0.001) in both management strategies, early invasive management for patients in the high and very high risk categories was associated with a lower rate of death or MI within 42 days compared with conservative management. No such benefit was seen in patients in the larger group of patients in the very low, low or moderate risk categories (p = 0.03 for the interaction between risk category and management assignment). CONCLUSIONS: Risk stratification may be an effective method for identifying those patients with unstable angina or NQMI most likely to benefit from early invasive management. Selective use of early invasive management can have a substantial impact in reducing morbidity and mortality in higher risk patients, but may not be warranted in lower risk patients.
----P Journal_Article 
----M M_Aged_MeSH M_Angina__Unstable_MeSH S_epidemiology_MeSH Angina__Unstable_epidemiology_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_C-Reactive_Protein_MeSH S_analysis_MeSH C-Reactive_Protein_analysis_MeSH M_Coronary_Angiography_MeSH P_Coronary_Artery_Bypass_MeSH M_Female_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Troponin_I_MeSH S_analysis_MeSH Troponin_I_analysis_MeSH 
****** 11585103
----K E
----T Brain natriuretic peptide-guided therapy for heart failure.
----A The drug treatment of heart failure, once simple, has become complex. Apart from a loop diuretic and digoxin, most patients should now be receiving an angiotensin-converting enzyme inhibitor (or angiotensin II receptor blocker), a beta-blocker and spironolactone. Newer drugs, such as endothelin-receptor antagonists and combined blockers of converting-enzyme and neutral endopeptidase, might soon become available. When to introduce these drugs and what dose is optimal for any individual, are questions that currently vex clinicians. We proposed that plasma levels of the cardiac hormone brain natriuretic peptide (BNP, or better, its 1-76 amino-acid N-terminal fragment, N-BNP), would provide an objective index for guiding drug treatment in patients with established, stable cardiac failure. In a pilot study, 69 patients were randomized to drug treatment based on clinical criteria, or based on plasma levels of N-BNP. After a median follow-up of 9.6 months, those in the N-BNP group had fewer clinical end-points than those in the group managed by clinical criteria alone (19 vs 54; P= 0.02). These preliminary data encourage the concept that the increasingly complex pharmacotherapy for heart failure, both chronic (as in this trial) and acute, might best be guided by an objective measure such as plasma levels of BNP or N-BNP.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Pilot_Projects_MeSH M_Point-of-Care_Systems_MeSH M_Treatment_Outcome_MeSH 
****** 11588403
----K E
----T Low-dose combination therapy: why include a diuretic?
----A Hypertension and its complications are more frequent and occur about a decade earlier in life among high-risk groups, especially in the Southeast. Moreover, socioeconomic status is inversely related to hypertension and cardiovascular complications. Low-income, young and middle-aged adults living in the Southeast may be at especially high risk. Data on inpatient admissions among hypertensive Medicaid beneficiaries living in this region may provide insights on the burden of hypertension-related disease and on opportunities for successful intervention. A study of hospitalization rates and costs among 44,440 hypertensive Medicaid beneficiaries in South Carolina from 1993-1996 showed that 16,883 (38%) were continuously enrolled in Medicaid. Of this group, 63% were African American and 74% were women. Among the continuously enrolled patients, 7637, or about 45%, were hospitalized during the 4-year period. These 7637 individuals accounted for 20,698 hospital admissions, i.e., 2.7 admissions per person, over the 4-year interval. Nearly two thirds of the hospitalizations included a cardiovascular or renal diagnosis. Hospital claims paid reached nearly $90 million for the 7637 hypertensive Medicaid recipients during the 4-year period. Among patients discharged from the hospital with congestive heart failure, 33% filled a prescription for an angiotensin-converting enzyme inhibitor within 90 days; 13% of patients discharged with an acute myocardial infarction filled a prescription for a beta blocker within 90 days. The data confirm that hypertensive Medicaid beneficiaries in the Southeast are hospitalized at high rates. Cardiovascular and renal morbidity account for the majority of the inpatient admissions. The findings suggest that the application of evidence-based guidelines would improve health, avoid cost, and reduce racial disparities in health outcomes.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Clinical_Trials_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 11589843
----K E
----T Cardiovascular safety of sublingual apomorphine in patients on stable doses of oral antihypertensive agents and nitrates.
----A Sublingual (SL) apomorphine (2 to 6 mg) has been shown to be effective for treatment of male erectile dysfunction. Many patients with erectile dysfunction are also being treated for systemic hypertension and/or cardiovascular disease. In a double-blind, randomized, placebo-controlled, crossover trial, SL apomorphine 5 mg and placebo were administered on alternate days to 162 men who were on long-term therapy (> or =4 weeks) with angiotensin-converting enzyme inhibitors, beta blockers, diuretics, calcium channel blockers, alpha(1) blockers, or short- or long-acting nitrates. Blood pressure and heart rate were measured before and after dosing; cardiac rhythm was recorded by 4-hour Holter monitoring. The only potentially clinically significant interactions between SL apomorphine and the antihypertensive agents or short-acting nitrates were greater orthostatic decreases in systolic blood pressure in the alpha-blocker and calcium channel blocker groups (-10 and -6 mm Hg vs placebo, respectively). Administration of SL apomorphine after dosing with long-acting nitrates resulted in significant decreases in blood pressure when patients were standing (mean systolic change, -5 to -9 mm Hg 30 to 60 minutes postdose, p <0.05; mean diastolic change, -3 to -4 mm Hg 50 to 60 minutes postdose, p <0.05). The most common adverse events with SL apomorphine were dizziness, nausea, and headache. Syncope occurred in 1 patient in the beta-blocker group; symptomatic hypotension occurred in 2 patients each in the short- and long-acting nitrate groups. Thus, in patients receiving common antihypertensive agents and short-acting nitrates, as well as in most patients receiving long-acting nitrates, SL apomorphine at higher than recommended doses produced no clinically significant changes in heart rate or blood pressure greater than changes seen with SL apomorphine alone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Sublingual_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Apomorphine_MeSH S_administration_&_dosage_MeSH Apomorphine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Apomorphine_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cross-Over_Studies_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Dopamine_Agonists_MeSH S_administration_&_dosage_MeSH Dopamine_Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Dopamine_Agonists_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Impotence_MeSH S_drug_therapy_MeSH Impotence_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_administration_&_dosage_MeSH Nitrates_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11589866
----K 4
----T Travoprost compared with latanoprost and timolol in patients with open-angle glaucoma or ocular hypertension.
----A PURPOSE: This study evaluated the safety and intraocular pressure-lowering efficacy of two concentrations of travoprost (0.0015% and 0.004%) compared with latanoprost 0.005% and timolol 0.5% in patients with open-angle glaucoma or ocular hypertension. METHODS: Eight hundred one patients with open-angle glaucoma or ocular hypertension were randomly assigned to travoprost 0.0015%, travoprost 0.004%, latanoprost 0.005%, or timolol 0.5%. The efficacy and safety of travoprost (0.0015% and 0.004%) daily was compared with latanoprost daily and timolol twice daily for a period of 12 months. RESULTS: Travoprost was equal or superior to latanoprost and superior to timolol with mean intraocular pressure over visits and time of day ranging from 17.9 to 19.1 mm Hg (travoprost 0.0015%), 17.7 to 19.1 mm Hg (travoprost 0.004%), 18.5 to 19.2 mm Hg (latanoprost), and 19.4 to 20.3 mm Hg (timolol). For all visits pooled, the mean intraocular pressure at 4 PM for travoprost was 0.7 mm Hg (0.0015%, P =.0502) and 0.8 mm Hg (0.004%, P =.0191) lower than for latanoprost. Travoprost 0.004% was more effective than latanoprost and timolol in reducing intraocular pressure in black patients by up to 2.4 mm Hg (versus latanoprost) and 4.6 mm Hg (versus timolol). Based on a criterion of 30% or greater intraocular pressure reduction from diurnal baseline or intraocular pressure 17 mm Hg or less, travoprost 0.0015% and 0.004% had an overall response to treatment of 49.3% and 54.7%, respectively, compared with 49.6% for latanoprost and 39.0% for timolol. Iris pigmentation change was observed in 10 of 201 of patients (5.0%) receiving travoprost 0.0015%, six of 196 of patients (3.1%) receiving travoprost 0.004%, 10 of 194 of patients (5.2%) receiving latanoprost, and none of the patients receiving timolol (0 of 196). The average ocular hyperemia score was less than 1 on a scale of 0 to 3, indicating that on average patients experienced between none/trace and mild for all treatment groups. There were no serious, unexpected, related adverse events reported for any therapy. CONCLUSIONS: Travoprost (0.0015% and 0.004%), a highly selective, potent prostaglandin F (FP) receptor agonist, is equal or superior to latanoprost and superior to timolol in lowering intraocular pressure in patients with open-angle glaucoma or ocular hypertension. In addition, travoprost 0.004% is significantly better than either latanoprost or timolol in lowering intraocular pressure in black patients. Travoprost is safe and generally well tolerated in the studied patient population.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cloprostenol_MeSH S_administration_&_dosage_MeSH Cloprostenol_administration_&_dosage_MeSH S_adverse_effects_MeSH Cloprostenol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Cloprostenol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Cloprostenol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Eye_Color_MeSH S_drug_effects_MeSH Eye_Color_drug_effects_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Iris_MeSH S_drug_effects_MeSH Iris_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Ophthalmic_Solutions_MeSH M_Pigmentation_Disorders_MeSH S_chemically_induced_MeSH Pigmentation_Disorders_chemically_induced_MeSH M_Prodrugs_MeSH S_therapeutic_use_MeSH Prodrugs_therapeutic_use_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11593094
----K E
----T Twenty-four hour ambulatory blood pressure in the Hypertension Optimal Treatment (HOT) study.
----A BACKGROUND AND AIMS: The Hypertension Optimal Treatment (HOT) study showed that when antihypertensive treatment reduces diastolic blood pressure well below 90 mmHg, there can be a further reduction of cardiovascular events, particularly myocardial infarction, with no evidence of a J-shaped curve at lower pressures. Office measurement, however, gives no information about blood pressure outside the office. This paper describes a HOT substudy in which patients underwent both office measurement and 24 h ambulatory blood pressure monitoring. METHODS: The mean age of the substudy population was 62 +/- 7 years. Substudy patients were treated for a median period of 2 years. All received the dihydropyridine calcium antagonist felodipine, while some also received an ACE-inhibitor, a beta-blocker or a diuretic. Average 24 h, day and night ambulatory blood pressure values were computed at baseline (n = 277) and during treatment (n = 347): 112 patients had been randomized to a target office diastolic blood pressure <or= 90 mmHg, 117 to <or= 85 mmHg and 118 to <or= 80 mmHg. Additional analyses included computation of: (1) trough-to-peak ratio and (2) the smoothness index (the ratio between the average of the 24 hourly blood pressure reductions after treatment and its standard deviation). RESULTS: Taking the subgroup as a whole, baseline 24 h average blood pressures (146 +/- 18/90 +/- 10 mmHg) were significantly and markedly lower than office blood pressures (170 +/- 14/105 +/- 3 mmHg, P < 0.01). Office, 24 h, day and night blood pressures were all significantly reduced by treatment, but there was a smaller fall in ambulatory, than in office pressures. The between group differences in office blood pressure were smaller than those observed in the overall HOT sample. Between-group differences in 24 h blood pressure were even smaller. Trough-to-peak ratios and smoothness indices were lowest in the highest blood pressure target group and highest in the lowest blood pressure target group. Office and ambulatory blood pressures were similar in the groups randomized to placebo (n = 170) or acetylsalicylic acid (n = 177). CONCLUSION: In conclusion, in the HOT study, treatment reduced not only office but also ambulatory blood pressure throughout the 24 h. The reduction was less marked for ambulatory than for office blood pressure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Determination_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Office_Visits_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH 
****** 11593098
----K E
----T Angiotensin converting enzyme gene polymorphism predicts blood pressure response to angiotensin II receptor type 1 antagonist treatment in hypertensive patients.
----A OBJECTIVES: To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment; more specifically, in response to treatment with irbesartan or atenolol. DESIGN AND METHODS: Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the beta1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction. RESULTS: The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18 +/- 11 SD versus -7 +/- 10 mmHg, P = 0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P = 0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment. CONCLUSIONS: ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Forecasting_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_genetics_MeSH Peptidyl-Dipeptidase_A_genetics_MeSH M_Polymorphism_(Genetics)_MeSH S_physiology_MeSH Polymorphism_(Genetics)_physiology_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11593101
----K E
----T Treatment with irbesartan or atenolol improves endothelial function in essential hypertension.
----A OBJECTIVES: To investigate if antihypertensive treatment could improve endothelium-dependent vasodilatation in hypertensive patients, and whether the angiotensin II subtype-1 (AT1)-receptor antagonist irbesartan and the beta1-receptor antagonist atenolol would differ in this respect. SUBJECTS AND METHODS: Thirty-four patients (28 men and six women) with mild-to-moderate essential hypertension (diastolic blood pressure 90-120 mmHg) were randomized to once daily 150-300 mg irbesartan or 50-100 mg atenolol in a double-blind fashion, preceded by a placebo run-in period. Forearm blood flow (FBF) was assessed by venous occlusion plethysmography during local intra-arterial infusions of methacholine and sodium nitroprusside, to evaluate endothelium-dependent and endothelium-independent vasodilatation, respectively. Measurements of FBF were undertaken at the end of the run-in placebo period and repeated after 3 months of active antihypertensive treatment. RESULTS: Irbesartan and atenolol induced a similar decline in blood pressure (from 171/107 to 158/98 mmHg, P < 0.05), and improved endothelium-dependent vasodilatation (e.g. an increase in FBF response to 4 microg/min methacholine from 325 +/- 29% to 411 +/- 41%, P < 0.05), with no difference between the two study drugs. No significant changes in endothelium-independent vasodilatation were induced by irbesartan or by atenolol. CONCLUSIONS: The present study shows that 3 months of antihypertensive therapy with irbesartan or atenolol improves endothelium-dependent vasodilatation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 11593109
----K E
----T A random comparison of fosinopril and nifedipine GITS in patients with primary renal disease.
----A OBJECTIVE: To investigate in a random comparison the capacity of an angiotensin converting enzyme inhibitor (fosinopril), and that of a long-acting dihydropiridine (nifedipine GITS) to modify the decay in renal function in patients with primary renal disease, exhibiting a progressive increase in serum creatinine during the previous 2 years. METHODS: A randomized, open-label, multicenter study with a minimum follow-up of 3 years. A total of 241 patients were included in the study. All of them were hypertensive and had a 25% or at least 0.5 mg/dl increase in the value of serum creatinine during the 24 months prior to entering the study. Initial doses of fosinopril and nifedipine GITS were 10 and 30 mg respectively, and titration to 30 and 60 mg was performed if needed to obtain the expected blood pressure goal (< 140/90 mmHg). Furosemide, atenolol, and doxazosin were added as second, third, and fourth drugs if necessary, for blood pressure control. The primary end-point of the study was the appearance of double the serum creatinine values and/or the need to enter a dialysis programme. Secondary end-points were cardiovascular events, death, changes in 24 h proteinuria, and the evolution of serum creatinine. Data reflect the analysis performed by intention to treat. RESULTS: Mean age of the group was 54 +/- 14, and 59% were males. Primary glomerulonephritis (31%), nephrosclerosis (26%) and polycystic kidney disease (19%) were the three most frequent diagnostic findings. After 3 years of follow-up, 21% (27/127) of patients treated with fosinopril, and 36% (40/112) of those receiving nifedipine GITS presented a primary end-point, (OR 0.47, 95% confidence intervals 0.26-0.84, P = 0.01). Renal survival was significantly better when fosinopril constituted the first step therapy (P = 0.002). These results did not seem to be influenced by the type of primary renal disease. Proteinuria decreased at the end of the study by a mean of 57% in the fosinopril group and increased by 7% in the group receiving dihydropiridine. Blood pressure control did not differ among groups for diastolic values. During follow-up, however, the patients receiving ACEi showed systolic blood pressure values 4-6 mmHg lower. CONCLUSION: In patients with chronic renal failure and hypertension due to primary renal disease, fosinopril significantly differed from nifedipine GITS by its capacity to slow the progressive decay in renal function. The drugs also differed by their capacity to lower blood pressure. The better control, in particular of systolic blood pressure, in the fosinopril arm could have contributed in a relevant manner to the attainment of a better outcome when the ACEi was employed.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Female_MeSH M_Fosinopril_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Kidney_Diseases_MeSH S_complications_MeSH Kidney_Diseases_complications_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 11595959
----K 1
----T [Interaction between sildenafil and antihypertensive drugs: what is evidence-based?]
----A Hypertension is an important risk factor for erectile dysfunction (ED). Consequently, there is a high coincidence between hypertension and ED. Oral sildenafil (Viagra) is an effective treatment for ED in patients with treated or untreated hypertension. The most common adverse events of sildenafil (headache, flushing, hypotension) result from its moderate vasodilating properties. The concomitant use of sildenafil and organic nitrates is contraindicated because it may lead to a potentiation of the decreases in blood pressure and thus cause life-threatening hypotension. In contrast, the concomitant use of sildenafil and different classes of antihypertensive agents (beta-blockers, alpha-blockers, diuretics, ACE inhibitors, calcium antagonists) may lead to additive but not to potentiating blood pressure decreases. Thus, this combination is unlikely to cause clinically significant hypotension or an increased incidence of adverse events. Sildenafil is an effective and well-tolerated treatment for ED in patients taking concomitant antihypertensive medication, including those on multidrug regimens.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Impotence_MeSH S_complications_MeSH Impotence_complications_MeSH S_drug_therapy_MeSH Impotence_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_adverse_effects_MeSH Phosphodiesterase_Inhibitors_adverse_effects_MeSH S_pharmacology_MeSH Phosphodiesterase_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Phosphodiesterase_Inhibitors_therapeutic_use_MeSH M_Piperazines_MeSH S_adverse_effects_MeSH Piperazines_adverse_effects_MeSH S_pharmacology_MeSH Piperazines_pharmacology_MeSH S_therapeutic_use_MeSH Piperazines_therapeutic_use_MeSH M_Placebos_MeSH M_Posture_MeSH M_Randomized_Controlled_Trials_MeSH M_Time_Factors_MeSH 
****** 11595610
----K E
----T Clinical profile and management of heart failure: rural community hospital vs. metropolitan heart center.
----A BACKGROUND: Knowledge on clinical characteristics and prognosis of patients with heart failure originates from studies of selected populations in clinical trials or from epidemiological observations. Reports on the large numbers of patients with heart failure treated in community hospitals are sparse. OBJECTIVE: Are there differences in patient characteristics and heart failure management between a metropolitan heart center (HC) and a rural community hospital (RCH)? PATIENTS AND METHODS: Retrospective analysis of medical charts from all patients admitted for heart failure (ICD 428.x, NYHA II-IV, EF<45%) between May 1997 and April 1998 and discharged alive from a rural community hospital. A similar, but prospective registry was available at the HC. Follow-up information was obtained by request at registration authorities. RESULTS: Patient groups comprised 120 in RCH and 146 in HC. Mean age was 75+/-11 and 66+/-11 years, respectively (P<0.001); 48% (RCH) vs. 74% (HC) of patients were male (P<0.001). On admission the proportion of functional class IV was 69% (RCH) vs. 17% (HC) (P<0.001). At discharge, the rate of ACE-inhibitors was 74% (RCH) vs. 98% (HC); 11% (RCH) vs. 43% (HC) of patients received beta-blocker therapy. Ninety-six percent of patients in HC underwent and 22% in RCH had undergone invasive diagnostics. One-year mortality rate of patients discharged alive was 26% in RCH and 19% in HC (P=n.s. after adjustment for age and gender). CONCLUSION: Heart failure management according to current guidelines, using beta-blockers and ACE inhibitors, and invasive cardiac examination was significantly less performed in the rural community hospital than in the metropolitan heart center. Therefore, strategies to improve heart failure management according to guidelines are urgently needed.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiac_Care_Facilities_MeSH S_standards_MeSH Cardiac_Care_Facilities_standards_MeSH S_statistics_&_numerical_data_MeSH Cardiac_Care_Facilities_statistics_&_numerical_data_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Guideline_Adherence_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospital_Mortality_MeSH M_Hospitals__Community_MeSH S_standards_MeSH Hospitals__Community_standards_MeSH S_statistics_&_numerical_data_MeSH Hospitals__Community_statistics_&_numerical_data_MeSH M_Hospitals__Rural_MeSH S_standards_MeSH Hospitals__Rural_standards_MeSH S_statistics_&_numerical_data_MeSH Hospitals__Rural_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Outcome_and_Process_Assessment_(Health_Care)_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11595611
----K E
----T Improved outcomes from a comprehensive management system for heart failure.
----A AIMS: Congestive heart failure (CHF) is associated with a high readmission rate after diagnosis. We assessed the ability of a comprehensive management program (CMP) for CHF to reduce readmissions with secondary endpoints of improving quality of life, exercise capacity and targeted drug doses. METHODS AND RESULTS: Patients (pts) with: New York Heart Association Class (NYHA) III or IV CHF; left ventricular ejection fraction <40%; and stable outpatient therapy were assigned to a CMP of cardiology assessment intensive education and referral to a tailored exercise program. Forty-two pts (35 M, 7 F, mean age 54 years, S.D. 12 years) were enrolled. Two pts were transplanted, two died during follow-up and two were lost to follow-up. Hospital admissions were reduced by 87.2%, (mean 1.05, S.D. 0.98, admissions per pt to mean 0.08, S.D. 0.28, admissions per pt at 6-month follow-up; P<0.0001). ACE-inhibitor dose increased by 42% (P<0.0008) and beta-blocker dose increased by 61% (P<0.0001). NYHA Class, 6-min walk and quality of life scores all improved significantly (P<0.0001). CONCLUSION: A CMP improves QOL and exercise capacity as well as substantially reducing hospital admissions in CHF pts. This study validates the benefit of intensive outpatient care of CHF.
----P Journal_Article 
----M M_Aged_MeSH M_Chronic_Disease_MeSH P_Disease_Management_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_rehabilitation_MeSH Heart_Failure__Congestive_rehabilitation_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Outcome_Assessment_(Health_Care)_MeSH S_methods_MeSH Outcome_Assessment_(Health_Care)_methods_MeSH S_organization_&_administration_MeSH Outcome_Assessment_(Health_Care)_organization_&_administration_MeSH M_Patient_Readmission_MeSH S_statistics_&_numerical_data_MeSH Patient_Readmission_statistics_&_numerical_data_MeSH M_Program_Evaluation_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11601952
----K E
----T Quality indicators for the management of heart failure in vulnerable elders.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_diagnosis_MeSH Cardiac_Output__Low_diagnosis_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH M_Digoxin_MeSH S_adverse_effects_MeSH Digoxin_adverse_effects_MeSH S_metabolism_MeSH Digoxin_metabolism_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH P_Frail_Elderly_MeSH M_Health_Services_for_the_Aged_MeSH S_standards_MeSH Health_Services_for_the_Aged_standards_MeSH M_Human_MeSH M_Medical_History_Taking_MeSH M_Monitoring__Physiologic_MeSH M_Outcome_and_Process_Assessment_(Health_Care)_MeSH S_standards_MeSH Outcome_and_Process_Assessment_(Health_Care)_standards_MeSH M_Patient_Education_MeSH M_Physical_Examination_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11602495
----K I
----T Treatment of isolated systolic hypertension is most effective in older patients with high-risk profile.
----A BACKGROUND: Although present guidelines suggest that treatment of hypertension is more effective in patients with multiple risk factors and higher risk of cardiovascular events, this hypothesis was never verified in older patients with systolic hypertension. METHODS AND RESULTS: Using data from the Systolic Hypertension in the Elderly Program, we calculated the global cardiovascular risk score according to the American Heart Association Multiple Risk Factor Assessment Equation in 4,189 participants free of cardiovascular disease (CVD) and in 264 participants with CVD at baseline. In the placebo group, rates of cardiovascular events over 4.5 years were progressively higher according to higher quartiles of CVD risk. The protection conferred by treatment was similar across quartiles of risk. However, the numbers needed to treat (NNTs) to prevent one cardiovascular event were progressively smaller according to higher cardiovascular risk quartiles. In participants with baseline CVD, the NNTs to prevent one cardiovascular event were similar to those estimated for CVD-free participants in the highest-risk quartile. CONCLUSIONS: Treatment of systolic hypertension is most effective in older patients who, because of additional risk factors or prevalent CVD, are at higher risk of developing a cardiovascular event. These patients are prime candidates for antihypertensive treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Reserpine_MeSH S_administration_&_dosage_MeSH Reserpine_administration_&_dosage_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Sex_Distribution_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 11603173
----K 1
----T [The comparison of clinical effectiveness of perindopril and acebutolol in the primary hypertension treatment]
----A Hypertension is one of the most important risk factors for ischaemic heart disease and stroke. The aim of our study was to assess the antihypertensive effect of angiotensine converting enzyme inhibitor (perindopril) versus beta blocker (acebutolol) in hypertensive patients. It was a double blind, placebo controlled study performed in the group of 31 patients (16 males, 15 females; mean age 46.6 +/- 8.7 years) with newly diagnosed (previously not treated) mild to moderate hypertension. Each patient in the wash-out period (two weeks) was given placebo and then was randomized to active treatment: perindopril (4 mg/day) or acebutolol (400 mg/day) for 3 weeks, following these drugs were cross matched (after one week wash out period). Blood pressure (BP) with mercury sphygmomanometer was measured three times: after 2 weeks of placebo treatment, after 3 weeks of perindopril and 3 weeks of acebutolol treatment. Both perindopril and acebutolol proved to be effective in monotherapy of hypertension. After 3 weeks of the treatment we observed BP systolic and diastolic normalization, but more patients had systolic BP normalization after perindopril treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_administration_&_dosage_MeSH Acebutolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH 
****** 11606149
----K E
----T Acute precipitants of congestive heart failure exacerbations.
----A BACKGROUND: Few studies have prospectively and systematically explored the factors that acutely precipitate exacerbation of congestive heart failure (CHF) in patients with left ventricular dysfunction. Knowledge of such factors is important in designing measures to prevent deterioration of clinical status. The objective of this study was to prospectively describe the precipitants associated with exacerbation of CHF status in patients enrolled in the Randomized Evaluation of Strategies for Left Ventricular Dysfunction Pilot Study. METHODS: We conducted a 2-stage, multicenter, randomized trial in 768 patients with CHF who had an ejection fraction of less than 40%. Patients were randomly assigned to receive enalapril maleate, candesartan cilexetil, or both for 17 weeks, followed by randomization to receive metoprolol succinate or placebo for 26 weeks. Investigators systematically documented information on clinical presentation, management, and factors associated with the exacerbation for any episode of acute CHF during follow-up. RESULTS: A total of 323 episodes of worsening of CHF occurred in 180 patients during 43 weeks of follow-up; 143 patients required hospitalization, and 5 died. Factors implicated in worsening of CHF status included noncompliance with salt restriction (22%); other noncardiac causes (20%), notably pulmonary infectious processes; study medications (15%); use of antiarrhythmic agents in the past 48 hours (15%); arrhythmias (13%); calcium channel blockers (13%); and inappropriate reductions in CHF therapy (10%). CONCLUSIONS: A variety of factors, many of which are avoidable, are associated with exacerbation of CHF. Attention to these factors and patient education are important in the prevention of CHF deterioration.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Precipitating_Factors_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11607795
----K E
----T Resistance to antihypertensive medication as predictor of renal artery stenosis: comparison of two drug regimens.
----A BACKGROUND: Renal artery stenosis is among the most common curable causes of hypertension. The definitive diagnosis is made by renal angiography, an invasive and costly procedure. The prevalence of renal artery stenosis is less than 1% in non-selected hypertensive patients but is higher when hypertension is resistant to drugs. OBJECTIVE: To study the usefulness of standardised two-drug regimens for identifying drug-resistant hypertension as a predictor of renal artery stenosis. DESIGN AND SETTING: Prospective cohort study carried out in 26 hospitals in The Netherlands. PATIENTS: Patients had been referred for analysis of possible secondary hypertension or because hypertension was difficult to treat. Patients < or =40 years of age were assigned to either amlodipine 10 mg or enalapril 20 mg, and patients >40 years to either amlodipine 10 mg combined with atenolol 50 mg or to enalapril 20 mg combined with hydrochlorothiazide 25 mg. Renal angiography was performed: (1) if hypertension was drug-resistant, ie if diastolic pressure remained > or =95 mm Hg at three visits 1-3 weeks apart or an extra drug was required, and/or (2) if serum creatinine rose by > or =20 micromol/L (> or =0.23 mg/dL) during ACE inhibitor treatment. RESULTS: Of the 1106 patients with complete follow-up, 1022 had been assigned to either the amlodipine- or enalapril-based regimens, 772 by randomisation. Drug-resistant hypertension, as defined above, was identified in 41% of the patients, and 20% of these had renal artery stenosis. Renal function impairment was observed in 8% of the patients on ACE inhibitor, and this was associated with a 46% prevalence of renal artery stenosis. In the randomised patients, the prevalence of renal artery stenosis did not differ between the amlodipine- and enalapril-based regimens. CONCLUSIONS: In the diagnostic work-up for renovascular hypertension the use of standardised medication regimens of maximally two drugs, to identify patients with drug-resistant hypertension, is a rational first step to increase the a priori chance of renal artery stenosis. Amlodipine- or enalapril-based regimens are equally effective for this purpose.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_diagnostic_use_MeSH Amlodipine_diagnostic_use_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_diagnostic_use_MeSH Antihypertensive_Agents_diagnostic_use_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_diagnostic_use_MeSH Atenolol_diagnostic_use_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Drug_Resistance_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_diagnostic_use_MeSH Enalapril_diagnostic_use_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_diagnostic_use_MeSH Hydrochlorothiazide_diagnostic_use_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Renal_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Renal_Artery_MeSH S_radiography_MeSH Renal_Artery_radiography_MeSH M_Renal_Artery_Obstruction_MeSH S_complications_MeSH Renal_Artery_Obstruction_complications_MeSH S_radiography_MeSH Renal_Artery_Obstruction_radiography_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11641310
----K E
----T Improvement in blood pressure, arterial stiffness and wave reflections with a very-low-dose perindopril/indapamide combination in hypertensive patient: a comparison with atenolol.
----A International guidelines recommend that antihypertensive drug therapy should normalize not only diastolic (DBP) but also systolic blood pressure (SBP). Therapeutic trials based on cardiovascular mortality have recently shown that SBP reduction requires normalization of both large artery stiffness and wave reflections. The aim of the present study was to compare the antihypertensive effects of the very-low-dose combination indapamide (0.625 mg) and perindopril (2 mg) (Per/Ind) with the beta-blocking agent atenolol (50 mg) to determine whether Per/Ind decreases SBP and pulse pressure (PP) more than does atenolol and, if so, whether this decrease is predominantly due to reduction of aortic pulse wave velocity (PWV) (automatic measurements) and reduction of wave reflections (pulse wave analysis, applanation tonometry). In a double-blind randomized study, 471 patients with essential hypertension were followed for 12 months. For the same DBP reduction, Per/Ind decreased brachial SBP (-6.02 mm Hg; 95% confidence interval, -8.90 to -3.14) and PP (-5.57; 95% confidence interval, -7.70 to -3.44) significantly more than did atenolol. This difference was significantly more pronounced for the carotid artery than for the brachial artery. Whereas the 2 antihypertensive agents decreased PWV to a similar degree, only Per/Ind significantly attenuated carotid wave reflections, resulting in a selective decrease in SBP and PP. The very-low-dose combination Per/Ind normalizes SBP, PP, and arterial function to a significantly larger extent than does atenolol, a hemodynamic profile that is known to improve survival in hypertensive populations with high cardiovascular risk.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aorta_MeSH S_drug_effects_MeSH Aorta_drug_effects_MeSH S_physiopathology_MeSH Aorta_physiopathology_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Asthenia_MeSH S_chemically_induced_MeSH Asthenia_chemically_induced_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Brachial_Artery_MeSH S_drug_effects_MeSH Brachial_Artery_drug_effects_MeSH S_physiopathology_MeSH Brachial_Artery_physiopathology_MeSH M_Carotid_Arteries_MeSH S_drug_effects_MeSH Carotid_Arteries_drug_effects_MeSH S_physiopathology_MeSH Carotid_Arteries_physiopathology_MeSH M_Comparative_Study_MeSH M_Cough_MeSH S_chemically_induced_MeSH Cough_chemically_induced_MeSH M_Dizziness_MeSH S_chemically_induced_MeSH Dizziness_chemically_induced_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Follow-Up_Studies_MeSH M_Headache_MeSH S_chemically_induced_MeSH Headache_chemically_induced_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indapamide_MeSH S_adverse_effects_MeSH Indapamide_adverse_effects_MeSH S_therapeutic_use_MeSH Indapamide_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_adverse_effects_MeSH Perindopril_adverse_effects_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Pulse_MeSH M_Treatment_Outcome_MeSH 
****** 11641316
----K E
----T Pulse pressure changes with six classes of antihypertensive agents in a randomized, controlled trial.
----A Pulse pressure has been more strongly associated with cardiovascular outcomes, especially myocardial infarction and heart failure, than has systolic, diastolic, or mean arterial pressure in a variety of populations. Little is known, however, of the comparative effects of various classes of antihypertensive agents on pulse pressure. In retrospective analyses of the Veterans Affairs Single-Drug Therapy for Hypertension Study, we compared changes in pulse pressure with 6 classes of antihypertensive agents: 1292 men with diastolic blood pressure of 95 to 109 mm Hg on placebo were randomized to receive hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem, prazosin, or placebo. Drug doses were titrated to achieve a goal diastolic blood pressure of <90 mm Hg during a 4- to 8-week medication titration phase. Pulse pressure change (placebo subtracted) was assessed from baseline to the end of the 3-month titration and 1-year maintenance. Mean baseline systolic, diastolic, and pulse pressures were 152, 99, and 53 mm Hg, respectively. Reductions in pulse pressure during titration were greater (P<0.001) with clonidine (6.7 mm Hg) and hydrochlorothiazide (6.2 mm Hg) than with captopril (2.5 mm Hg), diltiazem (1.6 mm Hg), and atenolol (1.4 mm Hg); reduction with prazosin (3.9 mm Hg) was similar to all but clonidine. After 1 year, pulse pressure was reduced significantly more (P<0.001) with hydrochlorothiazide (8.6 mm Hg) than with captopril and atenolol (4.1 mm Hg with both); clonidine (6.3 mm Hg), diltiazem (5.5 mm Hg), and prazosin (5.0 mm Hg) were intermediate. These data show that classes of antihypertensive agents differ in their ability to reduce pulse pressure. Whether these differences affect rates of cardiovascular events remains to be determined.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Clonidine_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prazosin_MeSH S_therapeutic_use_MeSH Prazosin_therapeutic_use_MeSH M_Pressure_MeSH P_Pulse_MeSH M_Randomized_Controlled_Trials_MeSH M_Systole_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11675840
----K E
----T Physicians' knowledge, attitudes, and practice of pharmacologic treatment of hypertension.
----A OBJECTIVE: To explore how well physicians who treat hypertension know the indications and contraindications for particular antihypertensive therapies, and how closely their opinions and practice of hypertension treatment agree with national guidelines. METHODS: We surveyed by mail a stratified random sample of 10,000 US cardiologists, internists, and general/family practitioners. This survey explored their knowledge, attitudes, and practices with respect to the treatment of hypertension. Responses were compared with national guidelines and product labeling at the time of the survey. Results were stratified by physician specialty. RESULTS: A total of 1,023 physicians, or 10.2% of the sample, responded to the survey. Only 37.3% answered all four knowledge questions correctly, including 25.7% of general/family practitioners, 38.3% of internists, and 49.5% of cardiologists (p < 0.001). In their attitudes with respect to evaluating high blood pressure and establishing treatment goals, most respondents agreed with established guidelines. However, when asked how they would treat uncomplicated, mild hypertension, only 23% limited their selection to diuretics and beta-blockers in accordance with the guidelines. Cardiologists in particular were more likely than internists or general/family practitioners to choose other drug classes, such as angiotensin-converting enzyme Inhibitors or calcium-channel blockers. CONCLUSIONS: The results of our survey suggest that national efforts to educate physicians about the increasingly complex armamentarium for hypertension, and to persuade them to base their prescribing on the results of randomized, controlled trials of primary prevention, must be continued.
----P Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Attitude_of_Health_Personnel_MeSH M_Female_MeSH P_Health_Knowledge__Attitudes__Practice_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Physician's_Practice_Patterns_MeSH M_Practice_Guidelines_MeSH M_Questionnaires_MeSH M_Specialties__Medical_MeSH M_Support__Non-U_S__Gov't_MeSH M_United_States_MeSH 
****** 11674903
----K E
----T What is the best treatment for slowing the progression to end-stage renal disease (ESRD) in African Americans with hypertensive nephropathy?
----A 
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_complications_MeSH Hypertension__Renal_complications_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_mortality_MeSH Kidney_Failure__Chronic_mortality_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH 
****** 11677866
----K 1
----T [Bisprolol in heart failure: efficacy and costs in a French setting according to CIBIS II]
----A After a significant mortality benefit with bisoprolol in heart failure was demonstrated in CIBIS-II, an economic evaluation has been performed in cost-effectiveness terms. Average direct costs per patient were based on clinical data from 231 French patients, and measured in the perspective of the French National Health Insurance, effectiveness being expressed in terms of life days gained per patient. The extra cost of bisoprolol treatment and follow-up (averaging FF 1300 per 1.3 years) is outweighed by the reduction in hospitalization costs (representing a saving of FF 10,500 per patient) and other medication costs. Finally, bisoprolol therapy induces benefits in terms of both cost and survival: on average FF 9500 and 11 life days per patient. Sensitivity analyses confirm these results.
----P Clinical_Trial Clinical_Trial__Phase_III Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cost_Control_MeSH M_Cost-Benefit_Analysis_MeSH M_Double-Blind_Method_MeSH M_Drug_Costs_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_France_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_economics_MeSH Hospitalization_economics_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Life_Expectancy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 11679383
----K E
----T Randomised trials of secondary prevention programmes in coronary heart disease: systematic review.
----A OBJECTIVE: To determine whether multidisciplinary disease management programmes for patients with coronary heart disease improve processes of care and reduce morbidity and mortality. DATA SOURCES: Randomised clinical trials of disease management programmes in patients with coronary heart disease were identified by searching Medline 1966-2000, Embase 1980-99, CINAHL 1982-99, SIGLE 1980-99, the Cochrane controlled trial register, the Cochrane effective practice and organisation of care study register, and bibliographies of published studies. DATA EXTRACTION: Studies were selected and data were extracted independently by two investigators, and summary risk ratios were calculated by using both the random effects model and the fixed effects model. DATA SYNTHESIS: A total of 12 trials (9803 patients with coronary heart disease) were identified. Disease management programmes had positive impacts on processes of care. Patients randomised to these programmes were more likely to be prescribed efficacious drugs (risk ratio 2.14 (95% confidence interval 1.92 to 2.38) for lipid lowering drugs, 1.19 (1.07 to 1.32) for beta blockers, and 1.07 (1.03 to 1.11) for antiplatelet agents). Five out of seven trials evaluating risk factor profiles showed significantly greater improvements with these programmes in comparison with usual care (with effect sizes in the moderate range). Summary risk ratios were 0.91 (0.79 to 1.04) for all cause mortality, 0.94 (0.80 to 1.10) for recurrent myocardial infarction, and 0.84 (0.76 to 0.94) for admission to hospital. Five of the eight trials evaluating quality of life or functional status reported better outcomes in the intervention arms. Only three of these trials reported the costs of the intervention-the interventions were cost saving in two cases. CONCLUSIONS: Disease management programmes improve processes of care, reduce admissions to hospital, and enhance quality of life or functional status in patients with coronary heart disease. The programmes' impact on survival and recurrent infarctions, their cost effectiveness, and the optimal mix of components remain uncertain.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Cost-Benefit_Analysis_MeSH M_Disease_Management_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11685175
----K E
----T Treatment of cardiac risk factors in diabetic patients: How well do we follow the guidelines?
----A BACKGROUND: Diabetic patients are at increased risk for both macrovascular and microvascular disease compared with nondiabetic patients. METHODS: We conducted a prospective observational study to assess the control of multiple predetermined cardiovascular risk factors in 235 treated diabetic patients undergoing elective cardiac catheterization at our institution between December 20, 1997, and February 15, 2000. The following parameters were used to define optimal treatment in these patients: hemoglobin (Hgb) A1c <7%, low-density lipoprotein cholesterol (LDL-c) <100 mg/dL, high-density lipoprotein cholesterol (HDL-c) >/=45 mg/dL for men and >/=55 mg/dL for women, triglyceride (TG) level <200 mg/dL, blood pressure (BP) <130/85 mm Hg, body mass index (BMI) <25, daily aspirin therapy, and current nonsmoking status. The use of b-blockers and angiotensin-converting enzyme inhibitors was also evaluated. RESULTS: The average patient age was 64 +/- 11 years; 155 (65%) were male. One hundred ninety-one (81%) patients had documented coronary artery disease at cardiac catheterization. The mean Hgb A1c level for all diabetic patients was 8.2% +/- 1.6%. Overall, 49 (21%) had an Hgb A1c level <7%. The fasting cholesterol panel for all patients revealed a mean LDL-c level of 103 +/- 41 mg/dL, a mean HDL level of 39 +/- 11 mg/dL, and a mean TG level of 164 +/- 128 mg/dL. One hundred sixteen (52%) patients had an LDL-c <100 mg/dL. Only 32 of 147 (22%) male patients and 14 of 80 (18%) female patients achieved an HDL-c >/=45 mg/dL or >/=55 mg/dL, respectively. One hundred seventy-seven of 232 (76%) patients had a TG level <200 mg/dL. Only 23 of 233 (10%) diabetics were controlled to a BP of <130/85 mm Hg, and 25 (11%) achieved a BMI <25. Only one patient (0.4%) had optimal control of all modifiable risk factors. CONCLUSIONS: These data demonstrate the poor control of numerous cardiovascular risk factors in treated diabetics undergoing elective cardiac catheterization.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Body_Mass_Index_MeSH M_Cardiovascular_Diseases_MeSH S_blood_MeSH Cardiovascular_Diseases_blood_MeSH S_diagnosis_MeSH Cardiovascular_Diseases_diagnosis_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_blood_MeSH Diabetes_Mellitus_blood_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_analogs_&_derivatives_MeSH Hemoglobin_A__Glycosylated_analogs_&_derivatives_MeSH S_analysis_MeSH Hemoglobin_A__Glycosylated_analysis_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_prevention_&_control_MeSH Hyperlipidemia_prevention_&_control_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Practice_Guidelines_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_epidemiology_MeSH Smoking_epidemiology_MeSH S_prevention_&_control_MeSH Smoking_prevention_&_control_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 11684917
----K E
----T Treatment of acute myocardial infarction.
----A Persons 75 years of age or older constitute 6.1% of the US population but account for 36% of acute myocardial infarctions (MI) and 60% of deaths. Unfortunately, despite the fact that patients over age 75 represent a large subgroup with an exceptionally high case-fatality rate, most randomized clinical trials have enrolled few patients in this group. As a result, therapeutic recommendations for managing acute MI in the very elderly are often extrapolated from studies conducted in younger patients. This article reviews current evidence-based guidelines for early treatment of acute MI in the elderly. As in younger patients, aspirin, beta blockers, and angiotensin-converting enzyme inhibitors should be considered standard therapy in appropriately selected elderly patients. Although the benefits of reperfusion therapy (i.e., thrombolysis and primary angioplasty) are less well established, advanced age per se should not be considered a contraindication to the use of these interventions. Given the relative paucity of data in the very elderly, additional studies are needed to define optimal pharmacologic and nonpharmacologic treatment of acute MI in this rapidly growing, high-risk population.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11684627
----K E
----T Bradykinin contributes to the vasodilator effects of chronic angiotensin-converting enzyme inhibition in patients with heart failure.
----A BACKGROUND: Bradykinin, an endogenous vasodilator peptide, is metabolized by ACE. The aims of the present study were to determine the doses of B9340, a bradykinin receptor antagonist, that inhibit vasodilatation to exogenous bradykinin and to assess the contribution of bradykinin to the maintenance of basal vascular tone in patients with heart failure receiving chronic ACE inhibitor therapy. METHODS AND RESULTS: Forearm blood flow was measured using bilateral venous occlusion plethysmography. On three occasions in a double-blind randomized manner, 8 healthy volunteers received intrabrachial infusions of placebo or B9340 (at 4.5 and 13.5 nmol/min). On each occasion, placebo or B9340 was coinfused with bradykinin (30 to 3000 pmol/min) and substance P (4 to 16 pmol/min). B9340 caused no change in basal FBF but produced dose-dependent inhibition of the vasodilatation to bradykinin (P<0.001) but not substance P. The effects of bradykinin antagonism were studied in 17 patients with NYHA grade II through IV heart failure maintained on chronic ACE inhibitor therapy. Incremental doses of B9340, but not HOE-140, produced a dose-dependent vasoconstriction (P=0.01). After withdrawal of ACE inhibitor therapy, B9340 produced no significant change in forearm blood flow. After reinstitution of therapy, B9340 again resulted in vasoconstriction (P<0.03). CONCLUSIONS: B9340 is a potent and selective inhibitor of bradykinin-induced vasodilatation. Bradykinin does not contribute to the maintenance of basal peripheral arteriolar tone in healthy humans or patients with heart failure but contributes to the vasodilatation associated with chronic ACE inhibitor therapy in patients with heart failure via the B(1) receptor.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Bradykinin_MeSH S_administration_&_dosage_MeSH Bradykinin_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Bradykinin_analogs_&_derivatives_MeSH S_antagonists_&_inhibitors_MeSH Bradykinin_antagonists_&_inhibitors_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Synergism_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Plethysmography_MeSH M_Receptors__Bradykinin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Bradykinin_antagonists_&_inhibitors_MeSH M_Reference_Values_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Substance_P_MeSH S_administration_&_dosage_MeSH Substance_P_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 11684630
----K E
----T Nonselective versus selective beta-adrenergic receptor blockade in congestive heart failure: differential effects on sympathetic activity.
----A BACKGROUND: Activation of the sympathetic nervous system has important prognostic implications in chronic heart failure. Nonselective versus selective beta-adrenergic receptor antagonists may have differential effects on norepinephrine release from nerve terminals mediated by prejunctional beta(2)-adrenergic receptors. METHODS AND RESULTS: Thirty-six patients with chronic heart failure were randomized to the nonselective beta-blocker carvedilol or the selective beta-blocker metoprolol (double-blind). Measurements of hemodynamics and cardiac and systemic norepinephrine spillover as well as microneurographic recordings of muscle sympathetic nerve traffic were made before and after 4 months of therapy. In the carvedilol group (n=17), there were significant reductions in both total body (-1.7+/-0.5 nmol/min, P<0.01) and cardiac norepinephrine spillover (-87+/-29 pmol/min, P<0.01). By contrast, in the metoprolol group (n=14), there were no significant changes in total body or cardiac norepinephrine spillover. Responses in the carvedilol group were significantly different from those observed in the metoprolol group (P<0.05). Both agents caused a reduction in heart rate and increases in pulse pressure, although mean arterial pressure did not change. Importantly, microneurographic measures of sympathetic nerve traffic to skeletal muscle did not change in either group. CONCLUSIONS: Therapy with carvedilol caused significant decreases in systemic and cardiac norepinephrine spillover, an indirect measure of norepinephrine release. Such changes were not observed in patients treated with metoprolol. There was no effect of either agent on sympathetic efferent neuronal discharge to skeletal muscle. These findings suggest that carvedilol, a nonselective beta-blocker, caused its sympathoinhibitory effect by blocking peripheral, prejunctional beta-adrenergic receptors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Muscle__Skeletal_MeSH S_innervation_MeSH Muscle__Skeletal_innervation_MeSH M_Norepinephrine_MeSH S_metabolism_MeSH Norepinephrine_metabolism_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH M_Substrate_Specificity_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH 
****** 11684376
----K E
----T Effects of hormonal replacement therapy in postmenopausal hypertensive patients.
----A OBJECTIVE: To evaluate the effect of hormonal replacement therapy (HRT) on blood pressure (BP) in postmenopausal hypertensive women. METHODS: Sixty women affected by hypertension were enrolled and randomized in two groups of treatment: transdermal continuous HRT in a sequential regimen (group A) and placebo (group P). At baseline, after 3 and 6 months of treatment, the BP with standard sphygmomanometer and with 24-h ambulatory recording method was evaluated in two periods (from day 10 through day 16 of the cycle and from day 20 through day 27 of the cycle). At the same time, we also evaluated total cholesterol, LDL-c, HDL-c, triglycerides, and fibrinogen levels. RESULTS: After 3 and 6 months of treatment, no significant variations of systolic and diastolic BP measured with standard sphygmomanometer were detected in both groups. On the contrary, in group A in comparison with basal values and group P, and without difference between the two phases of treatment, the 24-h recording showed a significant (P<0.05) decrease in BP. No significant variations were detected in group P versus baseline. In particular, we observed in group A at 3 months of treatment a significant (P<0.05) decrease only in daytime BP in comparison with basal values and group P, without difference between the two phases of treatment. Indeed, the decrease in daytime BP was significant (P<0.05) for both systolic and diastolic BP. At 3 and 6 months a significant (P<0.05) decrease in total cholesterol, LDL-c and fibrinogen levels was detected in group A versus baseline and group P. HDL-c and triglyceride concentrations showed no significant variations. CONCLUSIONS: The transdermal HRT induces a significant reduction of BP values and a favorable metabolic action in postmenopausal hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Circadian_Rhythm_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Estradiol_MeSH S_pharmacology_MeSH Estradiol_pharmacology_MeSH P_Estrogen_Replacement_Therapy_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Medroxyprogesterone_17-Acetate_MeSH S_pharmacology_MeSH Medroxyprogesterone_17-Acetate_pharmacology_MeSH M_Middle_Aged_MeSH M_Postmenopause_MeSH S_drug_effects_MeSH Postmenopause_drug_effects_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 11688609
----K I
----T Beta-blockers: a new therapy in congestive heart failure.
----A BACKGROUND: Until recently, use of beta-blockers was contraindicated in treatment of patients with congestive heart failure. However, empirical evidence suggests that adding beta-blockers to the standard therapy can slow the progression of heart failure and reduce mortality, including sudden cardiac death. PURPOSE: To analyze the results of major, prospective, randomized controlled trials on the effects of beta-blockers in congestive heart failure and to provide recommendations for clinical practice and patients' education. METHODS: MEDLINE (1989-2001) and biomedical databases (1995-2001) were searched for literature on the use of beta-blockers in patients with congestive heart failure. Information on major randomized controlled trials of at least 6 months' duration with mortality as a major end point were reviewed. RESULTS: Both selective and nonselective beta-blockers significantly reduce mortality due to all causes; decrease need for hospitalization due to cardiovascular causes; and improve patients' New York Heart Association functional classification, hemodynamic status, left ventricular ejection fraction, and signs and symptoms of congestive heartfailure. However, clinical use of beta-blockers remains limited. CONCLUSION: Strong empirical evidence supports adding beta-blockers to the standard therapy for congestive heart failure. Future efforts should be directed toward establishing the safety and efficacy of beta-blockers in patients with severe heartfailure.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Controlled_Clinical_Trials_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Patient_Education_MeSH M_Practice_Guidelines_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH 
****** 11688766
----K E
----T Efficacy, tolerability and influence on "quality of life" of nifedipine GITS versus amlodipine in elderly patients with mild-moderate hypertension.
----A OBJECTIVE: The main purpose of this study was to compare efficacy, tolerability and influence on quality of life (QOL) of nifedipine gastrointestinal therapeutic system (NI) 30-60 mg once a day vs amlodipine (AM) 5-10 mg once a day in elderly patients with mild-moderate hypertension. DESIGN: This was a randomized, double-blind, parallel-group, multicenter study. After a 2-week single-blind placebo run-in, patients were randomized to either NI 30 mg or AM 5 mg. Responders continued on the same dosage for 16 additional weeks, while non-responders were titrated to 60 mg NI or 10 mg AM. METHODS: Blood pressure was measured by mercury sphygmomanometer and efficacy equivalence of NI and AM tested by covariance analysis. Diastolic blood pressure (DBP) was the primary efficacy parameter, its baseline value being taken as covariate while centers effect and treatment interaction were included as fixed effects in the analysis model. The secondary efficacy variables systolic blood pressure (SBP) and scores for QOL were analyzed according to the same model. RESULTS: At the end of the study, overall mean DBPs, calculated as least-square means (LSMEANS), in the "by protocol" population were 87.5 mmHg for NI and 86.7 for AM (difference 0.8 mmHg with 90% CI -1.2 to 2.8 mmHg). In the "by intention to treat" (ITT) population LSMEANS were 87.6 mmHg for NI and 86.4 mmHg for AM (difference 1.2 mmHg with 90% CI -0.6 to 3.1 mmHg). SBP LSMEANS in the "by protocol" population were 147.7 mmHg for NI and 147.3 mmHg for AM (difference 0.3 mmHg, with 90% CI -3.7 to 4.3); corresponding values in the "by ITT" population were 148.0 mmHg for NI and 147.2 for AM (difference 0.8 mmHg, with 90% CI -2.8 to 4.6). Mean values for QOL parameters were not significantly different. A total of 173 episodes of adverse events were documented in 54 patients (26 NI and 28 AM), dropouts were 15 (20% of group) on NI and 21 (28%) on AM. CONCLUSIONS: NI 30-60 mg was shown to be as efficacious and safe as AM 5-10 mg in elderly patients with mild-moderate hypertension. QOL improved compared to baseline with no significant difference between the two drugs, thus confirming a positive class effect for calcium antagonists.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH P_Quality_of_Life_MeSH M_Therapeutic_Equivalency_MeSH 
****** 11692790
----K 1
----T [Are we treating coronary heart disease and heart failure appropriately in the clinic and ambulatory care? Secondary prevention and drug therapy 1998]
----A We examined retrospectively 186 patients with acute coronary syndrome (ACS) and 163 patients with cardiac insufficiency (CHF) regarding secondary prevention in hospital or externally. Of the Inhospital-patients with ACS 99% had antithrombotic medicaments (AT), 73% betablockers and 73% a statin. CHF-patients had ACEH in 69%. Externally 120 patients with known coronary heart disease (CHD) received in 91% AT, 66% betablocker, 30% statins and 111 CHF-patients in 49% ACEH. Compared to other studies medical therapy ameliorated in CHD and CHF either stationary and ambulatory. The reasons for low prescription of statins may be due to short time since positive results occurred and to the expensive costs in the setting of pressure because of high cost in health system.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Ambulatory_Care_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH P_Critical_Pathways_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Patient_Admission_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH M_Switzerland_MeSH M_Treatment_Outcome_MeSH 
****** 11693075
----K 1
----T [Pharmaceutical care in people who have had acute coronary episodes (TOMCOR study)]
----A BACKGROUND: This study evaluates the effects on coronary patients of a new practice in community pharmacies called Pharmaceutical Care (PhC) as compared to the traditional pattern of pharmacy practice. It attempts to ascertain whether pharmaceutical care is feasible in addition to ascertaining differences in effectiveness for coronary patients' pharmacotherapeutic health outcomes, potentially attributable to PhC. METHODS: A randomized prospective controlled-intervention study was conducted in 83 community pharmacies in the provinces of Asturias, Barcelona, Madrid and Biscay in a one-year monitoring of the drug-use of 735 patients at the start of the study (330 intervention patients and 405 control) and 600 at the end. RESULTS: Differences were fund in favor of the intervention group in: a) the use of health care services as a morbidity indicator such as frequency of hospital emergency room visits 1.27 I (CI95%; 1.10-1.44) and 1.63 C (CI95%; 1.36-1.90) or average length-of-stay in Intensive Care Units 2.46 I (CI95%; 1.56-3.36) and 5.87 C (CI95%; 3.57-8.17), both due to coronary causes; b) health-related quality of life score (physical functioning dimension difference of 4.7 (p < 0.05); c) average patient knowledge of coronary heart disease risk factors having improved by 10% (p < 0002-0.007 depending on dimension); d) patient knowledge of the name and identification of their drugs having improved by 10% (p < 0.001) along with their subjective perception of the antiagregans drugs relative importance having improved by 12% (p < 0.009) and effects of beta-blockers having improved by 25% (p < 0.02); e) average satisfaction with pharmaceutical care service and perception of pharmacist's professional competence having improved by 2% (p < 0.000 to 0.05 depending on dimension). CONCLUSIONS: A decrease in emergency health care demand due to coronary causes, a fewer number of patient hospitalizations and a shorter length-of-stay in Coronary Intensive Care Units due to hospitalization regarding coronary patients on pharmaceutical care would suggest that patients who suffered an acute coronary heart episode made a better use of drugs and would tend to be less ill. Furthermore, coronary patients who received pharmaceutical care services showed a better knowledge of the reasons for their pharmacotherapy and therefore took better advantage of health care resources and improved their health condition.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acute_Disease_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pharmaceutical_Services_MeSH S_statistics_&_numerical_data_MeSH Pharmaceutical_Services_statistics_&_numerical_data_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11691524
----K E
----T Lack of evidence for peripheral alpha(1)- adrenoceptor blockade during long-term treatment of heart failure with carvedilol.
----A OBJECTIVES: The purpose of this study was to determine whether carvedilol's alpha(1)-adrenoceptor antagonism persists during long-term therapy of patients with congestive heart failure (CHF). BACKGROUND: Carvedilol and metoprolol differ in that carvedilol also antagonizes beta(2)- and alpha(1)-adrenoceptors. We hypothesized that in contrast to metoprolol, carvedilol would increase calf vascular conductance (CVC), blunt neurally mediated vasoconstriction and attenuate neuroeffector transfer function gain. METHODS: We randomized 36 patients with CHF (age 55 +/- 1 years, ejection fraction 19 +/- 1%, means +/- SE) to either drug. Blood pressure (BP), heart rate, muscle sympathetic nerve activity (MSNA) and CVC were assessed before and after four months of treatment. The variability of BP and MSNA was determined using fast Fourier transformation. RESULTS: Paired data were obtained in 23 (carvedilol, 13; metoprolol, 10) subjects. Both beta-blockers decreased heart rate, but neither affected mean BP or CVC (carvedilol: 0.016 +/- 0.002 to 0.018 +/- 0.003 U; metoprolol: 0.020 +/- 0.002 to 0.020 +/- 0.004 U). Isometric handgrip exercise (30% of maximum) increased heart rate, mean BP and MSNA. The calf vasoconstrictor response to handgrip exercise was not affected by carvedilol (from 16 +/- 6 resistance U to 25 +/- 10 resistance U, NS). The gain of the transfer of oscillations in MSNA into BP under resting conditions was not attenuated by carvedilol. CONCLUSIONS: Carvedilol did not increase CVC, blunt the calf vasoconstrictor response to handgrip or attenuate the gain of the neuroeffector transfer function, indicating the absence of functionally important peripheral alpha(1)-adrenoceptor antagonism during long-term treatment of CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_Fibers_MeSH S_drug_effects_MeSH Adrenergic_Fibers_drug_effects_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacokinetics_MeSH Carbazoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Monitoring_MeSH M_Evidence-Based_Medicine_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Fourier_Analysis_MeSH M_Hand_Strength_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Isometric_Contraction_MeSH S_drug_effects_MeSH Isometric_Contraction_drug_effects_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Muscle__Skeletal_MeSH S_drug_effects_MeSH Muscle__Skeletal_drug_effects_MeSH M_Neuroeffector_Junction_MeSH S_drug_effects_MeSH Neuroeffector_Junction_drug_effects_MeSH M_Prognosis_MeSH M_Propanolamines_MeSH S_pharmacokinetics_MeSH Propanolamines_pharmacokinetics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Receptors__Adrenergic__alpha-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__alpha-1_antagonists_&_inhibitors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Vasoconstriction_MeSH S_drug_effects_MeSH Vasoconstriction_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11208254
----K E
----T Overview of recent clinical trials in heart failure: what is the current standard of care?
----A Heart failure develops as a consequence of cardiac injury. As the heart begins to fail to meet the body's metabolic demands, the renin angiotensin aldosterone system (RAAS) and the sympathetic nervous system are activated. These interrelated systems act in concert to facilitate cardiac output and tissue perfusion. Though these neurohormonal systems are initially compensatory, evidence suggests that they promote deleterious cardiac remodeling and myocyte destruction. Recent studies in patients with heart failure have targeted the RAAS and sympathetic nervous system for therapeutic intervention. This article reviews major recent multicenter, randomized, double-blind, and placebo-controlled trials in heart failure that have resulted in a new standard of care for patients with this devastating disease.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiology_MeSH S_standards_MeSH Cardiology_standards_MeSH P_Clinical_Trials_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH P_Guidelines_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Severity_of_Illness_Index_MeSH M_Survival_Analysis_MeSH M_Sympathetic_Nervous_System_MeSH S_physiology_MeSH Sympathetic_Nervous_System_physiology_MeSH M_Treatment_Outcome_MeSH 
****** 11699618
----K E
----T Use of cardiovascular drugs by home-dwelling coronary patients aged 75 years and older. A population-based cross-sectional survey in Helsinki, Finland.
----A OBJECTIVE: Elderly individuals constitute an increasing proportion of coronary patients, and up-to-date information is needed of their treatments in the community. METHODS: A random sample of 75-, 80-, 85-, 90- and 95-year-old residents (n = 3,921) of Helsinki, Finland, was studied during 1998-1999. They were sent a postal questionnaire with questions about health, diseases and current drug use. RESULTS: The response rate of home-dwelling elderly persons was 78% (n = 2,511). Of men and women, 75.8% and 79.8%, respectively, had some regular medication (P< 0.05 between genders). Of home-dwelling individuals with coronary heart disease (CHD, n = 717, 28.6%), 61.0% of women and 68.3% of men used aspirin, 58.4% and 52.9% nitrates, 54.7% and 52.4% beta-blockers, 20.0% and 13.7% (angiontensin-converting enzyme) ACE inhibitors and 25.1% and 21.1% calcium-channel blockers. Only 14.3% and 19.4% were on cholesterol-lowering drugs. The difference in ACE inhibitor, diuretic and digoxin use was statistically significant (P < 0.05) between genders (women used more). CONCLUSION: Cardiovascular drug use is very common among the oldest age cohorts, but assuming that knowledge from younger individuals applies, there is a suboptimal use of several evidence-based treatments, especially lipid-lowering drugs, aspirin and beta-blockers in elderly coronary patients.
----P Case_Reports Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Cross-Sectional_Studies_MeSH M_Drug_Monitoring_MeSH M_Evidence-Based_Medicine_MeSH M_Female_MeSH M_Finland_MeSH M_Human_MeSH M_Male_MeSH M_Population_Surveillance_MeSH M_Questionnaires_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11700777
----K E
----T Cost effectiveness of bisoprolol in the treatment of chronic congestive heart failure in Sweden: analysis using data from the Cardiac Insufficiency Bisoprolol Study II trial.
----A OBJECTIVE: To investigate the cost effectiveness of adding the beta-blocker bisoprolol to standard treatment in patients with congestive heart failure (CHF). DESIGN AND SETTING: A cost-effectiveness study was based on the Cardiac Insufficiency Bisoprolol Study II (CIBIS-II), a randomised clinical trial investigating the efficacy of adding bisoprolol to standard therapy of CHF. The cost-effectiveness analysis was carried out from a societal perspective. METHODS: Health effects were measured in terms of years of life gained. On the cost side, treatment costs for pharmaceuticals and hospitalisations were included. Data on healthcare resource consumption from CIBIS-II were used and were combined with average Swedish retail prices for medicines, and average costs for hospitalisations based on hospital admissions, in the base case. The costs of added years of life, i.e. consumption net of production during life-years gained were also included. RESULTS: If costs of added years of life were not included, then bisoprolol therapy increased life expectancy at an incremental cost of Swedish kronor (SEK) 13 094 (1999 values) per year of life gained. If costs of added years of life were included, then the incremental cost-effectiveness ratio of bisoprolol therapy was SEK 168 858 per year of life gained. CONCLUSIONS: For patients with CHF with the characteristics of those in CIBIS-II, the cost effectiveness of bisoprolol therapy compares favourably with that of other cardiovascular therapies.
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH P_Cost-Benefit_Analysis_MeSH P_Health_Care_Costs_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Hospitalization_MeSH S_economics_MeSH Hospitalization_economics_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH 
****** 11702517
----K 5
----T A comprehensive review of antihypertensive agents providing renal protection.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetic_Nephropathies_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH P_Kidney_Failure_MeSH 
****** 11703993
----K I
----T Pulse pressure and risk of cardiovascular events in the systolic hypertension in the elderly program.
----A Pulse pressure has been related to higher risk of cardiovascular events in older persons. Isolated systolic hypertension is common among the elderly and is accompanied by elevated pulse pressure. Treatment of isolated systolic hypertension may further increase pulse pressure if diastolic pressure is lowered to a greater extent than systolic pressure. Little is known regarding pulse pressure as a predictor of cardiovascular outcomes in elderly persons with isolated systolic hypertension, and the influence of treatment on the pulse pressure effect. We assessed the relation between pulse pressure, measured throughout the follow-up period, and the incidence of coronary heart disease (CHD), heart failure (HF), and stroke in 4,632 participants in the Systolic Hypertension in the Elderly Program, a 5-year randomized, placebo-controlled clinical trial of treatment of isolated systolic hypertension in older adults. In the treatment group, a 10-mm Hg increase in pulse pressure was associated with a statistically significant 32% increase in risk of HF and a 24% increase in risk of stroke after controlling for systolic blood pressure and other known risk factors, as well as with a 23% increase in risk of HF and a 19% increase in risk of stroke after controlling for diastolic blood pressure and other risk factors. Pulse pressure was not significantly associated with HF or stroke in the placebo group, nor with incidence of CHD in either the placebo or treatment group. These results suggest that pulse pressure is a useful marker of risk for HF and stroke among older adults being treated for isolated systolic hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_physiopathology_MeSH Cerebrovascular_Accident_physiopathology_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH P_Pulse_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH 
****** 11702031
----K 5
----T Quality of life in the elderly hypertensive.
----A The approach to the treatment of hypertension in the elderly hypertensive should take into account the effects of the different antihypertensive drugs on the quality of life, especially in the elderly where a small reduction in health status could have an impact on their independence.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Treatment_Outcome_MeSH 
****** 11711020
----K I
----T Does a change to long-acting antianginals provide better symptom control, treatment satisfaction, and quality of life?
----A 
----P Journal_Article 
----M M_Activities_of_Daily_Living_MeSH M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Delayed-Action_Preparations_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH P_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Male_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH P_Patient_Satisfaction_MeSH M_Practice_Guidelines_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Research_Design_MeSH S_standards_MeSH Research_Design_standards_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11759645
----K I
----T A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure.
----A BACKGROUND: Actions of angiotensin II may contribute to the progression of heart failure despite treatment with currently recommended drugs. We therefore evaluated the long-term effects of the addition of the angiotensin-receptor blocker valsartan to standard therapy for heart failure. METHODS: A total of 5010 patients with heart failure of New York Heart Association (NYHA) class II, III, or IV were randomly assigned to receive 160 mg of valsartan or placebo twice daily. The primary outcomes were mortality and the combined end point of mortality and morbidity, defined as the incidence of cardiac arrest with resuscitation, hospitalization for heart failure, or receipt of intravenous inotropic or vasodilator therapy for at least four hours. RESULTS: Overall mortality was similar in the two groups. The incidence of the combined end point, however, was 13.2 percent lower with valsartan than with placebo (relative risk, 0.87; 97.5 percent confidence interval, 0.77 to 0.97; P=0.009), predominantly because of a lower number of patients hospitalized for heart failure; 455 (18.2 percent) in the placebo group and 346 (13.8 percent) in the valsartan group (P<0.001). Treatment with valsartan also resulted in significant improvements in NYHA class, ejection fraction, signs and symptoms of heart failure, and quality of life as compared with placebo (P<0.01). In a post hoc analysis of the combined end point and mortality in subgroups defined according to base-line treatment with angiotensin-converting-enzyme (ACE) inhibitors or beta-blockers, valsartan had a favorable effect in patients receiving neither or one of these types of drugs but an adverse effect in patients receiving both types of drugs. CONCLUSIONS: Valsartan significantly reduces the combined end point of mortality and morbidity and improves clinical signs and symptoms in patients with heart failure, when added to prescribed therapy. However, the post hoc observation of an adverse effect on mortality and morbidity in the subgroup receiving valsartan, an ACE inhibitor, and a beta-blocker raises concern about the potential safety of this specific combination.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Quality_of_Life_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 11720061
----K 5
----T Increasing relevance of pharmacogenetics of drug metabolism in clinical practice.
----A Much of the individual variation in drug response is due to genetic drug metabolic polymorphisms. Clinically relevant examples include acetylator status; cytochrome P450 2D6, 2C9 and 2C19 polymorphisms; and thiopurine methyltransferase deficiency. It is important to be aware of which drugs are subject to pharmacogenetic variability. In the future, population-based pharmacogenetic testing will allow more individualized drug treatment and will avoid the current empiricism.
----P Journal_Article Review Review__Tutorial 
----M M_Acetyltransferases_MeSH S_genetics_MeSH Acetyltransferases_genetics_MeSH S_metabolism_MeSH Acetyltransferases_metabolism_MeSH P_Aryl_Hydrocarbon_Hydroxylases_MeSH M_Cytochrome_P-450_CYP2D6_MeSH S_genetics_MeSH Cytochrome_P-450_CYP2D6_genetics_MeSH S_metabolism_MeSH Cytochrome_P-450_CYP2D6_metabolism_MeSH M_Cytochrome_P-450_Enzyme_System_MeSH S_genetics_MeSH Cytochrome_P-450_Enzyme_System_genetics_MeSH S_metabolism_MeSH Cytochrome_P-450_Enzyme_System_metabolism_MeSH M_Drug_Therapy_MeSH S_methods_MeSH Drug_Therapy_methods_MeSH M_Enzymes_MeSH S_genetics_MeSH Enzymes_genetics_MeSH S_metabolism_MeSH Enzymes_metabolism_MeSH M_Genotype_MeSH M_Human_MeSH M_Methyltransferases_MeSH S_genetics_MeSH Methyltransferases_genetics_MeSH S_metabolism_MeSH Methyltransferases_metabolism_MeSH M_Pharmaceutical_Preparations_MeSH S_metabolism_MeSH Pharmaceutical_Preparations_metabolism_MeSH M_Pharmacogenetics_MeSH P_Steroid_16-alpha-Hydroxylase_MeSH M_Steroid_Hydroxylases_MeSH S_genetics_MeSH Steroid_Hydroxylases_genetics_MeSH S_metabolism_MeSH Steroid_Hydroxylases_metabolism_MeSH 
****** 11720598
----K E
----T Verapamil-sensitive left ventricular tachycardia in patients with coronary artery disease: clinical and electrophysiologic features consistent with triggered activity.
----A This is a retrospective review of three male patients with verapamil-sensitive left ventricular tachycardia, severe coronary artery disease, and past myocardial infarction. Each patient had severe left ventricular dysfunction (mean ejection fraction 34%). Each tachycardia had a right bundle branch block/left axis deviation morphology, which was sustained with isoproterenol. One patient had incessant tachycardia 3 days after coronary bypass surgery. Electrophysiology and clinical parameters were suggestive of triggered activity rather than reentry. Each tachycardia was terminated with verapamil but failed with adenosine, beta blockers, and class I/III antiarrhythmics. Prior cases of verapamil-sensitive ventricular tachycardia have been seen in patients without organic heart disease, and the putative mechanism appears to be reentry. These patients with ischemic coronary artery disease may exhibit a mechanism of triggered activity in the Purkinje system region, which is responsive to calcium channel blockade. Successful radiofrequency ablation was guided by Purkinje potentials.
----P Case_Reports Journal_Article 
----M M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Bundle-Branch_Block_MeSH S_physiopathology_MeSH Bundle-Branch_Block_physiopathology_MeSH S_surgery_MeSH Bundle-Branch_Block_surgery_MeSH S_therapy_MeSH Bundle-Branch_Block_therapy_MeSH M_Catheter_Ablation_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Human_MeSH M_Male_MeSH M_Retrospective_Studies_MeSH M_Tachycardia__Ventricular_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 11721720
----K E
----T Beneficial effects of diltiazem during myocardial reperfusion: a randomized trial in acute myocardial infarction.
----A BACKGROUND: Although in experimental models of coronary occlusion diltiazem administration has been shown to reduce the degree of stunning and of reperfusion injury, the majority of clinical trials has failed to demonstrate significant benefits. The aim of this study was to evaluate the effect of diltiazem, administered before coronary reperfusion, on infarct size, residual myocardial viability and recovery of left ventricular function. METHODS: We studied 90 patients admitted within 3 hours of the onset of symptoms of acute myocardial infarction. They were immediately randomized to either intravenous diltiazem (10 mg bolus + 10 mg/hour for 3 days) (group 1, n = 43) or placebo (group 2, n = 47) and subsequently treated with recombinant tissue-type plasminogen activator. All underwent serial echocardiograms upon admission, 4 days post-admission during low-dose dobutamine stress echo, at discharge and after 6 months. We calculated the dysfunction score (1 = hypokinesia, 2 = akinesia, 3 = dyskinesia) on admission and its percent reduction after dobutamine (viability) and at follow-up (recovery). The 12-lead electrocardiograms were continuously monitored for 3 days and coronary angioplasty was performed whenever the residual stenosis was > 60%. RESULTS: Upon admission, there were no differences in age, sex, infarct location and size, degree of ST-segment elevation, time from onset of symptoms and dysfunction score. Creatine kinase peaked early in 70% of patients in both groups; the incidences of recurrent ischemia, infarct-related vessel patency and the need for coronary angioplasty were also similar. The creatine kinase peak was significantly higher in group 2 (2931 +/- 2456 vs 1726 +/- 1004 IU/l, p < 0.05). Conversely, in group 1 the residual viability was significantly higher (51 +/- 23 vs 36 +/- 30% improvement in dysfunction score, p < 0.05) and the early recovery of regional function was significantly greater (35 +/- 34 vs 18 +/- 22% at discharge, p < 0.05). On the other hand, the delayed recovery was not significantly different (15 +/- 29 vs 21 +/- 32% from the time of discharge to 6 months of follow-up). CONCLUSIONS: Intravenous diltiazem, started before coronary reperfusion, has beneficial effects on the infarct size, residual viability and recovery of regional function. If confirmed by larger trials, these preliminary results suggest the use of diltiazem as adjunctive therapy in patients with acute myocardial infarction and undergoing reperfusion.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Angiography_MeSH M_Diltiazem_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Stress_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_enzymology_MeSH Myocardial_Infarction_enzymology_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Myocardial_Reperfusion_Injury_MeSH S_prevention_&_control_MeSH Myocardial_Reperfusion_Injury_prevention_&_control_MeSH M_Plasminogen_Activators_MeSH S_therapeutic_use_MeSH Plasminogen_Activators_therapeutic_use_MeSH M_Risk_Factors_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11721319
----K 1
----T Mechanical vs intrinsic components in the improvement of brachial arterial compliance. Comparison of the effects of atenolol versus ramipril in hypertensive patients.
----A The aim of this study was to compare the mechanical and intrinsic effects of an angiotensin converting enzyme inhibitor, vs a beta-blocker, on brachial arterial compliance. In a double blind study, 34 essential hypertensive patients were treated for 3 months with either ramipril 2.5-5.0 mg daily (n = 17, age 57 +/- 7 y, 11 males) or atenolol 50-100 mg daily (n = 17, age 53 +/- 8 y, 11 males). Blood pressure (BP), brachial artery diameter (D), brachial-radial pulse wave velocity (PWV) and effective compliance (Ceff), were measured before and at the end of the study. Isobaric evaluation (Ciso) was performed in the entire population studied at an average mean BP of 110 mmHg. Ramipril significantly reduced BP from 155 +/- 16/94 +/- 6 mmHg to 140 +/- 15/85 +/- 7 mmHg (p < 0.001) without affecting heart rate (HR; 74 +/- 10 vs. 75 +/- 12 bpm). In addition, it significantly improved both PWV (18%; p < 0.001) and arterial compliance (45%; p < 0.001), from which 35% was related to a pressure independent effect (p < 0.01). Atenolol also induced a reduction in both BP (159 +/- 17/96 +/- 10 to 133 +/- 13/81 +/- 8 mmHg; p < 0.001) and HR (76 +/- 10 to 57 +/- 7 bpm; p < 0.001). In a similar way, PWV (11%; p < 0.05) and Ceff (30%; p < 0.05) were significantly improved without significant change in Ciso. This suggests that blood pressure reduction was responsible for compliance improvement. In conclusion, it is suggested that atenolol induces only hemodynamic changes, mediated mainly by BP reduction. In contrast, the improved brachial buffering function observed after ramipril involves not only hemodynamic changes, but also changes mediated by other mechanisms, such as modification of wall structures.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Brachial_Artery_MeSH S_drug_effects_MeSH Brachial_Artery_drug_effects_MeSH S_physiopathology_MeSH Brachial_Artery_physiopathology_MeSH M_Comparative_Study_MeSH M_Compliance_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11723019
----K E
----T beta-blockers before percutaneous coronary intervention do not attenuate postprocedural creatine kinase isoenzyme rise.
----A BACKGROUND: beta-blocker (BB) use reduces infarct size in spontaneously occurring nonreperfused infarcts but probably does not change infarct size in patients treated with reperfusion therapy. A recent observational study suggested that BB use concurrent with percutaneous coronary intervention (PCI) decreased the risk of creatine kinase (CK)-MB elevation. The cogency of such a conclusion is dependent on the ability to risk-adjust for the multiple differences in patients treated with and without BBs. METHODS AND RESULTS: Using propensity score and multivariate regression analyses, 6200 consecutive patients were analyzed to assess the relationship between BB use before PCI and per protocol-measured CK and CK-MB rise. There were several highly significant (P<0.001) differences between patients with and without BB treatment (eg, age, prior infarction, unstable angina). Maximum CK and CK-MB levels were higher in patients taking BBs (CK median, 95 U [interquartile range: 61, 175]; CK-MB, 3 U [2, 5]) than in patients not taking BBs (CK, 91 U [60, 157]; CK-MB, 3 U [2, 4]) (P=0.011 and P=0.021 for CK and CK-MB, respectively). After adjustment for significant differences in baseline characteristics there was no difference in either maximum CK rise (P=0.21) or maximum CK-MB rise (P=0.99). CONCLUSIONS: The results of this large observation study do not support the contention that BB use before PCI decreases myocardial injury.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_adverse_effects_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_adverse_effects_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_enzymology_MeSH Coronary_Disease_enzymology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH M_Female_MeSH M_Human_MeSH M_Isoenzymes_MeSH S_blood_MeSH Isoenzymes_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Reperfusion_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Preoperative_Care_MeSH M_Prospective_Studies_MeSH M_Risk_Assessment_MeSH M_Treatment_Failure_MeSH M_Treatment_Outcome_MeSH 
****** 11723089
----K E
----T Reduced cardiovascular morbidity and mortality in hypertensive diabetic patients on first-line therapy with an ACE inhibitor compared with a diuretic/beta-blocker-based treatment regimen: a subanalysis of the Captopril Prevention Project.
----A OBJECTIVE: The Captopril Prevention Project (CAPPP) evaluated the effects of an ACE inhibitor-based therapeutic regimen on cardiovascular mortality and morbidity in hypertension. One planned subanalysis of the CAPPP was to evaluate the outcome in the diabetic patient group. RESEARCH DESIGN AND METHODS: In the CAPPP, 572 (4.9% of 10,985 hypertensive patients) had diabetes at baseline and were studied according to a prospective, randomized, open, blinded, end point trial design. Patients aged 25-66 years with diastolic blood pressure > or =100 mmHg were included and randomized to receive either captopril or conventional antihypertensive treatment (diuretics and/or beta-blockers). RESULTS: The primary end point, fatal and nonfatal myocardial infarction and stroke as well as other cardiovascular deaths, was markedly lower in the captopril than in the conventional therapy group (relative risk [RR] = 0.59; P = 0.018). Specifically, cardiovascular mortality, defined as fatal stroke and myocardial infarction, sudden death, and other cardiovascular death, tended to be lower in the captopril group (RR = 0.48; P = 0.084), and no difference was observed between the study groups for stroke (RR = 1.02; P = 0.96). Myocardial infarctions were less frequent in the captopril group than in the conventional therapy group (RR = 0.34; P = 0.002). Furthermore, total mortality was lower in the captopril as compared with the conventional therapy group (RR = 0.54; P = 0.034). Patients with impaired metabolic control seemed to benefit the most from ACE inhibitor-based therapy. CONCLUSIONS: Captopril is superior to a diuretic/beta-blocker antihypertensive treatment regimen in preventing cardiovascular events in hypertensive diabetic patients, especially in those with metabolic decompensation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Body_Mass_Index_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Morbidity_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prospective_Studies_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11724081
----K E
----T Prescribing patterns and therapeutic implications for diabetic hypertension in Bahrain.
----A OBJECTIVE: To determine drug prescription patterns and the extent of conformity with World Health Organization/international Society of Hypertension (WHO/ISH) guidelines in diabetic hypertension. DESIGN: Retrospective prescription-based survey. SETTING: Seven primary-care health centers, comprising approximately one-third of primary-care health centers in Bahrain. PATIENTS: Patients with type 2 diabetes and hypertension. MAIN OUTCOME MEASURE: The prescribing pattern of antihypertensive and antidiabetic drugs. RESULTS: Among a study sample of 1,463 patients with type 2 diabetes and hypertension, antidiabetic agents were prescribed as monotherapy in the following descending order: glyburide, gliclazide, insulin, and metformin. As combinations, sulfonylureas plus metformin was most popular, followed by metformin plus insulin, and sulfonylureas plus insulin. Sulfonylurea and metformin with insulin was rarely used. There was no significant difference in prescribing of glyburide and metformin between the elderly and young middle-aged diabetic patients; many patients older than 65 years were treated with a beta-blocker along with a long-acting sulfonylurea. Both as monotherapy and in overall use, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium-channel blockers were most often prescribed. Among 35.5% patients treated with antihypertensive combinations, various two- and three-drug combinations of beta-blockers, ACE inhibitors, calcium-channel blockers, and diuretics were often used. The proportion of patients taking atenolol 100 mg/d was higher with combination regimens. Hydrochlorothiazide 25 mg or equivalent thiazide diuretics were extensively used. CONCLUSIONS: The prescribing pattern of antihypertensives in diabetic hypertension differs in many instances from WHO/ISH guidelines, especially regarding the choice of antihypertensive drugs and their combinations. The appropriateness of antidiabetic drug choice is questionable in relation to the antihypertensive used.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bahrain_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_Drug_Utilization_Review_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Insulin_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Prescriptions__Drug_MeSH M_Retrospective_Studies_MeSH 
****** 11726010
----K E
----T Assessment of the association between blood pressure control and health care resource use.
----A BACKGROUND: Several studies have reported increased health care resource use among hypertensive patients with uncontrolled blood pressure (BP). OBJECTIVE: The purpose of this study was to investigate the relationship between BP control and health care resource use. METHODS: Data were obtained from the Caring for Hypertension on Initiation: Costs and Effectiveness (CHOICE) study, a multicenter feasibility study of actual physician and patient behavior and clinical outcomes in a naturalistic setting. Adult patients with newly diagnosed hypertension were randomized to either Group 1 (treatment with diuretics or beta-blockers) or Group 2 (treatment with calcium channel blockers or angiotensin-converting enzyme inhibitors) and followed for 5 +/- 1 months. Physicians practiced standard care while documenting medications, BP measurements, and health care resource use for their patients. A subsequent analysis evaluating the relationship between BP and physician visits was performed for the whole population and for a subpopulation of patients with at least 4 months of follow-up data. Cox regression was used to model time to next visit. RESULTS: A total of 512 patients with newly diagnosed hypertension were followed: 399 had follow-up data for at least 4 months. Baseline demographic characteristics were similar in the 2 groups. Kaplan-Meier curves and a log-rank test showed that the time to next visit for patients with uncontrolled BP was significantly shorter than for patients whose BP was controlled (P < 0.05). On average, patients with uncontrolled BP (> or = 140/90 mm Hg) had follow-up office visits approximately 13 days earlier than patients with controlled BP (< 140/90 mm Hg). This association remained significant after adjustment for repeated measures, and after exclusion of the first return visit. Cox regression analysis showed that higher systolic and diastolic BP measurements were significantly associated with a shorter time to next visit, after adjustment for age and sex. Total estimated costs during the study period were $170 per patient for medications and $283 per patient for office visits. CONCLUSIONS: In the CHOICE study, higher BP was associated with a shorter time to next visit. Office visits were the main cost driver in the short-term management of hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_economics_MeSH Calcium_Channel_Blockers_economics_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH S_statistics_&_numerical_data_MeSH Cost-Benefit_Analysis_statistics_&_numerical_data_MeSH M_Delivery_of_Health_Care_MeSH M_Diuretics_MeSH S_economics_MeSH Diuretics_economics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Feasibility_Studies_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 11727652
----K E
----T Initial antihypertensive therapy. What are the current drugs of choice?
----A The goal of antihypertensive treatment, in addition to lowering blood pressure, is to reduce the risk of cardiovascular events. Until recently, however, only conventional treatment with diuretics and beta-blockers had been studied in terms of cardiovascular end points. In this article, Dr Yeun reviews the results of recent trials comparing these agents with other classes of antihypertensive drugs. She examines the confounding elements in the trials, provides an interpretation of study results, and suggests a practical approach to initial treatment of uncomplicated hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH P_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 11728147
----K E
----T Combination treatment in stable effort angina using trimetazidine and metoprolol: results of a randomized, double-blind, multicentre study (TRIMPOL II). TRIMetazidine in POLand.
----A AIMS: To assess the antiischaemic efficacy and tolerability of the metabolic agent trimetazidine in combination with metoprolol in patients with stable effort angina. METHODS: This was a randomized, multicentre, double-blind, placebo-controlled parallel group study. A total of 426 male and female patients with stable, effort-induced angina and documented coronary artery disease received either placebo or trimetazidine 20 mg three times daily in addition to metoprolol 50 mg twice daily. Treadmill exercise tests were performed at weeks (-1), 0, 4 and 12. RESULTS: After 12 weeks, there were significantly greater improvements in the metoprolol + trimetazidine group than in the metoprolol + placebo group in: time to 1 mm ST segment depression, total workload, time to onset of angina, maximum ST segment depression, mean weekly number of angina attacks, mean weekly nitrate consumption, and grade of anginal pain. There was no evidence of any development of tolerance to trimetazidine. The tolerability of trimetazidine was excellent. CONCLUSIONS: Therapy with trimetazidine plus metoprolol produced significant improvements in exercise stress tests and the symptoms of angina relative to metoprolol alone. With its metabolic effect, devoid of any haemodynamic action, trimetazidine is useful for combination therapy in patients with stable angina insufficiently controlled by monotherapy with a beta-blocker.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Europe_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Trimetazidine_MeSH S_administration_&_dosage_MeSH Trimetazidine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11731997
----K E
----T Propranolol for the prevention of first esophageal variceal hemorrhage: a lifetime commitment?
----A Although beta blockers have had significant impact in the treatment of portal hypertension, the question of how long they should be continued for prevention of variceal hemorrhage remains unknown. Prospective studies on beta blockers to prevent variceal hemorrhage lack long-term follow-up, and indefinite administration of beta blockers for primary prevention of variceal bleeding has become standard practice. The aim of this study was to determine the outcomes of patients in whom beta blocker therapy was discontinued. Patients completing a prospective, randomized, double-blind, placebo-controlled trial of propranolol for the primary prevention of variceal hemorrhage were tapered off of propranolol and placebo and followed prospectively for subsequent events. Of the 49 patients in the follow-up study (25 former propranolol, 24 former placebo), 9 experienced variceal hemorrhage (6 former propranolol, 3 former placebo). Following withdrawal of propranolol, the freedom from variceal bleeding was not significantly different between these 2 groups of patients, suggesting that the protective effect of propranolol against variceal hemorrhage, noted previously, was no longer present. Seventeen patients died (12 former propranolol, 5 former placebo) during the follow-up study. Cumulative survival was longer in the placebo group. These trends for EVH and survival were opposite to those observed in the original study population while patients were taking medication. When propranolol is withdrawn, the risk of variceal hemorrhage returns to what would be expected in an untreated population. Patients who discontinue beta blockers experience increased mortality compared with an untreated population. These observations support the current practice of indefinite prophylactic therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH 
****** 11731729
----K E
----T Comparative hemodynamic effects of urapidil and labetalol after electroconvulsive therapy.
----A Urapidil, a postsynaptic alpha 1 -adrenergic antagonist, has been reported to improve intraoperative hemodynamic stability, although it has never been used to prevent the hemodynamic response of electroconvulsive therapy (ECT). This study was designed to evaluate the clinical effectiveness of urapidil, as an alternative to labetalol, in preventing the hemodynamic response of ECT. Twenty-seven patients undergoing a series of six consecutive ECT treatments were studied. Each patient received all three pretreatments twice: no drug, labetalol 0.2 mg/kg, or urapidil 25 mg. Systolic, diastolic, and mean blood pressure and heart rate (HR) were recorded during the awake state, after anesthesia induction, and 1, 2, 5, 10 and 30 minutes after electroencephalographic (EEG) seizure ended. The duration of the EEG convulsion was also recorded. After induction, the HR increased for no drug and urapidil pretreatments, whereas it decreased when labetalol was given. Labetalol and urapidil attenuated the peak increase of blood pressure and returned it to earlier baseline values. There were no differences in the duration of EEG convulsion between the three pretreatments. Urapidil seems to be a good alternative to labetalol for attenuating the hypertensive response to ECT in cases where there is a contraindication to beta-antagonists.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Electroconvulsive_Therapy_MeSH S_adverse_effects_MeSH Electroconvulsive_Therapy_adverse_effects_MeSH M_Electroencephalography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Labetalol_MeSH S_pharmacology_MeSH Labetalol_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Piperazines_MeSH S_pharmacology_MeSH Piperazines_pharmacology_MeSH 
****** 11734093
----K E
----T Actual practice in hypertension: implications for persistence with and effectiveness of therapy.
----A Hypertension is often poorly controlled despite its importance and despite the availability of very effective treatments. Many factors contribute to poor control, including failure of patients to attend physicians, failure of physicians to detect and adequately treat hypertension to goal levels, and failure of patients to persist with prescribed therapy. An under-recognized problem is the failure, both in writing and in the application by third party payers, of consensus guidelines to recognize the important difference between efficacy in clinical trials and effectiveness in clinical practice.The issue of applicability of guidelines to actual practice was studied in the context of a Canadian Family Medicine teaching practice. At the time of the study, consensus guidelines for management of hypertension recommended that drug therapy be initiated with a beta-blocker or diuretic, except for patients with complicated hypertension for whom these drug classes are relatively contraindicated. It was generally assumed that widespread use of other classes of drugs represented inappropriate and wasteful use of resources. By a retrospective chart audit, we determined the proportion of patients in a family practice for whom therapy with a beta-blocker or diuretic was contraindicated, and examined the compliance of the physicians in the practice with guidelines. We found that about half of hypertensives had conditions for which recommended therapy is not a beta-blocker or diuretic. Thus, failure of physicians to follow guidelines is apparently less inappropriate than is widely perceived.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Guideline_Adherence_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH P_Patient_Compliance_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11734686
----K 4
----T Ocular complications of pregnancy.
----A Pregnancy is often associated with ocular changes, most often transient in nature, though occasionally permanent. It can be associated with development of new conditions, or can exacerbate pre-existing conditions. The ocular effects of pregnancy may be divided into physiologic changes, pathologic conditions or modifications of pre-existing conditions. Pathologic conditions include entities such as pre-eclampsia and eclampsia, along with conditions that are seen with increased frequency during pregnancy such as central serous retinopathy. The most significant modified pre-existing condition is diabetes mellitus. The various effects of pregnancy on the eye will be reviewed in this article.
----P Journal_Article Review Review__Tutorial 
----M M_Eye_Diseases_MeSH S_etiology_MeSH Eye_Diseases_etiology_MeSH M_Female_MeSH M_Human_MeSH M_Pregnancy_MeSH P_Pregnancy_Complications_MeSH 
****** 11759128
----K E
----T The dose-related effects of bolus esmolol on heart rate and blood pressure following laryngoscopy and intubation.
----A Many researchers have studied esmolol and its effects on heart rate and blood pressure. All studied relatively large doses of esmolol. Therefore, the purpose of the present study was to determine whether small doses of esmolol would blunt the transient increases in blood pressure and heart rate caused by laryngoscopy. This double-blind, prospective, randomized study included 61 subjects. The subjects were randomized to 1 of 3 groups: group 1 received esmolol, 0.2 mg/kg; group 2 received esmolol, 0.4 mg/kg; and group 3 received saline placebo. Groups 1 and 2 had smaller increases in heart rate than group 3. We also found that the 0.4 mg/kg dose significantly blunted the increase in mean arterial pressure seen in group 3. This study shows that small doses of esmolol may block the increases in heart rate and blood pressure resulting from laryngoscopy and intubation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Monitoring_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Injections__Intravenous_MeSH M_Intraoperative_Care_MeSH S_methods_MeSH Intraoperative_Care_methods_MeSH M_Intubation__Intratracheal_MeSH S_adverse_effects_MeSH Intubation__Intratracheal_adverse_effects_MeSH M_Laryngoscopy_MeSH S_adverse_effects_MeSH Laryngoscopy_adverse_effects_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Prospective_Studies_MeSH M_Tachycardia_MeSH S_drug_therapy_MeSH Tachycardia_drug_therapy_MeSH S_etiology_MeSH Tachycardia_etiology_MeSH M_Time_Factors_MeSH 
****** 11736772
----K E
----T The effect of an infusion of esmolol on the incidence of myocardial ischaemia during tracheal extubation following coronary artery surgery.
----A The aim of this randomised controlled study was to determine whether an esmolol infusion affected the incidence of ST segment changes during weaning from intermittent positive pressure ventilation and tracheal extubation after coronary artery surgery. Thirty-one patients received an infusion of esmolol 0-300 microg x kg(-1) x min(-1) and 37 patients comprised the control group. ST segment changes were monitored using a continuous ambulatory surveillance system. The electrocardiogram, direct arterial pressure and pulse oximetry were monitored continuously. The period of analysis was from 120 min before until 180 min after tracheal extubation. Three patients in the esmolol group developed myocardial ischaemia during the study period compared with 12 in the control group (p = 0.05). Heart rate increased with time during the study period (p = 0.002) in the control group but was unchanged in the esmolol group. Mean heart rate was significantly higher in the control group than in the esmolol group from 40 min before until 180 min after tracheal extubation. Seven patients in the esmolol group suffered adverse events related to the esmolol infusion. Although the use of esmolol reduced the incidence of myocardial ischaemia, the incidence of adverse effects makes it unsuitable prophylaxis for patients after coronary artery surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiopulmonary_Bypass_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Device_Removal_MeSH S_adverse_effects_MeSH Device_Removal_adverse_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Intubation__Intratracheal_MeSH S_adverse_effects_MeSH Intubation__Intratracheal_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Postoperative_Care_MeSH S_methods_MeSH Postoperative_Care_methods_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 11740134
----K E
----T Different effects of calcium antagonist and beta-blocker therapy on left-ventricular diastolic function in ischemic heart disease. A direct comparison of the impact of mibefradil and atenolol.
----A OBJECTIVE: To compare the effect of a calcium antagonist and a beta-blocker on left-ventricular diastolic function in patients with ischemic heart disease. METHODS: 138 patients with chronic stable angina pectoris were randomized in a multicenter, double-blind trial to treatment with either mibefradil or atenolol for 6 weeks (50 mg once daily for 2 weeks followed by 100 mg once daily for 4 weeks). The ratio between early (E) and late (A) diastolic mitral flow velocities (E/A), the E wave deceleration time (DT) and the left ventricular isovolumetric relaxation time (IRT) were measured by Doppler echocardiography as parameters of left-ventricular diastolic function initially, after 4 and after 6 weeks of treatment. RESULTS: Mibefradil did not change the E/A ratio significantly (+4%, NS), while atenolol treatment resulted in a significant increase in the E/A ratio (+20%, p < 0.001). Mibefradil treatment, on the other hand, resulted in a significant decrease (-8%, p < 0.001) in IRT, while atenolol treatment did not change IRT. Neither mibefradil nor atenolol treatment changed DT significantly. CONCLUSIONS: Both mibefradil and atenolol treatment significantly improves echocardiographic indices of left-ventricular diastolic function in patients with chronic stable angina. However, they affect different parameters and thus apparently act through different mechanisms.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_ultrasonography_MeSH Angina_Pectoris_ultrasonography_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH S_physiology_MeSH Blood_Flow_Velocity_physiology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH S_physiology_MeSH Diastole_physiology_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Heart_Septum_MeSH S_drug_effects_MeSH Heart_Septum_drug_effects_MeSH S_physiopathology_MeSH Heart_Septum_physiopathology_MeSH S_ultrasonography_MeSH Heart_Septum_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Mibefradil_MeSH S_therapeutic_use_MeSH Mibefradil_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Mitral_Valve_MeSH S_drug_effects_MeSH Mitral_Valve_drug_effects_MeSH S_physiopathology_MeSH Mitral_Valve_physiopathology_MeSH S_ultrasonography_MeSH Mitral_Valve_ultrasonography_MeSH M_Time_Factors_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 11738224
----K E
----T The effects of chronic carvedilol therapy on QT dispersion in patients with congestive heart failure.
----A BACKGROUND: Carvedilol therapy reduces mortality from sudden cardiac death and progressive pump failure in congestive heart failure (CHF). However, the effect(s) of carvedilol on ventricular repolarization characteristics is unclear. AIM: The aim of the study was to investigate the effects of chronic carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) in patients with CHF. METHOD: Nineteen patients (age 53+/-12 years; 16 male, three female) with CHF (eight ischemic, 11 non-ischemic dilated cardiomyopathy) were prospectively included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 3.125 mg bid and uptitrated biweekly to the maximum tolerated dose. From standard 12-lead electrocardiograms the maximum and minimum QT intervals (QTmax, QTmin), QTd, corrected QT intervals (QTcmax, QTcmin) and corrected QTd (QTcd) values were calculated at baseline, after the 2nd and the 16th month of carvedilol therapy. RESULTS: A significant reduction was noted in the QTd and QTcd values with carvedilol therapy after the 16th month (QTd: 81+/-22 ms vs. 40+/-4.3 ms P<0.001; QTcd: 91+/-25 ms vs. 51+/-7 ms P<0.001), but not after the 2nd month (P>0.05). The resting heart rate was also significantly reduced after a 16-month course of carvedilol therapy (78+/-13 bpm vs. 66+/-15 bpm, P<0.05). Carvedilol therapy did not alter QTmax and QTcmax intervals (P>0.05), however, QT min and QTcmin significantly increased with carvedilol at the 16th month (P<0.001 and P<0.01, respectively). CONCLUSION: Long-term carvedilol therapy was associated with a reduction in QTd, an effect that might contribute to the favorable effects of carvedilol in reducing sudden cardiac death in CHF.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Diseases_MeSH S_complications_MeSH Myocardial_Diseases_complications_MeSH S_drug_therapy_MeSH Myocardial_Diseases_drug_therapy_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Turkey_MeSH 
****** 11738299
----K I
----T Aspirin impairs reverse myocardial remodeling in patients with heart failure treated with beta-blockers.
----A OBJECTIVES: We hypothesized that aspirin (ASA) might alter the beneficial effect of beta-blockers on left ventricular ejection fraction (LVEF) in patients with chronic heart failure. BACKGROUND: Aspirin blunts the vasodilation caused by both angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in hypertensive patients and in patients with heart failure. Several studies suggest that ASA also blunts some of beneficial effects of ACE inhibitors on mortality in patients with heart failure. To our knowledge, there have been no data evaluating the possible interaction of ASA and beta-blockers on left ventricular remodeling in patients with heart failure. METHODS: We retrospectively evaluated patients entered into the Multicenter Oral Carvedilol Heart failure Assessment (MOCHA) trial, a 6-month, double-blind, randomized, placebo-controlled, multicenter, dose-response evaluation of carvedilol in patients with chronic stable symptomatic heart failure. Multivariate analysis was performed to determine if aspirin independently influenced the improvement in LVEF. RESULTS: Over all randomized patients (n = 293), LVEF improved 8.2 +/- 0.8 ejection fraction (EF) units in ASA nonusers and 4.5 +/- 0.7 EF units in ASA users (p = 0.005). In subjects randomized to treatment with carvedilol (n = 231), LVEF improved 9.5 +/- 0.9 EF units in ASA nonusers and 5.8 +/- 0.8 EF units in ASA users (p = 0.02). In subjects randomized to treatment with placebo (n = 62), LVEF improved 2.8 +/- 1.2 EF units in ASA nonusers and 0.5 +/- 1.4 EF units in ASA users (p = 0.20). Aspirin did not significantly affect the heart rate or systolic blood pressure response in either the placebo or carvedilol groups. The effect of ASA became more significant on multivariate analysis. The change in LVEF was also influenced by carvedilol dose, etiology of heart failure, baseline heart rate, EF and coumadin use. The detrimental effect of ASA on the improvement in LVEF was dose-related and was present in both placebo and carvedilol groups, although the effect was statistically significant only in the much larger carvedilol group. CONCLUSIONS: Aspirin significantly affects the changes in LVEF over time in patients with heart failure and systolic dysfunction treated with carvedilol. The specific mechanism(s) underlying this interaction are unknown and further studies are needed to provide additional understanding of the molecular basis of factors influencing reverse remodeling in patients with heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_antagonists_&_inhibitors_MeSH Carbazoles_antagonists_&_inhibitors_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_antagonists_&_inhibitors_MeSH Propanolamines_antagonists_&_inhibitors_MeSH M_Retrospective_Studies_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 11738309
----K E
----T Effect of metoprolol and d,l-sotalol on microvolt-level T-wave alternans. Results of a prospective, double-blind, randomized study.
----A OBJECTIVES: The study evaluated the effects of metoprolol, a pure beta-blocker, and d,l-sotalol, a beta-blocker with additional class III antiarrhythmic effects, on microvolt-level T-wave alternans (TWA). BACKGROUND: Assessment of TWA is increasingly used for purposes of risk stratification in patients prone to sudden death. There are only sparse data regarding the effects of beta-blockers and antiarrhythmic drugs on TWA. METHODS: Patients with a history of documented or suspected malignant ventricular tachyarrhythmias were eligible. All patients underwent invasive electrophysiologic (EP) testing including programmed ventricular stimulation and determination of TWA at increasing heart rates using atrial pacing. Reproducibility of TWA at two consecutive drug-free baseline measurements was tested in a random patient subset. Following baseline measurements, all patients were randomized either to double-blind intravenous infusion of sotalol (1.0 mg/kg) or metoprolol (0.1 mg/kg). Results of TWA assessment at baseline and after drug exposure were compared. RESULTS: Fifty-four consecutive patients were studied. In 12 patients, repetitive baseline measurement of TWA revealed stable alternans voltage (V(alt)) values (9.1 +/- 5.8 microV vs. 8.5 +/- 5.7 microV, p = NS). After drug administration, V(alt) decreased by 35% with metoprolol (7.9 +/- 6.0 microV to 4.9 +/- 4.2 microV; p < 0.001) and by 38% with sotalol (8.6 +/- 6.8 microV to 4.4 +/- 2.3 microV; p = 0.001). In eight patients with positive TWA at baseline, repeated measurement revealed negative test results. CONCLUSIONS: In patients prone to sudden cardiac death, there is a reduction in TWA amplitude following the administration of antiadrenergic drugs. This result indicates that TWA is responsive to the pharmacologic milieu and suggests that, to assess a patient's risk of spontaneous ventricular arrhythmia, the patient should be tested while maintaining the pharmacologic regimen under which the risk of arrhythmia is being assessed. This applies particularly for beta-blocker therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH M_Survival_Rate_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH 
****** 11740831
----K E
----T How to avoid cardiac ischemic events associated with aortic surgery.
----A Whereas there is some degree of coronary artery disease (CAD) in most patients undergoing vascular surgery, there is no consensus regarding how to avoid perioperative cardiac ischemic events. Although this edition of Seminars in Vascular Surgery is devoted to aortic surgery, it must be remembered that the incidence of adverse cardiac outcomes after infrainguinal operations is at least as great as after aortic procedures. Thus, much of the information discussed herein will be applicable to patients undergoing all varieties of vascular surgery. Numerous strategies exist for preoperative cardiac testing before vascular operations. These strategies range from routine evaluation before surgery to a "minimalist" approach, treating all patients as though CAD was present. Although advocates of various algorithms often are unwavering in their convictions, there are no randomized, prospective studies comparing different strategies for evaluation and management of patients with CAD undergoing vascular surgery. Potential adverse effects of evaluation and cardiac intervention should be considered before undertaking screening studies. The authors analyzed the adverse outcomes of preoperative cardiac evaluation and intervention before vascular operations in patients treated at the Denver Department of Veterans Affairs Medical Center. Of 153 patients undergoing vascular procedures, 42 had extended cardiac evaluations. Sixteen (38%) patients had untoward events related to this evaluation. Extensive cardiac evaluation before vascular operations can result in morbidity, delays, and refusal to undergo vascular surgery. The underlying indication for vascular operations and the local iatrogenic cardiac complication rates should be considered before ordering special studies. Several recent randomized, prospective studies have established that perioperative beta-adrenergic blockade is beneficial in vascular patients with CAD. Beta-Blocker therapy can reduce the risk of perioperative adverse cardiac outcomes by 55%. The Coronary Artery Revascularization Prophylaxis (CARP) trial currently underway is a multicenter, prospective comparison of invasive intervention for CAD versus best medical care in patients undergoing aortic and lower extremity vascular surgery funded by the Department of Veterans Affairs Cooperative Studies Program.
----P Journal_Article Review Review_of_Reported_Cases 
----M M_Aortic_Diseases_MeSH S_complications_MeSH Aortic_Diseases_complications_MeSH S_surgery_MeSH Aortic_Diseases_surgery_MeSH M_Cardiovascular_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiovascular_Surgical_Procedures_adverse_effects_MeSH M_Coronary_Arteriosclerosis_MeSH S_etiology_MeSH Coronary_Arteriosclerosis_etiology_MeSH S_therapy_MeSH Coronary_Arteriosclerosis_therapy_MeSH M_Forecasting_MeSH M_Human_MeSH M_Incidence_MeSH M_Postoperative_Complications_MeSH S_epidemiology_MeSH Postoperative_Complications_epidemiology_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH M_Risk_Factors_MeSH 
****** 11742926
----K E
----T Postural response of low-frequency component of heart rate variability is an increased risk for mortality in patients with coronary artery disease.
----A STUDY OBJECTIVES: We examined whether autonomic functions assessed by heart rate variability (HRV) during standardized head-up tilt testing (HUTT) predict risk for death in stable patients with coronary artery disease (CAD). DESIGN AND SETTING: Retrospective cohort study in medium-sized university general hospital. MEASUREMENTS AND RESULTS: In a cohort of 250 patients with CAD who were undergoing elective coronary angiography, we analyzed HRV during standardized HUTT under paced breathing with discontinuation of treatment with all medications. During a subsequent mean follow-up period of 99 months, there were 13 cardiac deaths and 12 noncardiac deaths. Cox regression analysis adjusted for cardiovascular risks revealed that increased postural change (supine to upright) in the power of low-frequency component (LF) power predicted an increased risk for cardiac death (relative risk [per 1-ln ms(2) increment], 4.36; 95% confidence interval, 1.64 to 11.6), while neither the high-frequency component nor its response to HUTT predicted any form of death. When the patients were trichotomized by the level of postural LF change (large drop, < or = - 0.6 ln[ms(2)]; small drop and rise, > 0 ln[ms(2)]), the three groups did not differ in terms of clinical features or CAD severity at baseline or coronary interventions during the follow-up period; however, the 8-year cardiac mortality rates were 0%, 6%, and 12%, respectively (p = 0.008 [log rank test]). Additionally, the difference was enhanced when analyzed excluding 64 patients who had been treated with a beta-blocker during the follow-up period (0%, 7%, and 15%, respectively; p = 0.006 [log rank test]). CONCLUSIONS: The postural response of HRV predicts the risk for death in patients with CAD. Postural LF increase (LF rise), in particular, is an independent risk factor for cardiac death.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Autonomic_Nervous_System_MeSH S_physiopathology_MeSH Autonomic_Nervous_System_physiopathology_MeSH M_Cause_of_Death_MeSH M_Cohort_Studies_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Japan_MeSH S_epidemiology_MeSH Japan_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH P_Tilt-Table_Test_MeSH 
****** 11765303
----K E
----T A review of class III antiarrhythmic agents for atrial fibrillation: maintenance of normal sinus rhythm.
----A A noteworthy shift from class I to class III antiarrhythmic agents for suppression of atrial fibrillation has occurred. Sotalol, amiodarone, and dofetilide have been evaluated for their ability to maintain sinus rhythm in patients with chronic atrial fibrillation. All of these agents are moderately effective; however, amiodarone appears to be most efficacious. Aside from their common class III actions, these agents have profoundly different pharmacologic, pharmacokinetic, safety, and drug interaction profiles that help guide drug selection. Amiodarone and dofetilide are safe in patients who have had a myocardial infarction and those with heart failure. The safety of commercially available d,l-sotalol in these patients is poorly understood. Torsades de pointes is the most serious adverse effect of sotalol and dofetilide, and risk increases with renal dysfunction. Amiodarone has minimal proarrhythmic risk but has numerous noncardiac toxicities that require frequent monitoring. Overall, an ideal antiarrhythmic agent does not exist, and drug selection should be highly individualized.
----P Journal_Article Review Review__Tutorial 
----M M_Amiodarone_MeSH S_pharmacokinetics_MeSH Amiodarone_pharmacokinetics_MeSH S_pharmacology_MeSH Amiodarone_pharmacology_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH M_Clinical_Trials_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Phenethylamines_MeSH S_pharmacokinetics_MeSH Phenethylamines_pharmacokinetics_MeSH S_pharmacology_MeSH Phenethylamines_pharmacology_MeSH S_therapeutic_use_MeSH Phenethylamines_therapeutic_use_MeSH M_Sotalol_MeSH S_pharmacokinetics_MeSH Sotalol_pharmacokinetics_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Sulfonamides_MeSH S_pharmacokinetics_MeSH Sulfonamides_pharmacokinetics_MeSH S_pharmacology_MeSH Sulfonamides_pharmacology_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH 
****** 11745304
----K E
----T Angiotensin-converting enzyme inhibitors and the risk of cancer: a population-based cohort study in Denmark.
----A BACKGROUND: A recent observational study suggested that the use of angiotensin-converting enzyme (ACE) inhibitors protects against cancer in general and against breast and female reproductive tract cancers in particular. To explore these hypotheses, the authors examined cancer risk among users of ACE inhibitors in North Jutland County, Denmark. METHODS: Using data from the population-based Prescription Database of North Jutland County and the Danish Cancer Registry, cancer incidence among 17,897 individuals prescribed ACE inhibitors was compared with expected incidence based on county specific cancer rates during an 8-year study period with a mean follow-up of 3.7 years. Standardized incidence ratios (SIRs) with corresponding 95% confidence intervals (95% CIs) were calculated for cancers overall and at selected sites. In addition, the authors performed a direct comparison of users of ACE inhibitors with users of beta-blockers or calcium channel blockers (n = 47,579 individuals) by means of a Cox proportional hazards model. RESULTS: Overall, 909 cancer cases were observed among users of ACE inhibitors, with 846 expected based on general population rates, yielding an SIR of 1.07 (95% CI, 1.01-1.15). No risk reductions were observed for cancers of the breast and female reproductive tract, whereas nonsignificantly decreased SIRs were observed for cancers of the esophagus, stomach, and liver. Cancer of the kidney was found in significant excess (SIR, 1.6; 95% CI, 1.1-2.2). Stratification by duration of follow-up or number of prescriptions revealed no apparent trends, except for a tendency toward decreasing risk with increasing length of follow-up for smoking-related cancers. The direct comparison of users of ACE inhibitors with users of beta-blockers or calcium channel blockers yielded results comparable to those derived from the comparison with the general population, with a hazard ratio for cancer overall of 1.01 (95% CI, 0.93-1.09). CONCLUSIONS: This large, population-based cohort study did not confirm a protective effect of ACE inhibitors on the development of cancer. The excess of kidney cancer observed likely reflects a correlation between hypertension and kidney cancer. Further investigation is needed to evaluate the long-term effects of ACE inhibitors beyond the observation period of this and previous studies. Also, the suggestive evidence of decreased risks for upper digestive system cancers and for smoking-related cancers over time may warrant additional investigation.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Breast_Neoplasms_MeSH S_epidemiology_MeSH Breast_Neoplasms_epidemiology_MeSH S_prevention_&_control_MeSH Breast_Neoplasms_prevention_&_control_MeSH M_Cohort_Studies_MeSH M_Denmark_MeSH S_epidemiology_MeSH Denmark_epidemiology_MeSH M_Female_MeSH M_Genital_Neoplasms__Female_MeSH S_epidemiology_MeSH Genital_Neoplasms__Female_epidemiology_MeSH S_prevention_&_control_MeSH Genital_Neoplasms__Female_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Kidney_Neoplasms_MeSH S_epidemiology_MeSH Kidney_Neoplasms_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neoplasms_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH S_prevention_&_control_MeSH Neoplasms_prevention_&_control_MeSH P_Registries_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11744130
----K E
----T Milrinone versus dobutamine in heart failure subjects treated chronically with carvedilol.
----A OBJECTIVE: To compare the efficacy of milrinone and dobutamine in patients chronically treated with carvedilol. BACKGROUND: Milrinone and dobutamine are used to manage decompensated heart failure, but their efficacy in patients on beta-blocker therapy was unknown. METHODS: Twenty patients with decompensated heart failure were prospectively enrolled. Inotropic responses to milrinone (12.5, 25 or 50 microg/kg bolus infusions) or dobutamine (5, 10, 15 or 20 microg/kg/min infusions) were evaluated by right-heart catheterization. RESULTS: Milrinone increased cardiac index (2.0-2.6 l/min/m2, P=0.0001) without significantly altering heart rate (70-75 bpm, P=0.19). Milrinone decreased mean pulmonary artery pressure (36-29 mm Hg, P=0.0001), pulmonary capillary wedge pressure (24-18 mm Hg, P=0.0001) and mean arterial blood pressure (78-75 mm Hg, P=0.0002). Left ventricular stroke volume index increased in the milrinone group (31-35 ml/beat/m2, P=0.0001). Dobutamine produced an increase in cardiac index (2.4-3.3 l/min/m2, P=0.0001) only at doses that are not typically used to treat heart failure (15-20 microg/kg/min). At these doses, dobutamine increased heart rate (68-82 bpm, P=0.008), mean systemic pressure (90-117 mm Hg, P=0.0001) and mean pulmonary artery pressure (21-30 mm Hg, P=0.001). Dobutamine did not alter left ventricular stroke volume index or pulmonary capillary wedge pressure. Conclusions: Dobutamine and milrinone have different hemodynamic effects in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated heart failure.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Comparative_Study_MeSH M_Dobutamine_MeSH S_administration_&_dosage_MeSH Dobutamine_administration_&_dosage_MeSH S_agonists_MeSH Dobutamine_agonists_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Milrinone_MeSH S_administration_&_dosage_MeSH Milrinone_administration_&_dosage_MeSH S_antagonists_&_inhibitors_MeSH Milrinone_antagonists_&_inhibitors_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_therapeutic_use_MeSH Phosphodiesterase_Inhibitors_therapeutic_use_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Pulmonary_Wedge_Pressure_MeSH S_drug_effects_MeSH Pulmonary_Wedge_Pressure_drug_effects_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11747387
----K I
----T Management of hypertension in patients with type 2 diabetes mellitus: guidelines based on current evidence.
----A Hypertension and diabetes are becoming increasingly common. Most patients with both disorders have a markedly worsened risk for premature microvascular and macrovascular complications. The appropriate management of the hypertension seen in almost 70% of patients with type 2 diabetes mellitus remains controversial. However, over the past few years, many randomized, controlled trials have provided guidance for more effective therapy. These trials have established the need for a lower goal blood pressure (<130/80 mm Hg) than has previously been recommended. In addition, they have proven the efficacy of drugs from three major classes of antihypertensive agents; however, comparative trials have failed to show definite superiority of any particular class in either lowering blood pressure or reducing cardiovascular morbidity and mortality. To achieve therapy goals, multiple antihypertensive drugs are usually needed. On the basis of their apparent superiority in slowing diabetic nephropathy, angiotensin-converting enzyme inhibitors should probably be the first choice. Second and third choices should be a long-acting diuretic and a calcium-channel blocker or a beta-blocker, respectively. Attention should also be directed toward nonpharmacologic and pharmacologic control of hyperglycemia and dyslipidemia.
----P Journal_Article Review Review_Literature 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_therapy_MeSH Diabetic_Angiopathies_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Practice_Guidelines_MeSH M_Risk_Factors_MeSH 
****** 11748098
----K E
----T Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S.
----A BACKGROUND: Patients with low HDL cholesterol (HDL-C) and elevated triglyceride had an increased risk for coronary heart disease (CHD) events and received the greatest benefit with fibrate therapy in substudy analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study. METHODS AND RESULTS: In this post hoc analysis of the Scandinavian Simvastatin Survival Study, which enrolled patients with elevated LDL cholesterol (LDL-C) and CHD, subgroups defined by HDL-C and triglyceride quartiles were compared to examine the influence of HDL-C and triglyceride on CHD events and response to therapy. Patients in the lowest HDL-C (<1.00 mmol/L [39 mg/dL]) and highest triglyceride (>1.80 mmol/L [159 mg/dL]) quartiles (lipid triad; n=458) had increased proportions of other features of the metabolic syndrome (increased body mass index, hypertension, diabetes), men, prior myocardial infarction, prior revascularization, and beta-blocker use than patients in the highest HDL-C (>1.34 mmol/L [52 mg/dL]) and lowest triglyceride (<1.11 mmol/L [98 mg/dL]) quartiles (isolated LDL-C elevation; n=545). The major coronary event rate was highest in lipid triad patients on placebo (35.9%), and this subgroup had the greatest event reduction (relative risk 0.48, 95% CI 0.33 to 0.69); a significant treatment-by-subgroup interaction (P=0.03) indicated a greater treatment effect in the lipid triad subgroup than the isolated LDL-C elevation subgroup. CONCLUSIONS: Patients with elevated LDL-C, low HDL-C, and elevated triglycerides were more likely than patients with isolated LDL-C elevation to have other characteristics of the metabolic syndrome, had increased risk for CHD events on placebo, and received greater benefit with simvastatin therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_pathology_MeSH Coronary_Disease_pathology_MeSH M_Disease-Free_Survival_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Simvastatin_MeSH S_therapeutic_use_MeSH Simvastatin_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 11768738
----K 5
----T Carvedilol in the failing heart.
----A Patients with chronic heart failure due to left ventricular systolic dysfunction of ischemic or nonischemic etiology have shown improvement in morbidity and mortality with carvedilol therapy. In patients with symptomatic (New York Heart Association class II-IV) heart failure, carvedilol improves left ventricular ejection fraction and clinical status, and slows disease progression, reducing the combined risk of mortality and hospitalization. Despite the overwhelming evidence for their benefit, there continues to be a large treatment gap between those who would derive benefit and those who actually receive the drug. In this article, the pharmacology, clinical trial evidence, and the potential differences between carvedilol and other beta blockers are discussed. Carvedilol provides powerful therapy in the treatment of chronic heart failure caused by a variety of etiologies and in a wide array of clinical settings.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11751658
----K E
----T Longitudinal myocardial contraction improves early during titration with metoprolol CR/XL in patients with heart failure.
----A OBJECTIVE: To investigate diastolic and systolic left ventricular recovery during titration with metoprolol CR/XL (controlled release/extended release). DESIGN: Placebo run in, followed by an open study. SETTING: University hospital. PATIENTS: 14 patients with chronic heart failure. INTERVENTIONS: Metoprolol CR/XL titrated from 12.5 mg once daily to 200 mg once daily. Main outcome measures: M mode recordings of atrioventricular (AV) plane displacement, Doppler measurement of transmitral flow and pulmonary venous flow, two dimensional ejection fraction, and measurement of venous plasma concentration of noradrenaline. Patients were investigated after 2, 4, 6, and 24 weeks of treatment. RESULTS: A reduction of heart rate was observed on the first dose (12.5 mg once daily), from a mean (SD) of 74 (11) to 67 (11) beats/min, p < 0.05. This was accompanied by prominent effects on AV plane filling parameters, including an increase in early diastolic filling period from 87 (28) to 105 (33) ms (p < 0.05), and in the lateral AV plane fractional shortening from 8.7 (2.7)% to 10.2 (2.8)% (p < 0.05). An early trend towards improvement in global systolic left ventricular function was also seen, although this was not significant until six weeks. Ejection fraction increased from 33 (7.5)% to 38 (11)% (p < 0.05). CONCLUSIONS: First effects of left ventricular recovery during beta blocker treatment were seen in recordings of longitudinal performance, as expressed by AV plane displacement. Doppler flow dynamics as well as global systolic recovery appeared several weeks later, emphasising the importance of longitudinal performance in evaluating left ventricular function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Chronic_Disease_MeSH M_Delayed-Action_Preparations_MeSH M_Diastole_MeSH S_physiology_MeSH Diastole_physiology_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Systole_MeSH S_physiology_MeSH Systole_physiology_MeSH 
****** 11770869
----K E
----T Effect of sildenafil citrate upon myocardial ischemia in patients with chronic stable angina in therapy with beta-blockers.
----A BACKGROUND: It has been suggested that phosphodiesterase 5 (PDE5) inhibition is potentially hazardous and that it increases the risk of cardiac events in patients with coronary artery disease. This study sought to evaluate whether PDE5 inhibition with sildenafil exerts any effect on exercise-induced myocardial ischemia in patients on beta-blockers. METHODS: Fourteen patients underwent a baseline exercise test off-therapy and were then started on atenolol (100 mg once daily). After a run-in phase of 1 week, patients underwent a second exercise test and were randomized to receive either sildenafil (50 mg) or placebo given in a random order on two different occasions, 2 days apart. Exercise test was repeated 2 hours after the administration of sildenafil or placebo. RESULTS: All patients had a > 1 mm ST-segment depression while off-therapy. Eight patients had a negative exercise test response after atenolol, which was unaltered by the adjunct of either sildenafil or placebo. In the remaining subjects, atenolol significantly prolonged the time to 1 mm ST-segment depression and the exercise time. Sildenafil and placebo did not reverse the beneficial effect of atenolol upon exercise-induced myocardial ischemia. CONCLUSIONS: PDE5 inhibition does not worsen exercise capacity and exercise-induced myocardial ischemia in patients with chronic stable angina whose symptoms and exercise test response are well controlled by beta-blocker therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chronic_Disease_MeSH M_Drug_Interactions_MeSH M_Exercise_Test_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_contraindications_MeSH Phosphodiesterase_Inhibitors_contraindications_MeSH S_pharmacology_MeSH Phosphodiesterase_Inhibitors_pharmacology_MeSH M_Piperazines_MeSH S_contraindications_MeSH Piperazines_contraindications_MeSH S_pharmacology_MeSH Piperazines_pharmacology_MeSH 
****** 11755834
----K 4
----T A double-masked randomized comparison of the efficacy and safety of unoprostone with timolol and betaxolol in patients with primary open-angle glaucoma including pseudoexfoliation glaucoma or ocular hypertension. 6 month data.
----A PURPOSE: A long-term comparison of the ocular hypotensive efficacy and safety of unoprostone isopropyl 0.15% twice daily with that of timolol maleate 0.5% twice daily and betaxolol HCl 0.5% twice daily.DESIGN: This was a randomized, multicenter, double-masked, active-controlled 24-month clinical trial involving 27 centers in Europe and Israel. METHODS:The study population was composed of patients with primary open-angle glaucoma (including pseudoexfoliation) or ocular hypertension. After washout of antiglaucoma medications, intraocular pressure (IOP) was measured at 0, + 2, + 8, and + 12 hours. Patients were randomized in a 2:1:1 ratio to unoprostone, timolol, or betaxolol. Patients returned for examinations at 2 and 6 weeks and 3 and 6 months. RESULTS: 556 patients were randomized. Each drug produced a clinically and statistically (P <.001) significant reduction from baseline in 12-hour diurnal IOP at month 6 (- 4.3 mm Hg, unoprostone; - 5.8 mm Hg, timolol; - 4.9 mm Hg, betaxolol). Differences in adjusted treatment means between unoprostone and timolol and unoprostone and betaxolol were 1.57 mm Hg (95% CI: 1.00, 2.13) and 0.53 mm Hg (95% CI: - 0.03, 1.09), respectively. Unoprostone was clinically equivalent to betaxolol but did not have as great an IOP-lowering effect as timolol. Discontinued for inadequate control of IOP were 7%, 1%, and 4% of the patients for unoprostone, timolol, and betaxolol, respectively. There were no changes of note in visual acuity, pupil size, cup-to-disk ratio, visual fields, or iris color. Changes in heart rate and blood pressure were small, with no clinically significant differences between groups. CONCLUSIONS: Unoprostone provided a clinically significant IOP-lowering effect equivalent to betaxolol but not to timolol. The side effect profile of unoprostone appears to be comparable to other established IOP-lowering agents.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Betaxolol_adverse_effects_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dinoprost_MeSH S_administration_&_dosage_MeSH Dinoprost_administration_&_dosage_MeSH S_adverse_effects_MeSH Dinoprost_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Dinoprost_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Dinoprost_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Exfoliation_Syndrome_MeSH S_drug_therapy_MeSH Exfoliation_Syndrome_drug_therapy_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Pupil_MeSH S_drug_effects_MeSH Pupil_drug_effects_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Visual_Acuity_MeSH S_drug_effects_MeSH Visual_Acuity_drug_effects_MeSH M_Visual_Fields_MeSH S_drug_effects_MeSH Visual_Fields_drug_effects_MeSH 
****** 11777294
----K 5
----T Migraine: assessment and management.
----A Headaches occur at some time in the vast majority of the population. For most people headaches are a nuisance but for some they can be disabling. Two per cent of the population at any time have chronic daily headache, with or without analgesic dependence, but most disabling headaches are intermittent and migranous in nature. Before hoping to make an appropriate intervention, an accurate diagnosis must be made.The first part of this paper examines the differential diagnosis and in particular separates benign from sinister, acute from chronic and tension-type from migranous. The second half focuses on the management of migraine. An individualised approach is usually the most effective, with the patient drawing from the broad areas of attention to trigger factors and lifestyle, finding an acute or rescue medication that consistently returns them to normal activities within a few hours, and prophylaxis to reduce the rate of attack by 50% in those with high frequency migraine. The expession of migraine may well vary during an individual's life and in order to achieve the best lifelong control, adjustment of the blend of management options may be needed. The aim of the adviser is to enable patients to feel in control of their migraine rather than feeling that migraine controls them.
----P Journal_Article Review Review__Tutorial 
----M M_Analgesics_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Diagnosis__Differential_MeSH M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH 
****** 11773911
----K E
----T Clinical features and outcomes of elderly outpatients with heart failure followed up in hospital cardiology units: data from a large nationwide cardiology database (IN-CHF Registry).
----A BACKGROUND: Congestive heart failure (HF) represents a major public health problem with an age-related increasing prevalence. Despite the high mortality and morbidity in elderly patients with HF, limited clinical and prognostic data are available for development of appropriate prevention and treatment strategies. METHODS: A cohort of 3327 outpatients consecutively enrolled in the Registry of Italian Network on Congestive Heart Failure by 133 cardiology centers was studied. Univariate and multivariate analyses were performed to compare patients <70 and > or =70 years old and to evaluate associations between clinical variables and the 1-year mortality rate and hospitalizations. RESULTS: With respect to the 2294 patients <70 years old, the 1033 (31%) elderly patients were significantly more likely to be female, to be in New York Heart Association (NYHA) class III-IV, and to have preserved left ventricular systolic function (ejection fraction >40%), an ischemic/valvular etiology, and atrial fibrillation/flutter. Elderly patients received angiotensin-converting enzyme inhibitors, beta-blockers, and anticoagulants less frequently than younger patients did. The 1-year mortality rate was significantly higher in patients > or =70 years old (22% vs 13.7%, P <.001). Age was an independent predictor of 1-year mortality, increasing 2.8% by each year of age. Independent predictors of 1-year mortality in elderly patients were (1) > or =1 hospital admission in the previous year (relative risk [RR] 2.09, 95% CI 1.51-2.87), (2) systolic blood pressure (RR 0.98, 95% CI 0.97-0.99), (3) NYHA class III-IV (RR 1.57, 95% CI 1.20-2.07), and (4) age (RR 1.028, 95% CI 1.001-1.056). CONCLUSIONS: Our study confirms that elderly patients (1) are seen in a more advanced stage of HF, (2) are less likely to receive evidence-based treatments, (3) show more frequently preserved systolic function, and (4) have a worse prognosis. Consequently, there is a need to develop more effective and targeted management strategies for this escalating health problem.
----P Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Child_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Databases__Factual_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Outpatients_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11773912
----K E
----T Acute myocardial infarction in the young--The University of Michigan experience.
----A BACKGROUND: The purpose of this study was to assess frequency, risk factors, treatment, and complications of very young patients with acute myocardial infarction (MI) at the University of Michigan Medical Center (UMMC). METHODS: From a database of 976 consecutive patients admitted to the UMMC with acute MI between 1995 and 1998, we compared care and outcomes of patients divided into 3 age categories: <46 years, 46-54 years, and >54 years. Risk factors, presenting symptoms, type of MI, management, complications, and hospital outcomes of the 3 groups were evaluated. RESULTS: Young patients represented >10% of all patients with acute MI, and >25% of these individuals were women, a number considerably higher than seen in previous studies. This group of young patients was more likely to have Q-wave MI and risk factors such as family history and tobacco use and less likely to have a history of angina. Although all 3 groups received similar inpatient treatment, there was more attention paid to risk factor modification such as smoking cessation and referral to cardiac rehabilitation in younger individuals. Young patients had fewer in-hospital complications and a lower mortality rate. CONCLUSIONS: At the University of Michigan, >1 in 10 with acute MI is <46 years old. Data suggest that current management and aggressive risk factor modification are quite good in this particular group, and overall the mortality rate is very low.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_epidemiology_MeSH Hyperlipidemia_epidemiology_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Male_MeSH M_Michigan_MeSH S_epidemiology_MeSH Michigan_epidemiology_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH S_epidemiology_MeSH Smoking_epidemiology_MeSH 
****** 11780330
----K E
----T Relationship between age and effect of early and long-term captopril treatment in patients with acute myocardial infarction.
----A OBJECTIVE: To analyse the relationship between age and treatment with captopril after acute myocardial infarction (AMI). METHODS: In a randomized trial, 822 patients with a first AMI received conventional medical treatment, including intravenous thrombolytic therapy and oral aspirin or metoprolol, and then were randomly allocated to captopril [dosage from the first 6.25 mg to 25 mg/t.i.d, 209 younger patients (< or = 64 years), 269 elderly patients (65-75 years)] or conventional treatment only (131 younger patients, 213 elderly). Survival in the four groups was calculated with the Kaplan-Meier method. Multivariate analysis was performed to understand the degree that multi-variables (including age) affect survival in patients taking captopril in the hospital or during long term follow-up. RESULTS: The survival of patients who took captopril correlated significantly with age (P < 0.001). The survival of the elderly patients on captopril treatment did increase (P < 0.0001), but not of the younger ones (P > 0.05) during hospitalization. During follow-up, the survival of patients who took captopril correlated insignificantly with age (P > 0.05), but both the elderly and the younger patients have good survival rates (all P < 0.01) and lower cardiac events (all P < 0.01) when they took captopril. CONCLUSIONS: Captopril exerts a weak effect on the younger patients but a beneficial effect on the elderly patients during hospitalization after AMI. However, there is no difference between the younger and the elderly in the prognosis, both having good survival and lower cardiac events when they take captopril long term during follow-up.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11783600
----K E
----T Treatment of IgA nephropathy with angiotensin converting enzyme inhibitors: design of a prospective randomized multicenter trial.
----A Although several in vitro studies and clinical observations suggest that ACE-inhibitors (ACE-I) are a promising treatment for IgA nephropathy (IgAN), meta-analysis of published data is not yet conclusive. Therefore, a European double-blinded, prospective, randomized therapeutic trial was designed to evaluate ACE-I treatment benefits in young IgAN patients (<35 years old) with persistent moderate proteinuria (>1<3.5 g/day/1.73 m2) and fair renal function (creatinine clearance >50 mL/min/1.73 m2). Patients enrolled are randomly assigned to benazepril (0.2 mg/kg/day) or placebo. Patients should be enrolled within a five year recruitment period (end on December 2003) for a total duration of follow-up of six years (end on December 2004). Hypertension and some genetic, histological and immunological factors will be evaluated to clarify their eventual role in the final response to ACE-I treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Benzazepines_MeSH S_therapeutic_use_MeSH Benzazepines_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerulonephritis__IGA_MeSH S_drug_therapy_MeSH Glomerulonephritis__IGA_drug_therapy_MeSH S_urine_MeSH Glomerulonephritis__IGA_urine_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11782853
----K E
----T Dose-related effects of metoprolol on heart rate and pharmacokinetics in heart failure.
----A BACKGROUND: The pharmacokinetics and pharmacodynamics of immediate-release (IR) metoprolol, 50 mg 3 times daily, were compared with those of different doses of controlled-release/extended-release metoprolol (CR/XL) given once daily. METHODS AND RESULTS: Fifteen patients with chronic heart failure were randomized to a 3-way crossover study to receive metoprolol IR 50 mg 3 times daily, CR/XL 100 mg once daily, and CR/XL 200 mg once daily for 7 days. On the seventh day of each treatment, serial plasma samples were drawn and standardized exercise tests and a 24-hour Holter recording were performed. Metoprolol IR 50 mg produced peak plasma levels comparable to those observed for CR/XL 200 mg (285 v 263 nmol/L). The difference in mean 24-hour heart rate between CR/XL 100 mg and IR 50 mg was 1.0 bpm (95% confidence interval [CI]), -2.9 to 4.9; NS) compared with -3.8 bpm (95% CI, -7.6 to -0.04; P = .048) between CR/XL 200 mg and IR 50 mg. Submaximal exercise heart rate was lower for patients receiving CR/XL 200 mg than those receiving IR 50 mg. No difference in tolerance or exercise performance was observed between treatment regimens. CONCLUSIONS: Peak plasma levels produced by metoprolol 200 mg CR/XL were similar to those of 50 mg IR. Metoprolol CR/XL 200 mg was associated with a more pronounced suppression of heart rate than metoprolol IR 50 mg. It is suggested that patients can safely be switched from multiple dosing of metoprolol IR 50 mg to a once-daily dose of metoprolol CR/XL.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_blood_MeSH Metoprolol_blood_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11787477
----K E
----T The gain-of-function G389R variant of the beta1-adrenoceptor does not influence blood pressure or heart rate response to beta-blockade in hypertensive subjects.
----A Mutation scanning of the beta1-adrenoceptor gene has identified a polymorphism, G389R, that markedly affects G-protein coupling of the receptor and resulting cAMP production. We have investigated the effect of this functionally active polymorphism on clinical response to beta-adrenoceptor blockade. Two cohorts of untreated hypertensive patients randomly assigned to a beta1-selective beta-blocker at the start of antihypertensive therapy were studied retrospectively to see if the G389R polymorphism influenced the response in terms of blood pressure and heart rate. The blood pressure and heart rate responses to treatment were assessed 4 weeks later and compared with the G389R genotype, ascertained by PCR/restriction fragment length polymorphism. The falls in blood pressure and heart rate for the first group (n = 92) by genotype were: GG, 20.1 +/- 3.5/13.9 +/- 2.7 mmHg (systolic/diastolic blood pressure), 18.4 +/- 2.2 beats/min; GR, 20.0 +/- 2.2/15.0 +/- 1.3 mmHg, 16.5 +/- 1.5 beats/min; RR, 20.8 +/- 2.3/13.4 +/- 1.1 mmHg, 16.0 +/- 1.4 beats/min. For the second group (n = 55) the corresponding falls were: GG, 17.0 +/- 4.3/11.2 +/- 3.4 mmHg, 12.0 +/- 3.5 beats/min; GR, 16.6 +/- 1.8/14.4 +/- 1.1 mmHg, 13.1 +/- 2.1 beats/min; RR, 18.0 +/- 1.6/13.0 +/- 1.4 mmHg, 14.4 +/- 1.4 beats/min. The G389R genotype also failed to have a significant effect on pretreatment blood pressure or heart rate in either group. These data suggest that, despite clear functional differences between the G389R receptor variants expressed in vitro, the polymorphism does not affect the haemodynamic response of hypertensive subjects to chronic beta1-adrenoceptor blockade.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_genetics_MeSH Blood_Pressure_genetics_MeSH M_Female_MeSH M_Genotype_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_genetics_MeSH Heart_Rate_genetics_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Polymorphism_(Genetics)_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_genetics_MeSH Receptors__Adrenergic__beta-1_genetics_MeSH S_physiology_MeSH Receptors__Adrenergic__beta-1_physiology_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 11788225
----K I
----T Evidence-based evaluation of calcium channel blockers for hypertension: equality of mortality and cardiovascular risk relative to conventional therapy.
----A OBJECTIVES; We present a meta-analysis based on three recent, substantial, randomized outcome trials and several smaller trials that compared calcium channel blockers (CCBs) with conventional therapy (diuretics or beta-blockers) or with angiotensin-converting enzyme (ACE) inhibitors. BACKGROUND: There is continuing uncertainty about the safety and efficacy of CCBs in the treatment of hypertension. Previous meta-analyses conflict and suggest that CCBs increase myocardial infarction (MI) or protect from stroke. METHODS: Standard procedures for meta-analysis were used to analyze three major trials on 21,611 patients and another three lesser studies to a total of 24,322 patients. RESULTS: Calcium channel blockers have a strikingly similar risk of total and cardiovascular mortality and of major cardiovascular events to conventional therapy. Calcium channel blockers give a lower risk of nonfatal stroke (-25%, p = 0.001) and a higher risk of total MI (18%, p = 0.013), chiefly nonfatal (18%). After performing the Bonferroni correction for multiplicity, these p values become 0.004 and 0.052, respectively. When compared with ACE inhibitors in 1,318 diabetic patients, CCBs had a substantially higher risk of nonfatal (relative risk [RR] = 2.259) and total MI (RR = 2.204, confidence interval 1.501 to 3.238; p = 0.001 or 0.004 with Bonferroni correction). Total and cardiovascular mortality rates are similar. To confirm the hypothesis that ACE inhibitors are superior to CCBs in diabetic patients requires more trial data, especially with renal end points. CONCLUSIONS: Mortality (total and cardiovascular) and major cardiovascular events with CCBs were apparently similar to those events seen with conventional first-line therapy (diuretics or beta-blockers). Stroke reduction more than balanced increased MI. In diabetics, CCBs may be less safe than ACE inhibitors.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_complications_MeSH Cerebrovascular_Accident_complications_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH M_Comparative_Study_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11790928
----K E
----T Do ACE inhibitors or angiotensin II antagonists reduce total mortality and arrhythmic mortality? A critical review of controlled clinical trials.
----A ACE-inhibitors (ACE-I) represent effective drugs more and more widely used in acute myocardial infarction (AMI) patients, in post AMI patients and mainly, today, in CHF patients.A complete review of the scientific literature and of all the randomized controlled clinical trials (RCTs), where ACE-I have been tested directly or in association with other drugs, have been performed. ACE-I effects on total mortality (TM) and arrhythmic mortality (AM) and other composite clinical endpoints have been evaluated.It is well known that frequent ventricular arrhythmias (VA) and a high incidence of sudden death (SD) can be documented in CHF patients; nevertheless a direct relationship between VA, TM, and AM has not been clearly demonstrated; neither beneficial effects, on the same endpoints, of the treatment and suppression of ambient VA in CHF. Conversely, sometimes clear negative effects on both TM and AM have been observed.According to individual studies and two recent complete and large metanalysis, ACE-I were unable to reduce AM, but they reduced TM. Furthermore, they can affect and modify many, if not all, of the triggering factors of VA and SD in this context.Differently from ACE-I, betablockers (BB) have been clearly associated with a reduction in TM and AM, in the same context. Thus, at present time, ACE-I, with or without BB, should be considered the standard therapy in all patients with CHF, if not contraindicated.Angiotensin II antagonists (AII-a) probably represent a comparably effective treatment, in all CHF patients and mainly in those patients, suffering from side effects or showing intolerance to ACE-I, but we are still lacking definitive data from RCTs.In many RCTs, conducted with traditional antiarrhythmic drug therapy (ADT), these drugs have been widely used, contributing probably, in a consistent way, to some of the positive results of these studies. All primary and some secondary implantable defibrillators (ICD) RCTs, in the prevention of SD, have included these drugs as the standard treatment of the underlying cardiac disease, with or without CHF. The same therapeutical strategy is regularly applied in all biventricular pacing (BP) RCTs, with or without the ICD. These trials are supposed to assess the reduction in TM and AM, preventing deterioration or progression of CHF and improving the quality of the patients' s life.Finally, according to these clinical evidences, in the last part of the review, we stress the need for a more widespread implementation of ACE-I and AII-a in treating CHF patients.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin_II_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH S_mortality_MeSH Arrhythmia_mortality_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Cardiac_Pacing__Artificial_MeSH M_Combined_Modality_Therapy_MeSH M_Defibrillators__Implantable_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Prevalence_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11791022
----K E
----T The relation of anger expression with blood pressure levels and hypertension in rural and urban Japanese communities.
----A OBJECTIVE: To examine the relation of anger expression with blood pressure and hypertension among Japanese. DESIGN: A cross-sectional study. METHODS: Subjects were 4374 men and women aged 30-74 years from rural and urban communities. Anger expression was estimated using the anger-out and anger-in scores of the Spielberger Anger Expression Scale. Multiple linear regression analyses were performed to estimate the associations of anger expression scores with blood pressure. Proportions of hypertensives among the tertiles of anger expression scores and the relative odds of hypertension for low versus high tertiles of anger expression scales were calculated using logistic regression models. RESULTS: The anger-out score was inversely associated with systolic and diastolic blood pressure levels for men; a four-point (one standard deviation) lower anger-out score was associated with 1.6 mmHg [95% confidence interval (CI), 0.6-2.6] greater systolic blood pressure and 0.6 mmHg (95% CI, -0.03 to 1.2) greater diastolic pressure after adjustment for age, body mass index, alcohol intake, smoking category, and parental history of hypertension. The adjusted relative odds of hypertension for low versus high tertiles of anger-out was 1.60 (95% CI, 1.19-2.15). These inverse associations were more evident among men with low coping behavior than among those with high coping behavior. For women, the anger-out score was not associated with blood pressure. There was no relation between the anger-in score and either blood pressure or hypertension in either men or women. CONCLUSIONS: This study suggests that Japanese men who do not express their anger, especially when they have low coping behavior, may have an increased risk of high blood pressure.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Anger_MeSH S_physiology_MeSH Anger_physiology_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Japan_MeSH S_epidemiology_MeSH Japan_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Prevalence_MeSH M_Rural_Health_MeSH M_Rural_Population_MeSH M_Sex_Factors_MeSH M_Statistics_MeSH M_Urban_Health_MeSH 
****** 11791028
----K E
----T Effect of crossing over hypertensive patients from a beta-blocker to an angiotensin receptor antagonist on resistance artery structure and on endothelial function.
----A BACKGROUND: Treatment of essential hypertensive patients with an AT1 angiotensin receptor antagonist has previously resulted in correction of resistance artery structure and endothelial function, whereas in a parallel group treated with the beta-blocker atenolol there was no improvement of altered vascular structure and function. To test the hypothesis that patients previously treated with atenolol could present improvement of vascular structure and endothelial function if they were subjected to blockade of the renin-angiotensin system, we crossed over hypertensive patients that had been randomized to treatment with the beta-blocker atenolol to treatment with the AT1 antagonist irbesartan, and studied small artery structure and endothelial function before and after treatment. METHODS: Eleven essential hypertensive patients (51 +/- 2 years, range 38-65; 75% male) that had previously been randomized to treatment with atenolol and treated for 1 year with good blood pressure control, were crossed over to treatment with the AT1 antagonist irbesartan for 1 year. Small resistance arteries were dissected from gluteal subcutaneous biopsies that were performed before and after 1 year of treatment. The structure and endothelial function of the resistance arteries were studied on a pressurized myograph. RESULTS: Blood pressure control (129 +/- 3.3/85 +/- 1.8 mmHg) was identical to that achieved previously with atenolol (131 +/- 3.3/84 +/- 1.1 mmHg). Following 1 year of treatment, the arterial media width to lumen ratio (M/L) of resistance arteries (lumen diameter, 150-350 microm), which had remained unchanged under atenolol treatment, decreased from 8.44 +/- 0.45% when patients were on atenolol, to 6.46 +/- 0.30%, P < 0.01, when patients received irbesartan. Maximal acetylcholine-induced endothelium-dependent relaxation was 81.1 +/- 4.1% when patients were on atenolol, unchanged from before starting treatment with the beta-blocker, and was normalized by irbesartan (to 94.8 +/- 2.0%, P < 0.01). CONCLUSION: Crossing over essential hypertensive patients with well-controlled blood pressure from the beta-blocker atenolol to the AT1 receptor antagonist irbesartan resulted in correction of previously persistently altered vascular structure and endothelial function, suggesting a structural and endothelial vascular protective effect of antihypertensive treatment with the AT1 receptor antagonist.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_therapeutic_use_MeSH Acetylcholine_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_antagonists_&_inhibitors_MeSH Biphenyl_Compounds_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiology_MeSH Endothelium__Vascular_physiology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroprusside_MeSH S_therapeutic_use_MeSH Nitroprusside_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Receptors__Angiotensin_therapeutic_use_MeSH M_Sensitivity_and_Specificity_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_antagonists_&_inhibitors_MeSH Tetrazoles_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 11792127
----K I
----T First-line treatment for hypertension.
----A AIMS: To assess the effects of pravastatin on all-cause mortality and cause-specific mortality and to compare the effects for patients with prior coronary heart disease with those for patients without, using pooled data from the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study, the Cholesterol and Recurrent Events (CARE) study, and the West of Scotland Coronary Prevention Study (WOSCOPS). METHODS AND RESULTS: 13 173 patients with coronary heart disease and 6595 men with elevated cholesterol and no prior coronary disease received pravastatin, 40 mg daily, or placebo for an average of 5 to 6 years. Data were analysed according to a pre-specified, published protocol. For all three trials combined, the mortality among patients assigned pravastatin was significantly lower, at 7.9%, than the 9.8% among those assigned placebo, a relative risk reduction of 20% (95% confidence interval (CI) 12-27%, P<0.0001). Active treatment was associated with a reduction in coronary mortality (24%, 95% CI 14-33%). Larger reductions in absolute risk were estimated in those with prior coronary heart disease than in those without. CONCLUSION: Treatment with pravastatin over 5 years reduces all-cause mortality and coronary mortality in patients with and those without a history of coronary heart disease. The size of the benefit was related principally to the baseline risk.
----P Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Meta-Analysis_MeSH M_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11796456
----K 5
----T The pharmacologic treatment of uncomplicated arterial hypertension in patients with airway dysfunction.
----A Because many antihypertensive drugs can affect airway function, the treatment of hypertension in patients with airway dysfunction is complex. For example, the worsening or precipitation of asthma by beta-adrenoceptor antagonists is well-recognized, but beta(1)-adrenoceptor blockers that exert mild beta(2)-agonist effects, and those that modulate the endogenous production of nitric oxide, affect airway function to a lesser extent. Therapy with selective alpha(1)-blockers is not contraindicated in cases of chronic airway obstruction. Conversely, alpha(2)-agonists must not be given to asthmatic subjects because they can adversely affect the bronchi. Calcium channel blockers do not exert severe side effects on the airways. Angiotensin-converting enzyme inhibitors may cause cough and exacerbate or even induce asthma; however, angiotensin II type I (AT(1)) antagonists do not cause cough. 5-Hydroxytryptamine modifiers such as urapidil are a treatment option for patients with chronic airway obstruction. In patients with airway dysfunction, we suggest treatment with thiazide diuretics as the initial drug choice, and calcium channel blockers if the response is poor. In the case of no response, calcium channel blockers alone must be used. However, there is no strict rule because individual patients may respond differently to individual drugs and drug combinations. Consequently, it is important to adopt a flexible approach. For patients who are unresponsive to the aforementioned drugs, AT(1) receptor antagonists, newer beta(1)-adrenoceptor-blocking agents with ancillary properties (eg, celiprolol or nebivolol), and/or vasodilators can be considered.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Asthma_MeSH S_chemically_induced_MeSH Asthma_chemically_induced_MeSH M_Comparative_Study_MeSH M_Cough_MeSH S_chemically_induced_MeSH Cough_chemically_induced_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11801805
----K 5
----T Migraines.
----A A 26-year-old woman is evaluated for headaches, which began when she was 14 years old. She states that she initially sees bright zig-zag bands, which expand in the shape of a horseshoe in her right visual field. Twenty minutes later, she develops a throbbing headache over the left frontal area, associated with photophobia and nausea. The headaches last 1-3 days and they occur once a month. There is no medical history, and she takes only multivitamin supplements. Her sister has been diagnosed with migraines. Her examination is normal, including equal and reactive pupils, full extraocular movements, and normal strength and sensation. A magnetic resonance scan of the brain shows no abnormalities.
----P Case_Reports Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analgesics__Non-Narcotic_MeSH S_adverse_effects_MeSH Analgesics__Non-Narcotic_adverse_effects_MeSH S_therapeutic_use_MeSH Analgesics__Non-Narcotic_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Botulinum_Toxins_MeSH S_therapeutic_use_MeSH Botulinum_Toxins_therapeutic_use_MeSH M_Classic_Migraine_MeSH S_diagnosis_MeSH Classic_Migraine_diagnosis_MeSH S_drug_therapy_MeSH Classic_Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Classic_Migraine_prevention_&_control_MeSH M_Contraceptives__Oral__Hormonal_MeSH S_adverse_effects_MeSH Contraceptives__Oral__Hormonal_adverse_effects_MeSH S_therapeutic_use_MeSH Contraceptives__Oral__Hormonal_therapeutic_use_MeSH M_Dihydroergotamine_MeSH S_adverse_effects_MeSH Dihydroergotamine_adverse_effects_MeSH S_therapeutic_use_MeSH Dihydroergotamine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Serotonin_Agonists_MeSH S_adverse_effects_MeSH Serotonin_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH 
****** 11801272
----K 4
----T Primary drug treatment for glaucoma: beta-blockers versus other medications.
----A This set of Viewpoints articles examines the merits of beta-blockers versus other medications as the primary drug treatment for glaucoma. Ophthalmologists must balance issues such as efficacy, compliance, cost, and side effects when deciding on the appropriate medication to prescribe. Dr. Stamper stresses the advantages of tailoring the choice of medication to the needs of the individual patient. Drs. Wigginton and Higginbotham review the benefits of beta-blockers and present some of the disadvantages of the non-beta-blocker class of medications.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_economics_MeSH Adrenergic_alpha-Agonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_economics_MeSH Carbonic_Anhydrase_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Drug_Costs_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Ophthalmic_Solutions_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Patient_Compliance_MeSH M_Prostaglandins_MeSH S_adverse_effects_MeSH Prostaglandins_adverse_effects_MeSH S_economics_MeSH Prostaglandins_economics_MeSH S_therapeutic_use_MeSH Prostaglandins_therapeutic_use_MeSH 
****** 11804300
----K E
----T Difference in the occurrence of cardiovascular events according to class of antihypertensive agent, based on a follow-up study of Japanese hypertension patients.
----A We conducted a nested case-control study to evaluate the relationship between antihypertensive agent class and the incidence of initial cardiovascular events. A total of 7.443 patients being treated with an antihypertensive agent in 1985-1986 were enrolled for follow-up of up to 5 years. A total of 362 patients (186 males and 176 females) developed cardiovascular events. Age (5-year interval) and sex-matched controls were then randomly selected. A Multiple logistic regression analysis was done to control for the effects of confounding factors. The results showed that the use of diuretics and beta-blockers was associated with a reduced risk of cardiovascular events (odds ratio [OR] =0.65, 95% confidence interval [CI]: 0.49-0.86, and OR=0.75, 95% CI: 0.56-1.02, respectively), against a significantly raised risk associated with the use of calcium antagonists (OR=1.34, 95% CI: 1.03-1.80). However, as far as stroke was concerned, there was no significant association of risk with the use of any agent. The control group was found to be similar to the case group with respect to the changes in the treatment program during the follow-up period. The results suggest that the calcium antagonists used in Japan during the period of 1985-1990 constituted a potential risk for the occurrence of cardiovascular events.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH M_Case-Control_Studies_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH 
****** 11805171
----K 5
----T Megalin and cubilin are endocytic receptors involved in renal clearance of hemoglobin.
----A The kidney is the main site of hemoglobin clearance and degradation in conditions of severe hemolysis. Herein it is reported that megalin and cubilin, two epithelial endocytic receptors, mediate the uptake of hemoglobin in renal proximal tubules. Both receptors were purified by use of hemoglobin-Sepharose affinity chromatography of solubilized renal brush-border membranes. Apparent dissociation constants of 1.7 microM for megalin and 4.1 microM for cubilin were determined by surface plasmon resonance analysis. The binding was calcium dependent in both cases. Uptake of fluorescence-labeled hemoglobin by BN-16 cells was inhibited by anti-megalin and anti-cubilin antibodies as well as by receptor-associated protein, a chaperone for LDL-receptor family proteins. Partial inhibition by myoglobin was observed, whereas bovine serum albumin, intrinsic factor-cobalamin complexes, and beta2-microglobulin did not affect the uptake. By use of immunohistochemistry, it was demonstrated that uptake of hemoglobin in proximal tubules of rat, mouse, and dog kidneys occurs under physiologic conditions. Studies on normal and megalin knockout mouse kidney sections showed that megalin is responsible for physiologic clearance of hemoglobin. Labeling intensities in kidneys from normal and cubilin-malexpressing dogs were similar, which suggests that, in the normal state, the role of cubilin in uptake of hemoglobin is rather limited. However, cubilin is likely to assist hemoglobin endocytosis in settings of hemoglobinuria. In conclusion, the study provides a molecular explanation for long-standing observations of hemoglobin uptake in renal proximal tubules that involve the endocytic receptors megalin and cubilin. The findings may prove to be essential for further research on the pathophysiology of hemoglobinuric acute renal failure and proteinuria-associated tubulointerstitial nephritis.
----P Journal_Article 
----M M_Absorption_MeSH M_Animals_MeSH M_Cell_Line_MeSH M_Chromatography__Affinity_MeSH M_Dogs_MeSH M_Fluoresceins_MeSH M_Fluorescent_Dyes_MeSH M_Hemoglobins_MeSH S_metabolism_MeSH Hemoglobins_metabolism_MeSH M_Immunohistochemistry_MeSH M_Kidney_MeSH S_metabolism_MeSH Kidney_metabolism_MeSH M_LDL-Receptor_Related_Protein_2_MeSH S_genetics_MeSH LDL-Receptor_Related_Protein_2_genetics_MeSH S_metabolism_MeSH LDL-Receptor_Related_Protein_2_metabolism_MeSH M_Mice_MeSH M_Mice__Knockout_MeSH S_genetics_MeSH Mice__Knockout_genetics_MeSH M_Microvilli_MeSH S_metabolism_MeSH Microvilli_metabolism_MeSH M_Rats_MeSH M_Receptors__Cell_Surface_MeSH S_metabolism_MeSH Receptors__Cell_Surface_metabolism_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Transport_Vesicles_MeSH S_metabolism_MeSH Transport_Vesicles_metabolism_MeSH 
****** 11806165
----K 5
----T Updates in nephrology. A summary of common diagnoses encountered in the clinical practice.
----A This article includes a review of hypertension, nephrolithiasis and cystic diseases of the kidney, all quite common diagnoses. These days, as concerns are growing, some are considering diabetes mellitus to be a national epidemic. Thus, our entire article focuses on the diabetic renal disease. The current approach to the diagnosis and treatment of acute renal failure and chronic renal insufficiency is discussed, including treatment modalities such as dialysis and transplantation. This article is not at all intended to be a comprehensive review of each topic included, but rather it is an attempt to make the reader more familiar with the fascinating and continuously evolving field of nephrology.
----P Journal_Article Review Review__Tutorial 
----M M_Female_MeSH M_Forecasting_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Kidney_Diseases_MeSH S_diagnosis_MeSH Kidney_Diseases_diagnosis_MeSH S_therapy_MeSH Kidney_Diseases_therapy_MeSH M_Male_MeSH M_Nephrology_MeSH S_standards_MeSH Nephrology_standards_MeSH S_trends_MeSH Nephrology_trends_MeSH M_United_States_MeSH 
****** 11809349
----K E
----T Which patients with unstable angina or non-Q-wave myocardial infarction should have immediate cardiac catheterization? A clinical decision rule for predicting who will fail medical therapy.
----A Unstable angina and non-Q-wave myocardial infarction (MI) are common and costly clinical events, but there is considerable uncertainty about optimal clinical management of these syndromes. We developed a prediction rule to help clinicians determine which patients with unstable angina or non-Q-wave MI are likely to "fail" medical therapy and ultimately require cardiac catheterization within 6 weeks of presentation. Subjects were 733 patients presenting with unstable angina or non-Q-wave MI enrolled in the TIMI IIIB trial and randomized to initial medical management. We developed a prediction rule based on logistic regression analysis of baseline data from history, physical examination, electrocardiogram, and blood studies. The outcome of interest was "failure" of medical therapy, defined as need for coronary catheterization within 42 days. Significant predictors of "failing" medical therapy included ST segment depression >or= .1 mV (odds ratio, OR, = 2.7, 95% confidence interval, CI, 1.8-4.1), accelerated angina in the prior 2 months (OR = 1.8, 95% CI 1.2-2.6), nitrate use in the prior week (OR = 1.6, 95% CI 1.1-2.2), exertional angina in the prior 2 months (OR = 1.6, 95% CI 1.1-2.2), and cardiac troponin I (cTnI) >or= 0.4 ng/mL (OR = 1.4, 95% CI 1.1-1.9). We used these variables to build a risk score by assigning point values based on these ORs. The risk score had a moderate ability to predict which patients would subsequently fail medical therapy and undergo cardiac catheterization (c = 0.682). Out of a total risk score of 13, failure of medical therapy occurred in 86% of patients who had a risk score >or= 8 (n = 111), 78% of patients who had a risk score >or= 6 (n = 240), and 72% of patients who had a risk score >or= 4 (n = 438). At scores of < 2 (n = 88), 40% of patients failed medical therapy. Although the management of unstable angina is in constant evolution, clinicians will always be faced with determining which patients should be managed most invasively. The simple prediction rule we present can be applied to patients with unstable angina or non-Q-wave MI at the time of presentation to predict which patients have a high probability of failing medical therapy. Such a rule may be useful for identifying patients who should be considered for early cardiac catheterization.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Decision_Support_Techniques_MeSH M_Female_MeSH P_Heart_Catheterization_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Predictive_Value_of_Tests_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Failure_MeSH 
****** 11810791
----K I
----T [Are newer antihypertensive agents better than the older ones? Results of trials (CAPPP, STOP-2, NORDIL, INSIGHT and ALLHAT) with newer antihypertensive agents]
----A Until recently, no morbidity-mortality study had examined the effects of "newer" drugs, like angiotensin-converting enzyme inhibitors, calcium antagonists, and alpha-blockers compared to "old", but well-proven, thiazide diuretics, and beta-blockers in the treatment of essential hypertension. The prospective and randomised clinical trials, CAPPP, STOP-2, NORDIL, INSIGHT, and one arm of ALLHAT, with a total of about 58,000 middle-aged or elderly hypertensive patients have now been published. The primary outcome, composite cardiovascular (CV) death, cerebral stroke, and myocardial infarction, or composite fatal coronary heart disease and myocardial infarction, was the same, irrespective of the drug in all trials. Thus, prevention of CV complications depends on the lowering of blood pressure with well-tolerated medication, irrespective of class.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11812667
----K E
----T Neurohormonal activation in heart failure after acute myocardial infarction treated with beta-receptor antagonists.
----A BACKGROUND: Few studies have described how neurohormonal activation is influenced by treatment with beta-receptor antagonists in patients with heart failure after acute myocardial infarction. The aims were to describe neurohormonal activity in relation to other variables and to investigate treatment effects of a beta(1) receptor-antagonist compared to a partial beta(1) receptor-agonist. METHODS: Double-blind, randomized comparison of metoprolol 50-100 mg b.i.d. (n=74), and xamoterol 100-200 mg b.i.d (n=67). Catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), renin activity, and N-terminal pro-atrial natriuretic factor (N-ANF) were measured in venous plasma before discharge and after 3 months. Clinical and echocardiographic variables were assessed. RESULTS: N-ANF showed the closest correlations to clinical and echocardiographic measures of heart failure severity, e.g. NYHA functional class, furosemide dose, exercise tolerance, systolic and diastolic function. Plasma norepinephrine, dopamine and renin activity decreased after 3 months on both treatments, in contrast to a small increase in NPY-LI which was greater (by 3.9 pmol/l, 95% CI 1.2-6.6) in the metoprolol group. N-ANF increased on metoprolol, and decreased on xamoterol (difference: 408 pmol/l, 95% CI 209-607). Increase above median of NPY-LI (>25.2 pmol/l, odds ratio 2.8, P=0.0050) and N-ANF (>1043 pmol/l, odds ratio 2.8, P=0.0055) were related to long term (mean follow-up 6.8 years) cardiovascular mortality. CONCLUSIONS: Decreased neurohormonal activity, reflecting both the sympathetic nervous system and the renin-angiotensin system, was found 3 months after an acute myocardial infarction with heart failure treated with beta-receptor antagonists. The small increase in NPY-LI may suggest increased sympathetic activity or reduced clearance from plasma. The observed changes of N-ANF may be explained by changes in cardiac preload, renal function, and differences in beta-receptor mediated inhibition of atrial release of N-ANF. NPY-LI, and N-ANF at discharge were related to long term cardiovascular mortality.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atrial_Natriuretic_Factor_MeSH S_metabolism_MeSH Atrial_Natriuretic_Factor_metabolism_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Dopamine_MeSH S_metabolism_MeSH Dopamine_metabolism_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler_MeSH M_Epinephrine_MeSH S_metabolism_MeSH Epinephrine_metabolism_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_ultrasonography_MeSH Myocardial_Infarction_ultrasonography_MeSH M_Neuropeptide_Y_MeSH S_metabolism_MeSH Neuropeptide_Y_metabolism_MeSH M_Norepinephrine_MeSH S_metabolism_MeSH Norepinephrine_metabolism_MeSH M_Probability_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Xamoterol_MeSH S_administration_&_dosage_MeSH Xamoterol_administration_&_dosage_MeSH 
****** 11812672
----K I
----T Clinical trials update: The Heart Protection Study, IONA, CARISA, ENRICHD, ACUTE, ALIVE, MADIT II and REMATCH. Impact Of Nicorandil on Angina. Combination Assessment of Ranolazine In Stable Angina. ENhancing Recovery In Coronary Heart Disease patients. Assessment of Cardioversion Using Transoesophageal Echocardiography. AzimiLide post-Infarct surVival Evaluation. Randomised Evaluation of Mechanical Assistance for Treatment of Chronic Heart failure.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Angina_Pectoris_MeSH S_epidemiology_MeSH Angina_Pectoris_epidemiology_MeSH S_prevention_&_control_MeSH Angina_Pectoris_prevention_&_control_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH M_Arrhythmia_MeSH S_epidemiology_MeSH Arrhythmia_epidemiology_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Cardiology_MeSH S_methods_MeSH Cardiology_methods_MeSH P_Clinical_Trials_MeSH M_Comorbidity_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH M_Depressive_Disorder_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH S_epidemiology_MeSH Depressive_Disorder_epidemiology_MeSH M_Electric_Countershock_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Male_MeSH M_Nicorandil_MeSH S_administration_&_dosage_MeSH Nicorandil_administration_&_dosage_MeSH M_Piperazines_MeSH S_administration_&_dosage_MeSH Piperazines_administration_&_dosage_MeSH M_Sensitivity_and_Specificity_MeSH 
****** 11821634
----K 5
----T Psychological characteristics and responses to antihypertensive drug therapy.
----A The objective of this study was to explore the relationship between psychological characteristics and responses to antihypertensive drug therapy. Twenty-two hypertensive subjects underwent psychological evaluation and treatment with 1) a diuretic, hydrochlorothiazide (HCTZ); 2) an angiotensin-converting enzyme (ACE) inhibitor, quinapril; and 3) combined alpha + beta blockade (doxazosin + betaxolol). Anger-Out scores on the State-Trait Anger Expression Inventory were positively correlated with the HCTZ-induced fall in systolic blood pressure (p<0.01); Anger-In was negatively correlated with the quinapril-induced fall in systolic pressure (p<0.05). The target systolic blood pressure (130 mm Hg) was achieved with either HCTZ or quinapril in 79% of subjects without, vs. 25% of subjects with, childhood trauma (p=0.03). Responses to doxazosin + betaxolol were not correlated with psychological characteristics. The authors conclude that both inhibited anger expression and childhood trauma are associated with reduced response to a diuretic or ACE inhibitor. Combined alpha/beta blockade may be preferable to an ACE inhibitor or diuretic in treating selected hypertensive patients. Further studies should include examination of psychological factors in terms of the response to combined ACE inhibitor + diuretic therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Anger_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Questionnaires_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 11822998
----K E
----T Pilot study of secondary prevention of posttraumatic stress disorder with propranolol.
----A BACKGROUND: Preclinical considerations suggest that treatment with a beta-adrenergic blocker following an acute psychologically traumatic event may reduce subsequent posttraumatic stress disorder (PTSD) symptoms. This pilot study addressed this hypothesis. METHODS: Patients were randomized to begin, within 6 hours of the event, a 10-day course of double-blind propranolol (n = 18) versus placebo (n = 23) 40 mg four times daily. RESULTS: The mean (SD) 1-month Clinician-Administered PTSD Scale (CAPS) score of 11 propranolol completers was 27.6 (15.7), with one outlier 5.2 SDs above the others' mean, and of 20 placebo completers, 35.5 (21.5), t = 1.1, df = 29, p =.15. Two propranolol patients' scores fell above, and nine below, the placebo group's median, p =.03 (sign test). Zero of eight propranolol, but six of 14 placebo, patients were physiologic responders during script-driven imagery of the traumatic event when tested 3 months afterward, p =.04 (all p values one-tailed). CONCLUSIONS: These pilot results suggest that acute, posttrauma propranolol may have a preventive effect on subsequent PTSD.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Accidents__Traffic_MeSH S_psychology_MeSH Accidents__Traffic_psychology_MeSH M_Adult_MeSH M_Arousal_MeSH S_drug_effects_MeSH Arousal_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Emergency_Service__Hospital_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Pilot_Projects_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Stress_Disorders__Post-Traumatic_MeSH S_diagnosis_MeSH Stress_Disorders__Post-Traumatic_diagnosis_MeSH S_prevention_&_control_MeSH Stress_Disorders__Post-Traumatic_prevention_&_control_MeSH S_psychology_MeSH Stress_Disorders__Post-Traumatic_psychology_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 11823672
----K E
----T Effect of controlled release/extended release metoprolol on carotid intima-media thickness in patients with hypercholesterolemia: a 3-year randomized study.
----A BACKGROUND AND PURPOSE: Beta-adrenergic blockade has in several studies been shown to improve survival after myocardial infarction. In animal experiments beta-blockers have also shown an antiatherosclerotic effect. The aim of this study was to test the hypothesis that the beta-blocker metoprolol succinate controlled release/extended release (CR/XL), when given to patients with hypercholesterolemia on concomitant lipid-lowering therapy, provides an additional antiatherosclerotic effect to that provided by the statins, measured as carotid intima-media thickness (IMT). METHODS: We conducted a randomized, double-blind, placebo-controlled, single center trial to compare the effect of metoprolol CR/XL (100 mg once daily) and placebo on the progression of carotid IMT during 36 months of treatment in patients with hypercholesterolemia and signs of early atherosclerosis in the carotid artery. Most patients were prescribed lipid-lowering treatment with statins. RESULTS: A highly significant difference in the progression rate of the composite variable of carotid bulb IMT+common carotid IMT was observed between the metoprolol CR/XL and placebo groups after 1 year of treatment (-0.08 versus -0.01 mm; P=0.004), an effect that was sustained after 3 years of follow-up (-0.06 versus +0.03 mm; P=0.011). The patients had high levels of total cholesterol at randomization: 9.4 mmol/L in the metoprolol CR/XL group and 8.6 mmol/L in the placebo group. During the study the 2 randomization groups were treated with lipid-lowering drugs, mainly statins, to a similar extent, and total cholesterol was reduced to 6.4 mmol/L at end of follow-up in both groups. CONCLUSIONS: The results from the present study in patients with hypercholesterolemia under concomitant lipid-lowering therapy are the first clinical data to show an antiatherosclerotic effect of beta-blockade as additional therapy to statins. The data indicate that statin treatment and treatment with beta-blockers affect different mechanisms in the atherosclerotic process and have additive beneficial effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carotid_Artery_Diseases_MeSH S_complications_MeSH Carotid_Artery_Diseases_complications_MeSH S_diagnosis_MeSH Carotid_Artery_Diseases_diagnosis_MeSH S_prevention_&_control_MeSH Carotid_Artery_Diseases_prevention_&_control_MeSH M_Delayed-Action_Preparations_MeSH S_administration_&_dosage_MeSH Delayed-Action_Preparations_administration_&_dosage_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Hypercholesterolemia_MeSH S_blood_MeSH Hypercholesterolemia_blood_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Treatment_Outcome_MeSH M_Tunica_Intima_MeSH S_drug_effects_MeSH Tunica_Intima_drug_effects_MeSH S_ultrasonography_MeSH Tunica_Intima_ultrasonography_MeSH M_Tunica_Media_MeSH S_drug_effects_MeSH Tunica_Media_drug_effects_MeSH S_ultrasonography_MeSH Tunica_Media_ultrasonography_MeSH M_Vascular_Patency_MeSH S_drug_effects_MeSH Vascular_Patency_drug_effects_MeSH 
****** 11826413
----K E
----T TIPS versus drug therapy in preventing variceal rebleeding in advanced cirrhosis: a randomized controlled trial.
----A Prevention of variceal rebleeding is mandatory in cirrhotic patients. We compared the efficacy, safety, and cost of transjugular intrahepatic portosystemic shunt (TIPS) versus pharmacologic therapy in preventing variceal rebleeding in patients with advanced cirrhosis. A total of 91 Child-Pugh class B/C cirrhotic patients surviving their first episode of variceal bleeding were randomized to receive TIPS (n = 47) or drug therapy (propranolol + isosorbide-5-mononitrate) (n = 44) to prevent variceal rebleeding. Mean follow-up was 15 months. Rebleeding occurred in 6 (13%) TIPS-treated patients versus 17 (39%) drug-treated patients (P =.007). The 2-year rebleeding probability was 13% versus 49% (P =.01). A similar number of reinterventions were required in the 2 groups; these were mainly angioplasty +/- restenting in the TIPS group (90 of 98) and endoscopic therapy for rebleeding in the medical group (45 of 62) (not significant). Encephalopathy was more frequent in TIPS than in drug-treated patients (38% vs. 14%, P =.007). Child-Pugh class improved more frequently in drug-treated than in TIPS-treated patients (72% vs. 45%; P =.04). The 2-year survival probability was identical (72%). The identified cost of therapy was double for TIPS-treated patients. In summary, medical therapy was less effective than TIPS in preventing rebleeding. However, it caused less encephalopathy, identical survival, and more frequent improvement in Child-Pugh class with lower costs than TIPS in high-risk cirrhotic patients. This suggests that TIPS should not be used as a first-line treatment, but as a rescue for failures of medical/endoscopic treatments (first-option therapies).
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Health_Care_Costs_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH M_Hepatic_Encephalopathy_MeSH S_etiology_MeSH Hepatic_Encephalopathy_etiology_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_MeSH S_physiopathology_MeSH Liver_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH S_adverse_effects_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_adverse_effects_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Retreatment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Varicose_Veins_MeSH S_complications_MeSH Varicose_Veins_complications_MeSH S_etiology_MeSH Varicose_Veins_etiology_MeSH 
****** 11826546
----K 1
----T [Effectiveness and tolerance of fosinopril in the treatment of arterial hypertension of mild and medium severity]
----A BACKGROUND: The standard of hypertension control in the population is not satisfactory, only 20% patients with hypertension achieve target values of blood pressure (BP). Extensive prospective studies revealed that diuretics, beta-blockers as well as the majority of calcium channel blockers and ACE inhibitors can significantly reduce the incidence of complications of hypertension and are therefore considered drugs of first choice in the treatment of hypertension. The additive effects of ACE inhibitors are manifested in particular after larger doses. OBJECTIVE OF TRIAL: To assess the effectiveness and tolerance of the modern long-acting ACE inhibitor--fosinopril--in the treatment of mild and medium severe hypertension and its effect on some anthropometric and laboratory parameters. RESULTS: Fosinopril as monotherapy in amounts of 10, 20 and 40 mg led to normalization of BP in 85% of the group (n = 203) and was very well tolerated. Only 11% of the group needed a combination with hydrochlorothiazide--12.5 g/day--after which normal BP levels were attained. Only 4% of the patients did not complete the study on account of undesirable effects, incl. 3 patients where cough was the reason for discontinuation. After 12 weeks treatment the systolic BP was reduced on average by 31 mm Hg and the diastolic BP by 16 mm Hg. The heart rate (HR) declined on average by 3 beats/min. (p 0.001). After four weeks treatment a significant decline of the blood sugar level occurred which was even more marked after 12 weeks of treatment (on average by 0.27 mmol/l and at the same time a significant drop of sodium occurred (by 2 mmol/l), of total and LDL-cholesterol (by 0.26 and 0.23 mmol/l). An expected increase of the potassium level occurred (by 0.1 mmol/l) and creatinine (by 3.4 mumol/l in plasma). CONCLUSION: Fosinopril treatment with 10-40 mg/day was effective in monotherapy of hypertension in 85% patients and was well tolerated. After 12 weeks treatment a significant decline of the BP, HR occurred as well as the expected decline of the plasma Na/K ratio and improvement of some metabolic parameters.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Fosinopril_MeSH S_administration_&_dosage_MeSH Fosinopril_administration_&_dosage_MeSH S_adverse_effects_MeSH Fosinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 11830324
----K I
----T Lebrec D, Poynard T, Hillon P, Benhamou J-P. Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis. A controlled study [N Engl J Med 1981;305:1371-1374].
----A 
----P Historical_Article Journal_Article 
----M M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_history_MeSH Gastrointestinal_Hemorrhage_history_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_History_of_Medicine__20th_Cent__MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_history_MeSH Liver_Cirrhosis_history_MeSH M_Propranolol_MeSH S_history_MeSH Propranolol_history_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Vasodilator_Agents_MeSH S_history_MeSH Vasodilator_Agents_history_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11833829
----K 5
----T Health-related quality of life in patients treated for hypertension: a review of the literature from 1990 to 2000.
----A BACKGROUND: The goals of antihypertensive therapy are to achieve and maintain blood pressure control by the least intrusive means possible to prevent future cardiovascular and renal events. To achieve these goals, pharmacologic agents must be chosen so as to minimize drug-related adverse events, increase patient adherence to treatment regimens, and minimize the negative impact on health-related quality of life (HRQL). Although the effects of antihypertensive therapy on HRQL have been extensively investigated, there is little synthesis of the research findings. OBJECTIVE: This review was undertaken to provide a synthesis of the available data on the impact of antihypertensive therapy on HRQL and to provide recommendations for future research. METHODS: A MEDLINE literature search was conducted to identify English-language articles published from 1990 to 2000 that included random assignment to antihypertensive treatment and HRQL as an outcome. In addition, reference lists of published reviews and other trials were reviewed to identify other studies of HRQL and antihypertensive therapy. RESULTS: A total of 48 articles were included in the review. Results among studies were frequently inconsistent, which is likely due to the wide variety of dimensions studied and instruments used as well as a number of methodological weaknesses, including small sample sizes, short-term assessments, and failure to account for missing data. CONCLUSION: A standardized approach to the assessment of HRQL in hypertensive patients is needed so that research in this area can be of value to clinical practice and to hypertensive patients and their families.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH P_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11836877
----K 1
----T [Risk factors for morbidity and mortality in patients with essential hypertension, followed for 25 years]
----A BACKGROUND: Among hypertensive patients, other risk factors for mortality and morbidity, besides blood pressure, must be considered when therapeutic decisions are done. AIM: To assess the incidence and relevance of cardiovascular risk factors in a cohort of patients with essential hypertension. MATERIAL AND METHODS: A cohort of 1,072 treated patients with essential hypertension was followed for a period up to 25 years. Four hundred eighty six were men and 586 were women, age ranged from 31 to 70 years. At entry, 56% of subjects did not have any organic complications associated to hypertension (stage I WHO criteria), 30% had mild alterations (Stage II) and 14% had major complications (myocardial infarction, stroke, heart failure or renal failure). Likewise, 43.8% had mild, 14.5%, moderate and 41.7%, severe hypertension. Patients were treated with monotherapy or combined therapy based on diuretics, beta blockers, calcium antagonists and angiotensin converting enzyme inhibitors. Goal of therapy was 140/90 mm Hg. Risk factors associated diseases and complications were registered carefully. Causes of death were obtained from hospital records and death certificates. Mortality was analyzed using life tables (intention to treat method included). RESULTS: Blood pressure dropped significantly during follow up from a mean of 182/110 to 154/92 mm Hg. During follow up, 143 patients died and 429 complications (lethal or non lethal) were recorded. Twenty four percent of patients smoked, 24% reported alcohol intake, 56% had hypercholesterolemia, 11% were obese, 13% had diabetes and 3% had gout. The proportional hazard model showed that the existence of previous complications, the presence of more than 3 risk factors, and age over 60 and mean systolic and diastolic pressure during therapy, were independent and significant risk factors for mortality. CONCLUSIONS: The incidence of risk factors among our hypertensive patients is very similar to that of other national or international cohorts.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Chi-Square_Distribution_MeSH M_Chile_MeSH S_epidemiology_MeSH Chile_epidemiology_MeSH M_Cohort_Studies_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH 
****** 11835919
----K E
----T Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).
----A In hypertensive patients, pulse pressure has been related to hypertension-induced target organ damage and risk of cardiovascular events. However, correlates of pulse pressure reduction during antihypertensive treatment have been less extensively investigated. We related pulse pressure changes to clinical and echocardiographic findings before and after 2 years of antihypertensive treatment in 767 patients aged 55 to 80 years (mean 66) in the Losartan Intervention For End point reduction in hypertension study. Over 2 years, blood pressure and pulse pressure were reduced from 173/98 to 147/84 mm Hg and from 75 to 63 mm Hg, respectively, both p <0.001. In linear multivariate analysis controlling for initial pulse pressure, 2-year reduction in pulse pressure correlated negatively with age and concomitant diabetes mellitus, and positively with body height and 2-year reduction in mean blood pressure (multiple R(2) = 0.42, p <0.01). When dividing the study population into 2 groups using a prognostically validated partition for pulse pressure, patients with pulse pressure > or =63 mm Hg after 2 years of antihypertensive treatment (n = 349) were older and shorter, included more women and patients with isolated systolic hypertension, diabetes mellitus, albuminuria, and echocardiographic left ventricular hypertrophy at baseline, and also had a smaller decrease in mean blood pressure and the urinary albumin/creatinine ratio over 2 years (all p <0.05). Thus, in hypertensive patients with electrocardiographic left ventricular hypertrophy, older age, less reduction in mean blood pressure, concomitant diabetes mellitus, and shorter stature are associated with attenuated pulse pressure reduction during antihypertensive treatment.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Albumins_MeSH S_metabolism_MeSH Albumins_metabolism_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Creatinine_MeSH S_urine_MeSH Creatinine_urine_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pulse_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11840225
----K E
----T Efficacy and safety of sibutramine for weight loss in obese patients with hypertension well controlled by beta-adrenergic blocking agents: a placebo-controlled, double-blind, randomised trial.
----A Sibutramine is a serotonin-noradrenaline reuptake inhibitor that is effective for long-term weight reduction and maintenance in obese patients when used as an adjunct to dietary and behavioural measures. Because the inhibition of noradrenaline reuptake may be expected to increase systolic and diastolic blood pressure (SBP and DBP) and pulse rate (PR), a 12-week multi-centre, placebo-controlled, double-blind study was designed to evaluate the efficacy and tolerability of sibutramine for weight loss in obese patients whose hypertension was well controlled (DBP < or = 95 mm Hg) by beta-adrenergic blocking agents (beta-blockers), with or without concomitant thiazide diuretics. Of the 61 patients randomised to sibutramine 20 mg once daily or placebo, 55 patients (90%) completed the study. After 12 weeks, sibutramine-treated patients lost significantly more weight than placebo-treated patients: mean weight reductions were 4.2 kg (4.5%) in the sibutramine group vs 0.3 kg (0.4%) in the placebo group (P<0.001). Greater weight reduction on sibutramine was accompanied by trends for greater mean reductions in serum triglycerides and very low density lipoprotein cholesterol. Sibutramine was well tolerated, and most adverse events were mild or moderate in severity. No sibutramine patient discontinued treatment because of an adverse event. Mean supine and standing DBP and SBP were not statistically significantly different between the sibutramine group and the placebo group at any post-baseline visit during the 12-week trial. At week 12, mean increases from baseline supine SBP and DBP, respectively, were 1.6 and 1.7 mm Hg for the sibutramine group vs increases of 0.4 and 1.3 mm Hg for the placebo group. At week 12, mean increases from baseline standing SBP and DBP, respectively, were 1.5 and 1.8 mm Hg for the sibutramine group vs an increase of 0.3 and a decrease of 0.8 mm Hg for the placebo group (P > 0.05 for treatment comparison). A statistically significant mean increase of 5.6 bpm (+/-8.25, s.d.) in supine PR from a baseline of 62 bpm was reported in sibutramine-treated patients at week 12, whereas placebo-treated patients had a mean supine PR decrease of 2.2 bpm (+/-6.43) (P < 0.001). In summary, sibutramine was well tolerated and effective in weight reduction. The addition of sibutramine did not result in an increase in BP in obese patients whose hypertension was well controlled by a beta-blocker. However, based on the potential for changes in BP and PR, obese patients being treated with sibutramine should be monitored periodically for changes in BP and PR and managed appropriately.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Appetite_Depressants_MeSH S_adverse_effects_MeSH Appetite_Depressants_adverse_effects_MeSH S_therapeutic_use_MeSH Appetite_Depressants_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cyclobutanes_MeSH S_adverse_effects_MeSH Cyclobutanes_adverse_effects_MeSH S_therapeutic_use_MeSH Cyclobutanes_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH S_drug_therapy_MeSH Obesity_drug_therapy_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Weight_Loss_MeSH S_drug_effects_MeSH Weight_Loss_drug_effects_MeSH S_physiology_MeSH Weight_Loss_physiology_MeSH 
****** 11835110
----K E
----T Evidence for age-based rationing in a Swiss university hospital.
----A AIM: To test the hypothesis that rationing of medical management mainly based on age exists in our health care system today. METHODS: We studied 303 consecutive patients hospitalised for acute coronary syndrome (ACS) and 163 consecutive patients hospitalised with congestive heart failure (CHF). They were divided into two age groups; patients aged less than 75 years and those equal to or older than 75 years. RESULTS: Our main findings were a significant underuse of stress tests (p < 0.001) and coronary angiography (p < 0.0001) in elderly patients with ACS and a significant underuse of echocardiography (p < 0.0001) in patients with CHF of the same age group. In patients with ACS, there was also a trend towards underuse of statins in elderly patients with hypercholesterolaemia. In addition, we noted that the use of beta-blockers in ACS and of ACE inhibitors in CHF was better than in previous published studies but that many patients were still not treated according to evidence based medicine. CONCLUSION: The lower rates of diagnostic tests performed and the lower statin use observed in elderly patients suggest "hidden" rationing of health care in elderly patients.
----P Journal_Article 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH M_Female_MeSH P_Health_Care_Rationing_MeSH M_Health_Services_Misuse_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Hospitals__University_MeSH S_utilization_MeSH Hospitals__University_utilization_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH M_Switzerland_MeSH M_Syndrome_MeSH 
****** 11845882
----K E
----T Beta-receptor downregulation in congenital heart disease: a risk factor for complications after surgical repair?
----A BACKGROUND: Neurohormonal activation in children with heart failure due to congenital heart disease leads to downregulation of myocardial beta-receptors that may influence the postoperative course after cardiothoracic surgery. METHODS: Myocardial biopsies of 26 children (aged 14+/-4 months) were obtained from the right atrium during cardiac surgery. Patients were allocated to either of two groups based on the duration of their intensive care unit stay: group 1 comprised those who stayed less than 7 days (n = 17), whereas group 2 comprised those who stayed more than 7 days, plus 3 infants who died during the early postoperative course (n = 9). For beta1- and beta2-mRNA quantitation, real-time polymerase chain reaction with fluorescence-labeled products was used. RESULTS: Values for myocardial beta1-receptor gene expression were twice as high in group 1 children compared with group 2 (beta1-receptor 0.12+/-0.07 versus 0.06+/-0.03, p = 0.0016; beta2-receptor 0.12+/-0.07 versus 0.06+/-0.03, p = 0.0071). Beta-receptor gene expression in 16 children who received standard treatment for heart failure averaged lower than in the 10 children who received additional propranolol. CONCLUSIONS: Beta-receptor downregulation due to congestive heart failure has an impact on the postoperative course in children with congenital disease and depends on heart failure therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Biopsy_MeSH M_Child__Preschool_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Down-Regulation_MeSH S_drug_effects_MeSH Down-Regulation_drug_effects_MeSH S_physiology_MeSH Down-Regulation_physiology_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Defects__Congenital_MeSH S_pathology_MeSH Heart_Defects__Congenital_pathology_MeSH S_physiopathology_MeSH Heart_Defects__Congenital_physiopathology_MeSH S_surgery_MeSH Heart_Defects__Congenital_surgery_MeSH M_Heart_Failure__Congestive_MeSH S_pathology_MeSH Heart_Failure__Congestive_pathology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_surgery_MeSH Heart_Failure__Congestive_surgery_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Infant_MeSH M_Length_of_Stay_MeSH M_Male_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_pathology_MeSH Postoperative_Complications_pathology_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Prospective_Studies_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH S_physiology_MeSH Receptors__Adrenergic__beta_physiology_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11851582
----K I
----T beta-Blocker therapy in heart failure: scientific review.
----A CONTEXT: Care of patients with heart failure has been revolutionized throughout the past decade. A paradigm shift in the strategy for treating heart failure caused by systolic dysfunction is in progress. Despite the initial perception about beta-blockers' safety, they are now the most extensively studied class of agents in the treatment of heart failure and have emerged as an important intervention to improve the clinical outcomes of heart failure patients. OBJECTIVE: To provide scientific rationale for the use of beta-blockers for patients with heart failure. DATA SOURCES: All English-language articles of large, randomized controlled clinical trials assessing the mortality benefits of beta-blockers in patients with heart failure were identified to provide the scientific rationale for the use of beta-blockers in heart failure. Basic science studies were reviewed to provide an overview of the potential physiologic role of beta-blockers in heart failure. Finally, clinical guidelines for the treatment of patients with heart failure were assessed to determine current recommendations for the use of these agents. STUDY SELECTION AND DATA EXTRACTION: Randomized controlled clinical trials of beta-blockers that included more than 300 subjects and assessed mortality as a primary end point. DATA SYNTHESIS: Of the 4 beta-blockers tested in large randomized controlled clinical trials of patients with heart failure, 3 are available in the United States, bisoprolol, carvedilol, and metoprolol; 2 of these, carvedilol and metoprolol, have Food and Drug Administration indications for the treatment of heart failure. Compared with placebo treatment, beta-blocker use is associated with a consistent 30% reduction in mortality and a 40% reduction in hospitalizations in patients with class II and III heart failure. CONCLUSIONS: Tested in more than 10,000 patients, beta-blockers reduce morbidity and mortality in class II through IV heart failure. Along with angiotensin-converting enzyme inhibitors, digoxin, and diuretics, beta-blockers have strengthened the armamentarium to improve clinical outcomes of heart failure patients. The science supporting beta-blockers must be translated into practice safely and rationally if the agents are to achieve their full potential.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 11862577
----K E
----T Effects of metoprolol CR/XL on mortality and hospitalizations in patients with heart failure and history of hypertension.
----A BACKGROUND: We describe the effect of controlled-release/extended-release (CR/XL) metoprolol succinate once daily on mortality and hospitalizations among patients with a history of hypertension complicated by chronic systolic heart failure. METHODS AND RESULTS: We enrolled 3,991 patients with chronic heart failure of New York Heart Association functional class II-IV with an ejection fraction of < or = 0.40, stabilized with optimum standard therapy, in a double-blind randomized placebo-controlled study. A total of 1,747 patients (44%) had a history of hypertension; 871 were randomized to receive metoprolol CR/XL and 876 to receive placebo. Treatment with metoprolol CR/XL compared with placebo resulted in a significant reduction in total mortality (relative risk [RR], 0.61; 95% confidence interval [CI], 0.44-0.84; P =.0022), mainly because of reductions in sudden death (RR, 0.51; 95% CI, 0.33-0.79; P =.0022) and mortality from worsening heart failure (RR, 0.49; 95% CI, 0.25-0.99; P =.042). Total number of hospitalizations for worsening heart failure was reduced by 30% in the metoprolol CR/XL group compared with placebo (P =.015). Metoprolol CR/XL was well tolerated: 12% fewer patients withdrew from study medication (all-cause) compared with placebo (P =.048). CONCLUSIONS: A subgroup analysis of MERIT-HF shows that patients with heart failure and a history of hypertension received a similar benefit from metoprolol CR/XL treatment as all patients included in the total study.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11863244
----K E
----T Effect of amlodipine compared to atenolol on small arteries of previously untreated essential hypertensive patients.
----A In a previous retrospective study, long-term treatment of essential hypertensive patients with a slow-release calcium channel blocker resulted in normal resistance artery structure and endothelial function, which did not occur with a beta-blocker. In the present prospective study, 19 previously untreated essential hypertensive patients (aged 47 +/- 2 years, 75% male) were treated for 1 year in a double-blind randomized study with the long-acting calcium channel blocker amlodipine or the beta-blocker atenolol. Resistance arteries (lumen diameter, 150 to 350 microm) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph. Blood pressure (BP) control (129 +/- 2/85 +/- 2 mm Hg) was identical in both groups for the last 6 months of the study. After 1 year of treatment with amlodipine, the media-to-lumen ratio (M/L) of resistance arteries decreased from 7.89% +/- 0.40% to 6.81% +/- 0.41% (P < .05). Acetylcholine-induced endothelium-dependent relaxation tended to improve from 84.3% +/- 5.5% to 90.5% +/- 4.8% (P = .06), whereas sodium nitroprusside-induced relaxation was unchanged in the patients treated with amlodipine. In the beta-blocker-treated group there was no significant change in M/L or acetylcholine-induced relaxation. In conclusion, treatment with the calcium channel blocker amlodipine corrected altered resistance artery structure and tended to improve endothelial function in essential hypertensive patients, whereas similar good control of BP with the beta-blocker atenolol did not. Whether the vascular protective effect of amlodipine will result in improved outcomes in hypertension remains to be demonstrated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Buttocks_MeSH S_blood_supply_MeSH Buttocks_blood_supply_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH M_Vasodilation_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 11868043
----K E
----T Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure.
----A BACKGROUND: A deleterious effect of complete left bundle-branch block (LBBB) on left ventricular function has been established. Nevertheless, the independent effect of a widened QRS on mortality rate in congestive heart failure (CHF) is still controversial. Therefore, we carried out this analysis to determine whether LBBB is an independent predictor of mortality in CHF. METHODS AND RESULTS: We analyzed the large Italian Network on CHF Registry of unselected outpatients with CHF of different causes. The registry was established by the Italian Association of Hospital Cardiologists in 1995. Complete 1-year follow-up data were available for 5517 patients. The main underlying cardiac diagnosis was ischemic heart disease in 2512 patients (45.6%), dilated cardiomyopathy in 1988 patients (36.0%), and hypertensive heart disease in 714 patients (12.9%). Other causes were recorded in the remaining 303 cases (5.5%). LBBB was present in 1391 patients (25.2%) and was associated with an increased 1-year mortality rate from any cause (hazard ratio, 1.70; 95% confidence interval, 1.41 to 2.05) and sudden death (hazard ratio, 1.58; 95% confidence interval, 1.21 to 2.06). Multivariate analysis showed that such an increased risk was still significant after adjusting for age, underlying cardiac disease, indicators of CHF severity, and prescription of angiotensin-converting enzyme inhibitors and beta-blockers. CONCLUSION: LBBB is an unfavorable prognostic marker in patients with CHF. The negative effect is independent of age, CHF severity, and drug prescriptions. These data may support the rationale of randomized trials to verify the effects on mortality rate of ventricular resynchronization with multisite cardiac pacing in patients with CHF and LBBB.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Bundle-Branch_Block_MeSH S_complications_MeSH Bundle-Branch_Block_complications_MeSH S_mortality_MeSH Bundle-Branch_Block_mortality_MeSH M_Cause_of_Death_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Registries_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11868804
----K E
----T Treatment patterns among newly diagnosed heart failure patients in general practice.
----A AIM: To examine treatment patterns of heart failure (HF) in general practice and to evaluate factors influencing the choice of that treatment, such as age, sex, severity of disease and co-morbidity. METHODS: We used previously identified and confirmed incident cases of HF (patients aged 40-84 years) from the General Practice Research Database in the UK (n = 938). We collected recorded information on demographics. co-morbidity and drug treatment prescribed 1 year before and after the incident diagnosis in 1996. RESULTS: Most of the study cohort was over 60 years old and presented with several concomitant diseases. Use of most cardiovascular drugs significantly increased after the diagnosis of HF. There was a greater than threefold increase in the use of angiotensin-converting enzyme inhibitors, while use of nitrates decreased after diagnosis of HF among men. Use of beta-blockers and calcium channel blockers slightly decreased after diagnosis. CONCLUSION: We found that well-established treatment practices were followed by general practitioners. Severity of the disease favoured use of diuretics and a previous ischaemic heart disease and hypertension favoured use of beta-blockers and aspirin. Women and elderly patients were less likely to receive treatment with angiotensin-converting enzyme inhibitors.
----P Journal_Article 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comorbidity_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Physician's_Practice_Patterns_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH 
****** 11871761
----K 4
----T Propranolol ameliorates thrombocytopenia in patients with cirrhosis.
----A BACKGROUND: Propranolol causes splanchnic arterial vasoconstriction owing to the unopposed alpha vasoconstriction resulting from the blockade of beta-2 adrenoceptors. It is therefore hypothesized that this drug may cause vasoconstriction in the splenic arterial circulation and, thus, modify the manifestations of hypersplenism, such as thrombocytopenia. The aim of the present study was to test this hypothesis. METHODS: Nineteen patients with cirrhosis and thrombocytopenia (fewer than thrombocytes 7 x 10(4)/mm3) were include. The subjects of the study. All of them were studied in the morning after an overnight fast. To evaluate splenic arterial hemodynamics, the pulsatility index was measured by Doppler ultrasonography. Platelet counts and platelet-associated immunoglobulin G levels were also recorded. The subjects were then randomized to receive propranolol (n = 10) or placebo (n = 9). The measurements were repeated after 1 week of propranolol or placebo administration. The dose of propranolol was determined so that a 20% to 25% reduction in heart rate was achieved. RESULTS: Placebo administration caused no significant changes in splenic artery hemodynamics. In contrast, propranolol administration significantly increased the intra splenic artery pulsatility index (from 1.10+/-0.06 to 1.24+/-0.08; P < 0.01). Placebo administration caused no significant changes in the platelet count. In contrast, propranolol administration significantly increased the platelet count (from 4.5+/-0.3 to 6.1+/-0.73 x 10(4)/mm3; P < 0.05). Furthermore, the change in platelet count was significantly correlated with either the change in extrasplenic artery pulsatility index (r = 0.78, P < 0.05) or the change in intrasplenic artery pulsatility index (r = 0.78, P < 0.01). Platelet-associated immunoglobulin G levels were not modified in either of the two groups. CONCLUSIONS: Propranolol ameliorates thrombocytopenia in patients with cirrhosis. This effect may be caused mainly by hemodynamic changes in the spleen, rather than being caused by immunological mechanisms.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Count_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Splenic_Artery_MeSH S_drug_effects_MeSH Splenic_Artery_drug_effects_MeSH S_ultrasonography_MeSH Splenic_Artery_ultrasonography_MeSH M_Thrombocytopenia_MeSH S_etiology_MeSH Thrombocytopenia_etiology_MeSH S_prevention_&_control_MeSH Thrombocytopenia_prevention_&_control_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11871210
----K 1
----T [Is heart rate reduction beneficial to patients with heart insufficiency? Focus on beta-blockade]
----A The aim of this review was to assess the effect of pharmacological reduction of the heart rate on prognosis in patients with chronic heart failure. Although a high heart rate is associated with a reduced life expectancy and causes a number of unwanted pathophysiological effects on the failing heart, there is no documentation that the beneficial effect of beta-blockers or other heart failure agents on survival is mediated through a reduction in heart rate.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH M_Controlled_Clinical_Trials_MeSH M_English_Abstract_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 11875324
----K E
----T Twenty-four hour ambulatory blood pressure in the International Nifedipine GITS Study Intervention as a Goal in Hypertension Treatment (INSIGHT).
----A OBJECTIVES : The International Nifedipine GITS Study Intervention as a Goal in Hypertension Treatment (INSIGHT) showed, by means of office blood pressure measurements, that long-term treatment with nifedipine GITS is as effective as diuretics in preventing cardiovascular and cerebrovascular complications. However, since office blood pressure measurements reflect to a limited extent blood pressure outside the office, a side-arm INSIGHT study in which patients underwent both office measurement and 24 h ambulatory blood pressure monitoring was also performed. DESIGN AND METHODS : The study had a randomized, double-blind, parallel group design. After 4 weeks of placebo, mild-to-moderate essential hypertensive patients were randomized to nifedipine GITS 30 mg or amiloride 2.5 + hydrochlorothiazide 5 mg for 3.1 years. Dose titration was performed by dose doubling and addition of atenolol 25-50 mg or enalapril 5-10 mg, or other drugs when needed. Analysis was carried out by intention-to-treat and included computation of 24 h, day and night ambulatory blood pressure and heart rate values. Additional analyses included computation of the trough-to-peak ratio and the smoothness index (the ratio between the average of the 24-hourly blood pressure reductions after treatment and its standard deviation). RESULTS : A total of 151 patients were recruited and 149 were valid for analysis: 78 patients had 24 h ambulatory recordings both at baseline and during treatment and 134 during treatment. Office, 24 h and day and night blood pressures were all significantly and similarly reduced by both treatments. Office and ambulatory heart rate was left unchanged by diuretics, while it was slightly reduced by nifedipine. Median trough-to-peak ratios were always > 0.5 and superimposable between the two treatment groups. Similarly, smoothness indices of systolic and diastolic blood pressures were comparably high for nifedipine and diuretics, thus demonstrating a similar well-balanced antihypertensive response to both drugs. No significant differences were observed between the two treatment groups in the number of cardiovascular events (17 in the nifedipine-based and 26 in the diuretics-based treatment group). CONCLUSIONS : In the INSIGHT study, the long-term antihypertensive effect on 24 h blood pressure and the cardiovascular protection of nifedipine was similar to that of diuretics.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amiloride_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_Determination_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH P_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Goals_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Office_Visits_MeSH M_Risk_Factors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 11877357
----K E
----T Change in diastolic left ventricular filling after one year of antihypertensive treatment: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.
----A BACKGROUND: It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. METHODS AND RESULTS: Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all P<0.001). Directionally opposite changes in isovolumic relaxation time (IVRT) and deceleration time indicate improvement in active LV relaxation and passive chamber stiffness during early diastole. Prevalences of normal LV filling increased, abnormal relaxation and pseudonormalization decreased, and restrictive filling pattern remained unchanged (P<0.05). Patients with reduction in LV mass had smaller left atrial diameter, shortened IVRT, increased E/A ratio, and prolonged LV inflow deceleration time (all P<0.001). Patients without LV mass reduction had no change in diastolic filling parameters (P=NS). IVRT shortening was independently associated with reduction in LV mass. Increase in E/A ratio was independently associated with reduction in diastolic BP, and increase in the deceleration time was independently associated with reduced end-systolic relative wall thickness. CONCLUSIONS: Antihypertensive therapy resulting in LV mass or relative wall thickness regression is associated with significant improvement of diastolic filling parameters related to active relaxation and passive chamber stiffness compared with patients without regression, independent of BP reduction; however, abnormalities of diastolic LV filling remain common.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Atria_MeSH S_drug_effects_MeSH Heart_Atria_drug_effects_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_diagnosis_MeSH Hypertrophy__Left_Ventricular_diagnosis_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH M_Remission_Induction_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 11880723
----K 4
----T Management of refractory glaucoma in childhood.
----A Glaucoma in children is characterized by marked intraocular pressure (IOP) elevation with resultant atrophy of the optic nerve and loss of retinal ganglion cells. In very young children, secondary expansion of the globe with damage to anterior segment structures, such as the cornea and zonule, often occurs. Permanent, severe visual dysfunction may result from optic nerve damage as well as from amblyopia arising from anisometropia and corneal opacification. The treatment of childhood glaucoma often involves surgery. Goniotomy and trabeculotomy remain the first line surgical procedures for open-angle glaucoma in children. Trabeculectomy with adjunctive antifibrosis therapy, aqueous shunt surgery, and cyclodestructive procedures are undertaken when angle surgery fails to control the IOP or is unlikely to succeed. The choice of surgical procedure is individualized according to factors such as the age of the patient, the specific type of glaucoma, the number of prior surgical procedures, and the visual potential of the eye. Achieving and maintaining an adequate IOP to prevent progressive optic nerve damage, avoiding complications, and preserving vision are the goals that must be considered in deciding on a surgical plan.
----P Journal_Article Review Review__Tutorial 
----M M_Child_MeSH M_Child__Preschool_MeSH M_Filtering_Surgery_MeSH S_methods_MeSH Filtering_Surgery_methods_MeSH M_Glaucoma_MeSH S_congenital_MeSH Glaucoma_congenital_MeSH S_etiology_MeSH Glaucoma_etiology_MeSH S_surgery_MeSH Glaucoma_surgery_MeSH M_Glaucoma_Drainage_Implants_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH 
****** 11881864
----K 5
----T Modulation of beta-adrenergic receptor subtype activities in perioperative medicine: mechanisms and sites of action.
----A This review focuses on the mechanisms and sites of action underlying beta-adrenergic antagonism in perioperative medicine. A large body of knowledge has recently emerged from basic and clinical research concerning the mechanisms of the life-saving effects of beta-adrenergic antagonists (beta-AAs) in high-risk cardiac patients. This article re-emphasizes the mechanisms underlying beta-adrenergic antagonism and also illuminates novel rationales behind the use of perioperative beta-AAs from a biological point of view. Particularly, it delineates new concepts of beta-adrenergic signal transduction emerging from transgenic animal models. The role of the different characteristics of various beta-AAs is discussed, and evidence will be presented for the selection of one specific agent over another on the basis of individual drug profiles in defined clinical situations. The salutary effects of beta-AAs on the cardiovascular system will be described at the cellular and molecular levels. Beta-AAs exhibit many effects beyond a reduction in heart rate, which are less known by perioperative physicians but equally desirable in the perioperative care of high-risk cardiac patients. These include effects on core components of an anaesthetic regimen, such as analgesia, hypnosis, and memory function. Despite overwhelming evidence of benefit, beta-AAs are currently under-utilized in the perioperative period because of concerns of potential adverse effects and toxicity. The effects of acute administration of beta-AAs on cardiac function in the compromised patient and strategies to counteract potential adverse effects will be discussed in detail. This may help to overcome barriers to the initiation of perioperative treatment with beta-AAs in a larger number of high-risk cardiac patients undergoing surgery.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Cardiac_Surgical_Procedures_MeSH M_Disease_Models__Animal_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Human_MeSH M_Perioperative_Care_MeSH S_methods_MeSH Perioperative_Care_methods_MeSH M_Receptors__Adrenergic__beta_MeSH S_physiology_MeSH Receptors__Adrenergic__beta_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11882098
----K E
----T Family physicians' and general practitioners' approaches to drug management of diabetic hypertension in primary care.
----A RATIONALE, AIMS AND OBJECTIVES: To compare the pharmacotherapeutic approaches to diabetic hypertension of family physicians (FPs) and general practitioners (GPs). METHODS: A retrospective prescription-based study was conducted in 15 out of a total of 20 health centres, involving 115 primary care physicians--77 FPs and 38 GPs, representing 74% of the primary care physicians of Bahrain. Prescriptions were collected during May and June 2000 to comprise a study population of 1266 diabetic-hypertensive patients. RESULTS: As monotherapy, angiotensin-converting enzyme (ACE) inhibitors (37.9%) and beta-blockers (38.3%) were the most commonly prescribed classes of antihypertensives by FPs and GPs, respectively. Calcium channel blockers (CCBs) were ranked third by both categories of physicians. For two-drug combinations, a beta-blocker and an ACE inhibitor was the combination of choice for both physician categories. Patients managed by the FPs were more likely to receive a beta-blocker-CCB combination (17.4 vs. 14.9%) or a diuretic-ACE inhibitor combination (16.7 vs. 11.4%) and less likely to receive a beta-blocker-diuretic combination (11.8 vs. 16.7%) than those managed by the GPs. The proportion of patients receiving antihypertensive combinations was 40.6 and 38.5% for FPs and GPs, respectively. While the GPs prescribed CCB as a monotherapy to the elderly most often, the FPs choice was a beta-blocker. Diuretics were less preferred by both FPs and GPs. Beta-blocker-ACE inhibitor was again the most preferred combination of both FPs and GPs. FPs prescribed CCB-beta-blocker combinations more often than GPs (P = 0.01), whereas CCB-ACE inhibitor combinations were less preferred (P = 0.09). A trend towards excessive use of short-acting nifedipine as monotherapy for elderly patients, both by FPs and by GPs, was noticed. Glibenclamide, alone or in combination with metformin, was the foremost antidiabetic drug prescribed by FPs and GPs. Middle-aged (45-64 years) patients seen by GPs were more likely to receive glibenclamide than those treated by FPs (P = 0.001) and less likely to receive gliclazide (P = 0.01). Combinations of a beta-blocker with either glibenclamide or insulin were prescribed considerably more often by GPs. CONCLUSIONS: Within the same practice setting, a substantial difference was observed between FPs and GPs in terms of preference for different classes of drugs in the management of diabetic hypertension. The compliance of both FPs and GPs was suboptimal; overall, the compliance of the FPs was closer to the recommended guidelines, however. Educational programmes should specifically address these inadequacies in order to improve the quality of health care.
----P Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bahrain_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Drug_Utilization_Review_MeSH M_Family_Practice_MeSH S_education_MeSH Family_Practice_education_MeSH S_standards_MeSH Family_Practice_standards_MeSH M_Female_MeSH P_Guideline_Adherence_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Practice_Guidelines_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11884971
----K E
----T Monitoring one-year compliance to antihypertension medication in the Seychelles.
----A OBJECTIVE: To examine the compliance to medication among newly diagnosed hypertensive patients screened from the general population of the Seychelles, a rapidly developing country. METHODS: Among the 1067 participants to a population-based survey for cardiovascular risk factors, hypertension was discovered in 50 (previously unaware of having hypertension and having blood pressure > or = 160/95 mmHg over 3 visits). These 50 patients were placed on a daily one-pill regimen of medication (bendrofluazide, atenolol, or a combination of hydrochlorothiazide and atenolol) and compliance to the regimen was assessed over 12 months using electronic pill containers. Satisfactory compliance was defined as taking the medication on 6 or 7 days a week on average (which corresponds to a mean compliance level of > or = 86%). FINDINGS: In the first month, fewer than half (46%) of the new hypertension patients achieved satisfactory compliance, and only about one-quarter (26%) achieved this level by the twelfth month. Compliance was better among the 23 participants who regularly attended medical follow-up, with nearly three-quarters of these patients (74%) achieving satisfactory compliance during the first month and over one-half (55%) by the twelfth month. There was a direct association between mean 12-month compliance level and having a highly skilled occupation; having good health awareness; and regularly attending medical appointments. In contrast, there was an inverse relationship between mean compliance level and heavy drinking. CONCLUSION: The low proportion of people selected from the general population who were capable of sustaining satisfactory compliance to antihypertension medication may correspond to the maximum effectiveness of medication interventions based on a screening and treatment strategy in the general population. The results stress the need for both high-risk and population approaches to improve hypertension control.
----P Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Bendroflumethiazide_MeSH S_administration_&_dosage_MeSH Bendroflumethiazide_administration_&_dosage_MeSH M_Cross-Sectional_Studies_MeSH M_Drug_Monitoring_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Office_Visits_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH M_Self_Administration_MeSH S_utilization_MeSH Self_Administration_utilization_MeSH M_Seychelles_MeSH S_epidemiology_MeSH Seychelles_epidemiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11889011
----K I
----T Tolerability of beta-blocker initiation and titration in the Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF).
----A BACKGROUND: beta-Blockade improves survival when administered over a long period of time to patients with heart failure. However, the time course of any possible deterioration during the titration phase has not been reported. METHODS AND RESULTS: We looked at evidence of clinical deterioration in the Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF) by analyzing events and symptoms during the first 90 days. During titration, the Kaplan-Meier curves for the combined end point of all-cause mortality/all-cause hospitalization were similar in all patients randomized, with no significant difference in favor of placebo at any visit or in any of the analyzed subgroups (New York Heart Association class II, III/IV, or III/IV with ejection fraction <0.25, heart rate less-than-or-equal 76 bpm, and systolic blood pressure less-than-or-equal 120 mm Hg). The curves started to diverge in favor of beta-blockade after 60 days. Low heart rate was the main factor that limited titration. In New York Heart Association class III/IV, 5.9% of the patients receiving placebo discontinued study medicine during the first 90 days compared with 8.1% of those receiving metoprolol CR/XL (P=0.037 unadjusted, P=NS adjusted); corresponding figures in those with New York Heart Association class III/IV and ejection fraction <0.25 were 7.1% and 8.0% (P=NS). From day 90 until the end of the study, more patients in the placebo group discontinued study medicine in all subgroups. There was no change in diuretic or ACE inhibitor dosing with beta-blocker titration. Most patients reported no change in symptoms of breathlessness or fatigue during the titration phase. CONCLUSIONS: When carefully titrated, metoprolol CR/XL can be given safely to the overwhelming majority of patients with stable mild to moderate heart failure, with minimal side effects or deterioration.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Delayed-Action_Preparations_MeSH S_adverse_effects_MeSH Delayed-Action_Preparations_adverse_effects_MeSH S_therapeutic_use_MeSH Delayed-Action_Preparations_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Fatigue_MeSH S_chemically_induced_MeSH Fatigue_chemically_induced_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH M_Patient_Dropouts_MeSH S_statistics_&_numerical_data_MeSH Patient_Dropouts_statistics_&_numerical_data_MeSH M_Respiration_MeSH S_drug_effects_MeSH Respiration_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11888754
----K E
----T Amiodarone versus digoxin and metoprolol combination for the prevention of postcoronary bypass atrial fibrillation.
----A OBJECTIVE: This prospective randomized study aims at evaluation and comparison of the prophylactic effects of amiodarone versus digoxin and metoprolol combination in postcoronary bypass atrial fibrillation. METHODS: A total of 241 consecutive patients undergoing elective coronary artery bypass grafting were randomly allocated into three groups. Patients in Group1 (n=77) received metoprolol 100 mg/24 h per oral (P.O.), preoperatively, 2x0.5 mg digoxin intravenously on the operating day and digoxin 0.25 mg P.O.+metoprolol 100 mg P.O. on the first postoperative day until discharge. Patients in Group 2 (n=72) received totally 1200 mg intravenous/24 h amiodarone which the 300 mg - bolus dose/1 h was given as soon as the operation had been finished. On the next day patients were administered 450 mg/24 h amiodarone i.v. and 600 mg/day in three doses P.O. were given until discharge. Group 3 (n=92) was the control group with no antiarrhythmic prophylaxis. RESULTS: Preoperative patient characteristics and operative parameters were similar in three groups. Atrial fibrillation occurred in 13 patients (16.8%) in Group 1, six patients (8.3%) in Group 2 and 31 patients (33.6%) in Group 3. CONCLUSION: Both study groups were effective in the prevention of postcoronary bypass atrial fibrillation with respect to control (P<0.01 in Group 1 and P<0.001 in Group 2).
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH P_Coronary_Artery_Bypass_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Prospective_Studies_MeSH 
****** 11890356
----K 5
----T Pharmacological treatment of portal hypertension.
----A In liver cirrhosis, increased resistance to portal blood flow is the primary factor in the pathophysiology of portal hypertension. The recognition of a dynamic component in hepatic resistance due to the active-reversible contraction of different elements of the portohepatic bed, has led to the active development of hepatic vasodilators. On the other hand, a significant increase in portal blood flow caused by arteriolar splanchnic vasodilation and hyperkinetic circulation, aggravates portal hypertension and provides the rational for the use of splanchnic vasoconstrictors, such as beta-blockers, vasopressin derivatives and somatostatin and its analogs. This review covers current developments in the treatment of portal hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Liver_Cirrhosis_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH 
****** 11895062
----K I
----T Role of race in the pharmacotherapy of heart failure.
----A OBJECTIVE: To review the literature assessing the differences in response to angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in black patients compared with the response in non-black patients in the management of systolic heart failure. DATA SOURCES: A MEDLINE search (January 1966-May 2001) was performed using heart failure, blacks, Negroid race, adrenergic beta-antagonists, and angiotensin-converting enzyme inhibitors as key words. English-language articles were identified. Additional pertinent articles were identified from review of the references of these articles. STUDY SELECTION AND DATA EXTRACTION: All identified references were reviewed. All articles deemed relevant to the subject of this article were included. DATA SYNTHESIS: It has been suggested that the antihypertensive effect of ACE inhibitors and beta-blockers may be less in black patients than in other racial groups. Retrospective reanalyses of major heart failure trials have suggested that black patients may not realize a significant benefit in morbidity or mortality when heart failure is managed with ACE inhibitors or beta-blockers. It has also been suggested that black patients may respond more favorably than non-black patients to the combination of hydralazine and isosorbide dinitrate. CONCLUSIONS: Published reanalyses of ACE inhibitor and beta-blocker trials in heart failure provide weak data to support a lack of benefit in black patients. The published literature on this topic is limited by its retrospective nature. Firm conclusions regarding the influence of race on effectiveness of ACE inhibitors and beta-blockers cannot be made until prospective trials, with planned analysis of the effect of race, have been performed.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Drug_Therapy_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Randomized_Controlled_Trials_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11899501
----K 1
----T [Clinical study of the month. Effects of valsartan in chronic heart failure: the VAL-HeFT study]
----A Current guidelines recommend drugs which reduce neurohormonal activation as standard therapy for heart failure: angiotensin converting-enzyme (ACE) inhibitors, beta-blockers and spironolactone. The Valsartan Heart Failure Trial (Val-HeFT) tested the efficacy of the angiotensin-receptor blocker valsartan in addition to prescribed therapy. A total of 5010 patients with heart failure of NYHA class II, III or IV were randomly assigned to receive 160 mg of valsartan or placebo twice daily. Further angiotensin antagonism by valsartan did not improve survival but was beneficial in terms of morbidity and mortality, because of reduced rate of hospitalization, significant improvements in NYHA class, ejection fraction, signs and symptoms of heart failure, and quality of life. Valsartan had highly favourable effects in patients not receiving ACE inhibitors but an adverse effect in patients receiving both ACE inhibitors and beta-blockers. The effects of adding valsartan are depending on the importance of previous neurohormonal inhibition.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_pathology_MeSH Heart_Failure__Congestive_pathology_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_physiology_MeSH Receptors__Angiotensin_physiology_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Survival_Analysis_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH S_pharmacology_MeSH Tetrazoles_pharmacology_MeSH M_Treatment_Outcome_MeSH M_Valine_MeSH S_administration_&_dosage_MeSH Valine_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_pharmacology_MeSH Valine_pharmacology_MeSH M_Ventricular_Dysfunction__Left_MeSH 
****** 11903524
----K E
----T Topiramate in migraine prevention: a double-blind, placebo-controlled study.
----A OBJECTIVE: To evaluate the efficacy of topiramate in the preventative treatment of episodic migraine. BACKGROUND: Topiramate is a broad-spectrum antiepileptic drug effective for treatment of multiple seizure types in adults and children. Antiepileptic agents have demonstrated efficacy in migraine prevention, and open-label experience from our clinic has suggested that topiramate might be effective for this use. We consequently conducted a single-center, double-blind, placebo-controlled trial to evaluate the efficacy and safety of topiramate for the preventative treatment of migraine. METHODS: Forty patients, aged 19 to 62 years (mean, 38.2 years), were randomly assigned in a 1:1 ratio to receive topiramate (n = 19; all women) or placebo (n = 21; 20 women, 1 man). Following a prospective baseline phase of 4 weeks, the study drug dose was titrated weekly in 25-mg increments over 8 weeks to 200 mg per day or to the maximum tolerated dose. The titration phase was followed by an 8-week maintenance phase. RESULTS: During the entire double-blind phase, topiramate-treated patients experienced a significantly lower 28-day migraine frequency (3.31 +/- 1.7 versus 3.83 +/- 2.1; P =.002) compared to placebo, irrespective of use of concomitant migraine prevention medications. The mean 28-day migraine frequency was reduced by 36% in patients receiving topiramate as compared with 14% in patients receiving placebo (P =.004). Twenty-six percent of the patients on topiramate and 9.5% of the patients on placebo achieved a 50% reduction in migraine frequency (P >.05). The mean dose of topiramate was 125 mg per day (range, 25 to 200 mg per day). Topiramate was well tolerated; 2 of 19 topiramate-treated patients discontinued treatment due to adverse events. Adverse effects that occurred more frequently in topiramate-treated patients included paresthesia, weight loss, altered taste, anorexia, and memory impairment. CONCLUSIONS: Preventative therapy with topiramate significantly reduced migraine frequency. Larger multicenter clinical studies may further delineate the role of topiramate in migraine prevention.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Analgesics_MeSH S_administration_&_dosage_MeSH Analgesics_administration_&_dosage_MeSH M_Anorexia_MeSH S_chemically_induced_MeSH Anorexia_chemically_induced_MeSH M_Anticonvulsants_MeSH S_adverse_effects_MeSH Anticonvulsants_adverse_effects_MeSH S_pharmacology_MeSH Anticonvulsants_pharmacology_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Dysgeusia_MeSH S_chemically_induced_MeSH Dysgeusia_chemically_induced_MeSH M_Female_MeSH M_Fructose_MeSH S_adverse_effects_MeSH Fructose_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Fructose_analogs_&_derivatives_MeSH S_pharmacology_MeSH Fructose_pharmacology_MeSH S_therapeutic_use_MeSH Fructose_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Memory_Disorders_MeSH S_chemically_induced_MeSH Memory_Disorders_chemically_induced_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Paresthesia_MeSH S_chemically_induced_MeSH Paresthesia_chemically_induced_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Weight_Loss_MeSH S_drug_effects_MeSH Weight_Loss_drug_effects_MeSH 
****** 11903031
----K E
----T beta-Blockers and reduction of cardiac events in noncardiac surgery: scientific review.
----A CONTEXT: Recent studies suggest that perioperatively administered beta-blockers may reduce the risk of adverse cardiac events in patients undergoing major noncardiac surgery. OBJECTIVE: To review the efficacy of perioperative beta-blockade in reducing myocardial ischemia, myocardial infarction, and cardiac or all-cause mortality from randomized trials. DATA SOURCES: A MEDLINE and conventional search of English-language articles published since 1980 was performed to gather information related to perioperative cardiac complications and beta-blockade. Reference lists from all relevant articles and published recommendations for perioperative cardiac risk management were reviewed to identify additional studies. STUDY SELECTION AND DATA EXTRACTION: Prospective randomized studies (6) were included in the analysis if they discussed the impact of beta-blockade on perioperative cardiac ischemia, myocardial infarction, and mortality for patients undergoing major noncardiac surgery. Articles were examined for elements of trial design, treatment protocols, important biases, and major findings. These elements were then qualitatively compared. DATA SYNTHESIS: We identified 5 randomized controlled trials: 4 assessed myocardial ischemia and 3 reported myocardial infarction, cardiac, or all-cause mortality. All studies sought to achieve beta-blockade before the induction of anesthesia by titrating doses to a target heart rate. Of studies reporting myocardial ischemia, numbers needed to treat were modest (2.5-6.7). Similarly modest numbers needed to treat were observed in studies reporting a significant impact on cardiac or all-cause mortality (3.2-8.3). The most marked effects were seen in patients at high risk; the sole study reporting a nonsignificant result enrolled patients with low baseline risk. As a group, studies of perioperative beta-blockade have enrolled relatively few carefully selected patients. In addition, differences in treatment protocols leave questions unanswered regarding optimal duration of therapy. CONCLUSIONS: Despite heterogeneity of trials, a growing literature suggests a benefit of beta-blockade in preventing perioperative cardiac morbidity. Evidence from these trials can be used to formulate an effective clinical approach while definitive trials are awaited.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Algorithms_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Human_MeSH M_Intraoperative_Complications_MeSH S_mortality_MeSH Intraoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Intraoperative_Complications_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH P_Perioperative_Care_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH P_Surgical_Procedures__Operative_MeSH S_mortality_MeSH Surgical_Procedures__Operative_mortality_MeSH M_Sympatholytics_MeSH S_adverse_effects_MeSH Sympatholytics_adverse_effects_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH 
****** 11907634
----K 5
----T Morbidity and mortality in cardiovascular disorders: impact of reduced heart rate.
----A 
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Body_Constitution_MeSH S_physiology_MeSH Body_Constitution_physiology_MeSH M_Clinical_Trials_MeSH M_Follow-Up_Studies_MeSH M_Heart_Diseases_MeSH S_drug_therapy_MeSH Heart_Diseases_drug_therapy_MeSH S_epidemiology_MeSH Heart_Diseases_epidemiology_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH S_physiopathology_MeSH Heart_Diseases_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Life_Expectancy_MeSH M_Longevity_MeSH S_physiology_MeSH Longevity_physiology_MeSH M_Risk_Factors_MeSH 
****** 11910343
----K E
----T Effects of long-term propranolol and octreotide on postprandial hemodynamics in cirrhosis: a randomized, controlled trial.
----A BACKGROUND & AIMS: Postprandial increases in portal pressure may influence esophageal variceal rupture. The effects of chronic propranolol and octreotide (100 and 200 microg subcutaneously in a single dose) on postprandial hemodynamics were evaluated. METHODS: FIRST STUDY: 36 cirrhotic patients were studied at baseline and 30 and 60 minutes after a standard meal and then treated with propranolol (139 +/- 9 mg/d during 39 +/- 2 days). SECOND STUDY: After baseline measurements, patients were randomized into 3 groups: (1) placebo, (2) octreotide (100 microg), or (3) octreotide (200 microg) (n = 12 for each group). Thirty minutes postinjection a new baseline was established and measurements were repeated 30 and 60 minutes after the meal. RESULTS: First study: Baseline portal pressure was 18.1 +/- 1.2 mm Hg, 30 and 60 minutes after the meal it was 21.5 +/- 0.8 mm Hg and 20.5 +/- 0.8 mm Hg, respectively (both P < 0.01 vs. baseline). Cardiac index (CI) was 4.5 +/- 0.2, 4.8 +/- 0.2, and 4.9 +/- 0.2 L x min(-1) x m(-2), respectively (both P < 0.05 vs. baseline). Peripheral vascular resistance was 1012 +/- 56, 902 +/- 51 (P = NS), and 884 +/- 49 dynes x sec x cm(-5) (P< 0.05 vs. baseline), respectively. Second study: Propranolol and placebo did not blunt postprandial increase in portal pressure. Octreotide (100 microg) partially ameliorated postprandial increase in portal pressure. Octreotide (200 microg) significantly enhanced the portal hypotensive effect of propranolol and blunted the postprandial increase in portal pressure. CONCLUSIONS: Octreotide blunts postprandial increase in portal pressure not prevented by long-term propranolol administration.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Catheterization_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Hepatic_Veins_MeSH M_Human_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Liver_Cirrhosis_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Octreotide_MeSH S_administration_&_dosage_MeSH Octreotide_administration_&_dosage_MeSH M_Portal_Pressure_MeSH S_drug_effects_MeSH Portal_Pressure_drug_effects_MeSH M_Postprandial_Period_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Vasoconstrictor_Agents_MeSH S_administration_&_dosage_MeSH Vasoconstrictor_Agents_administration_&_dosage_MeSH 
****** 11910301
----K E
----T Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial.
----A BACKGROUND: Our aim was to determine if gene polymorphisms in the renin-angiotensin-aldosterone system (RAAS) were related to the degree of change in left ventricular hypertrophy (LVH) during antihypertensive treatment. METHODS AND RESULTS: Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months. The angiotensinogen T174M and M235T, the angiotensin-converting enzyme I/D, the AT1-receptor A1166C and the aldosterone synthase (CYP11B2) -344 C/T polymorphisms were analysed and related to the change in left ventricular mass (LVM). Patients with the angiotensinogen 174 TM genotype treated with irbesartan responded with the greatest reduction in LVM (-23 +/- 31SD g/m2 for TM and +0.5 +/- 18 g/m2 for TT, P = 0.005), independent of blood pressure reduction. Both the angiotensinogen 235 T-allele (P = 0.02) and the AT1-receptor 1166 AC genotype responded with the greatest reduction in LVM when treated with irbesartan (-0.1 +/- 19 g/m2 for AA and -18 +/- 30 g/m2 for AC, P = 0.02), independent of blood pressure reduction. These polymorphisms were not associated with the change in LVM during treatment with atenolol. DISCUSSION: The angiotensinogen T174M and M235T and the AT1-receptor A1166C polymorphisms were related to the change in LVH during antihypertensive treatment with an AT1-receptor antagonist; of these angiotensinogen T174M was the most powerful. This highlights the role of the RAAS for left ventricular hypertrophy and the potential of pharmacogenetics as a tool for guidance of antihypertensive therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Alleles_MeSH M_Angiotensinogen_MeSH S_genetics_MeSH Angiotensinogen_genetics_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_genetics_MeSH Hypertrophy__Left_Ventricular_genetics_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Polymorphism_(Genetics)_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_genetics_MeSH Receptors__Angiotensin_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 11910315
----K E
----T Double-blind, placebo-controlled crossover comparison of five classes of antihypertensive drugs.
----A OBJECTIVE: Hypertension guidelines recommend initial treatment with a beta-blocker or diuretic and adding the other drug where blood pressure is not controlled. We hypothesized that systematic rotation through the major classes of antihypertensive drugs would demonstrate substantial differences in the pattern of an individual patient's response, and suggest a more rational approach to choosing best treatment. DESIGN: Thirty-four young hypertensives (age 28-55, median 47) rotated in a double-blind, Latin-square, crossover fashion through 6 weeks of treatment each with amlodipine, doxazosin, lisinopril, bisoprolol, bendrofluazide and placebo. Blood pressure was measured at each visit. 'Best' drug, defined by efficacy and tolerability, was repeated at the end. RESULTS: Rotation doubled the number of patients reaching target blood pressure (systolic < 140 mmHg) on one drug (P = 0.03). All five drugs were represented among the 'best' drugs. In six patients, the blood pressure on 'best' drug was at least 10 mmHg lower than on any other. Response to the 'best' drug was highly correlated (r = 0.79) with its previous administration. By contrast, there were only weak correlations between responses to pairs of drugs, except for angiotensin-converting enzyme (ACE) inhibitor (A) with beta-blocker (B), and calcium blocker (C) with diuretic (D) - each r = 0.71, P < 0.005). In these young patients, the majority of patients (23/34) responded best to a drug suppressing the renin system (A and B). CONCLUSIONS: Patients vary reproducibly in their response to initial treatment, and switching among drugs can increase the efficacy of monotherapy. The results support an AB/CD scheme for choosing therapy, in which the first drug is taken from one of these pairs, and uncontrolled patients switch to one of the other pair.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH M_Bendroflumethiazide_MeSH S_administration_&_dosage_MeSH Bendroflumethiazide_administration_&_dosage_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_administration_&_dosage_MeSH Doxazosin_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lisinopril_MeSH S_administration_&_dosage_MeSH Lisinopril_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11913603
----K E
----T African-American ethnicity in epidemiological studies of calcium antagonists in relation to cancer.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_African_Continental_Ancestry_Group_MeSH S_genetics_MeSH African_Continental_Ancestry_Group_genetics_MeSH M_Age_Distribution_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neoplasms_MeSH S_chemically_induced_MeSH Neoplasms_chemically_induced_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH S_ethnology_MeSH Neoplasms_ethnology_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11912816
----K E
----T Implications of the United Kingdom Prospective Diabetes Study (UKPDS) results on patient management.
----A The goal of treatment of type 2 diabetes is to treat early and balance the risk/benefit ratio of aggressive therapeutic intervention for the patient. The results of the UKPDS trial have shown that treatment to improve overall glucose control significantly reduces the risk of microvascular complications and thereby improves the quality of life for persons with diabetes. Optimal medical management includes a team approach and uses continuous communication and education, medical treatment, lifestyle modifications, and behavior changes to improve glycemic control.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Combined_Modality_Therapy_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_metabolism_MeSH Diabetes_Mellitus__Type_II_metabolism_MeSH S_psychology_MeSH Diabetes_Mellitus__Type_II_psychology_MeSH S_therapy_MeSH Diabetes_Mellitus__Type_II_therapy_MeSH M_Diabetic_Diet_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_metabolism_MeSH Hemoglobin_A__Glycosylated_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Intensive_Care_MeSH S_methods_MeSH Intensive_Care_methods_MeSH S_standards_MeSH Intensive_Care_standards_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 11916185
----K E
----T Transjugular intrahepatic portosystemic shunt versus endoscopic therapy: randomized trials for secondary prophylaxis of variceal bleeding: an updated meta-analysis.
----A 
----P Comment Editorial Meta-Analysis 
----M M_Comparative_Study_MeSH M_Endoscopy__Digestive_System_MeSH S_methods_MeSH Endoscopy__Digestive_System_methods_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH S_methods_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_methods_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Risk_Assessment_MeSH M_Treatment_Outcome_MeSH 
****** 11918251
----K I
----T Effects of beta-blockers on sexual performance in men with coronary heart disease. A prospective, randomized and double blinded study.
----A In a prospective trial assessing the effects of beta-blockers on sexual function men with coronary heart disease were randomized to a 4 month treatment with sustained release metoprolol 95 mg or placebo. A standardized and validated self-report questionnaire (KEED = Kolner Erhebungsbogen der Erektilen Dysfunktion) dealing with several aspects of sexual performance in men had to be answered at the beginning and at the end of the study. Based on 65 patients completing the study, sex life seemed unaffected by metoprolol treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Human_MeSH M_Impotence_MeSH S_chemically_induced_MeSH Impotence_chemically_induced_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11923805
----K 2
----T Effects of bisoprolol fumarate on left ventricular size, function, and exercise capacity in patients with heart failure: analysis with magnetic resonance myocardial tagging.
----A BACKGROUND: Recent data suggest that beta-blockers can be beneficial in subgroups of patients with chronic heart failure (CHF). For metoprolol and carvedilol, an increase in ejection fraction has been shown and favorable effects on the myocardial remodeling process have been reported in some studies. We examined the effects of bisoprolol fumarate on exercise capacity and left ventricular volume with magnetic resonance imaging (MRI) and applied a novel high-resolution MRI tagging technique to determine myocardial rotation and relaxation velocity. METHODS: Twenty-eight patients (mean age, 57 +/- 11 years; mean ejection fraction, 26 +/- 6%) were randomized to bisoprolol fumarate (n = 13) or to placebo therapy (n = 15). The dosage of the drugs was titrated to match that of the the Cardiac Insufficiency Bisoprolol Study protocol. Hemodynamic and gas exchange responses to exercise, MRI measurements of left ventricular end-systolic and end-diastolic volumes and ejection fraction, and left ventricular rotation and relaxation velocities were measured before the administration of the drug and 6 and 12 months later. RESULTS: After 1 year, heart rate was reduced in the bisoprolol fumarate group both at rest (81 +/- 12 before therapy versus 61 +/- 11 after therapy; P <.01) and peak exercise (144 +/- 20 before therapy versus 127 +/- 17 after therapy; P <.01), which indicated a reduction in sympathetic drive. No differences were observed in heart rate responses in the placebo group. No differences were observed within or between groups in peak oxygen uptake, although work rate achieved was higher (117.9 +/- 36 watts versus 146.1 +/- 33 watts; P <.05) and exercise time tended to be higher (9.1 +/- 1.7 minutes versus 11.4 +/- 2.8 minutes; P =.06) in the bisoprolol fumarate group. A trend for a reduction in left ventricular end-diastolic volume (-54 mL) and left ventricular end-systolic volume (-62 mL) in the bisoprolol fumarate group occurred after 1 year. Ejection fraction was higher in the bisoprolol fumarate group (25.0 +/- 7 versus 36.2 +/- 9%; P <.05), and the placebo group remained unchanged. Most changes in volume and ejection fraction occurred during the latter 6 months of treatment. With myocardial tagging, insignificant reductions in left ventricular rotation velocity were observed in both groups, whereas relaxation velocity was reduced only after bisoprolol fumarate therapy (by 39%; P <.05). CONCLUSION: One year of bisoprolol fumarate therapy resulted in an improvement in exercise capacity, showed trends for reductions in end-diastolic and end-systolic volumes, increased ejection fraction, and significantly reduced relaxation velocity. Although these results generally confirm the beneficial effects of beta-blockade in patients with chronic heart failure, they show differential effects on systolic and diastolic function.
----P Clinical_Trial Journal_Article Letter Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH P_Exercise_Tolerance_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_anatomy_&_histology_MeSH Heart_Ventricles_anatomy_&_histology_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Human_MeSH M_Magnetic_Resonance_Imaging_MeSH S_methods_MeSH Magnetic_Resonance_Imaging_methods_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Respiratory_Function_Tests_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 11926017
----K E
----T Current standard of care in patients affected by coronary heart disease in Italy: the MC'95 study.
----A BACKGROUND: The aims of MC'95 were to verify i) whether the main risk factors for coronary heart disease had been recorded in the hospital medical records of patients admitted for coronary events; ii) how modifiable risk factors had been managed by drug therapy and lifestyle advices following hospitalization; iii) whether first-degree blood relatives of patients had been screened for coronary heart disease risk factors. METHODS: The survey concerned 40 hospital units across Italy admitting patients with acute coronary events or offering interventional cardiology or cardiac surgery. Two thousand and four hospital records (50 for each unit) of consecutive patients (< or = 74 years, 21% women) discharged within 6 months before initiation of the study (November 1995) were reviewed and the patients were invited for a follow-up examination from 6 to 9 months after hospital discharge. RESULTS: The prevalence of patients positive for risk factors reported was: 58.5% for high total cholesterol (> or = 5.2 mmol/l), 46.9% for high blood pressure (> or = 140/90 mmHg), 35.2% for smoking, 20.2% for high blood glucose (> 7 mmol/l), and 14.2% for obesity (body mass index > or = 30 kg/m2). A number of medical records did not provide complete information on risk factors: 24.1% for body mass index, 11.0% for serum cholesterol, and 11.6% for a family history of premature coronary heart disease. Eighty-nine percent of the patients attended the follow-up examination. Their care during the follow-up period was managed by general practitioners (30.5%), cardiologists (37.2%) and/or at hospital outpatient clinics (42.4%). At follow-up examination the prevalence of hypercholesterolemia increased to 62.2%, that of uncontrolled hypertension decreased to 32.2%, and the percentage of smokers decreased to 13.6%. The adherence to the drug treatment prescribed at discharge was as follows: 69.6% for lipid-lowering agents, 81.2% for ACE-inhibitors and beta-blockers, and 90.8% for antiplatelet agents. A family history of premature heart disease was reported in 55.1% of patients but screening for coronary heart disease risk factors was extended to relatives in less than 25% of cases. CONCLUSIONS: The prevalence of modifiable risk factors is high in patients with different clinical manifestations of coronary heart disease. The prescriptions for secondary prevention and their efficacy after hospital discharge and the surveying of relatives for primary prevention need to be improved. For this purpose, a more coordinated intervention of primary care physicians, cardiologists and cardiac surgeons is mandatory.
----P Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Drug_Therapy_MeSH S_standards_MeSH Drug_Therapy_standards_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Male_MeSH M_Medical_Records_MeSH S_standards_MeSH Medical_Records_standards_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Patient_Admission_MeSH S_standards_MeSH Patient_Admission_standards_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11927527
----K I
----T Metoprolol CR/XL in female patients with heart failure: analysis of the experience in Metoprolol Extended-Release Randomized Intervention Trial in Heart Failure (MERIT-HF).
----A BACKGROUND: Underrepresentation of women in heart failure clinical trials has limited conclusions regarding the effect of various management strategies on survival in women with heart failure and decreased left ventricular ejection fraction (LVEF). METHODS AND RESULTS: MERIT-HF (Metoprolol Extended-Release Randomized Intervention Trial in Heart Failure) was a randomized, placebo-controlled study, the purpose of which was to evaluate the effect of metoprolol controlled-release/extended-release (CR/XL) in 3991 patients with New York Heart Association class II to IV heart failure and LVEF < or =0.40. We performed a post hoc analysis to evaluate the effect of metoprolol CR/XL on outcome in women (n=898), including the outcome in 183 women with severe heart failure (New York Heart Association class III/IV and LVEF < 0.25). Treatment with metoprolol CR/XL in women resulted in a 21% reduction in the primary combined end point of all-cause mortality/all-cause hospitalizations (164 versus 137 patients; P=0.044). The number of cardiovascular hospitalizations was reduced by 29% (164 versus 120; P=0.013), and hospitalization for worsening heart failure was reduced by 42% (95 versus 56; P=0.021). Similar results were noted in the subgroup of women with severe heart failure, with a 57% reduction in cardiovascular hospitalizations (63 versus 30; P=0.005) and a 72% reduction in hospitalization due to worsening heart failure (46 versus 14; P=0.0004). A pooling of mortality results from MERIT-HF, the Cardiac Insufficiency Bisoprolol Study (CIBIS II), and the Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) showed very similar survival benefits in women and men. CONCLUSIONS: The beneficial effects of metoprolol CR/XL extend to women with heart failure, including women with clinically stable severe heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Delayed-Action_Preparations_MeSH M_Drug_Therapy__Combination_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11927206
----K E
----T The effect of patient selection on comorbidity-adjusted operative mortality risk. Implications for outcomes studies of surgical procedures.
----A Consumers of outcomes research may assume that risk-adjustment procedures based on patients' comorbid conditions will control for baseline prognostic differences between comparison groups, so that differences in risk-adjusted outcomes represent effects other than those due to differences in comorbidity severity. However, surgeons may differ in their threshold to operate on patients with different intensities of the same comorbidity, which may not be accounted for using commonly employed risk-adjustment methods. We developed a model to explore the effect that selection based on comorbidity severity could have on estimates of the risk-adjusted relative risk (RR) of operative death. Larger effects on the apparent RR of operative death were observed when both the proportion of patients in the high-risk ("selected") stratum and the relative increase in the risk of death due to being in the high-risk stratum were large. Biased estimates of the risk-adjusted RR of operative death will be observed if surgeons differentially select patients based on comorbidity severity and if differences in comorbidity severity are not captured by the risk-adjustment methodology.
----P Journal_Article 
----M P_Comorbidity_MeSH M_Human_MeSH M_Models__Statistical_MeSH P_Patient_Selection_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Surgical_Procedures__Operative_MeSH S_mortality_MeSH Surgical_Procedures__Operative_mortality_MeSH 
****** 11927787
----K E
----T More on isolated systolic hypertension, diabetes, nephropathy and hypertension, and use of low-sodium diets in obese hypertensives.
----A The authors evaluated the treatment of isolated systolic hypertension based on medical record review of charts between 1998 and 1999 in a multispecialty physician practice group. Two age-stratified random samples of ambulatory medical records were examined (393 patients aged > or =65 years and 251 patients aged 50-64 years). The samples corresponded to the practices of 35 primary care physicians who were surveyed about their hypertension care. Isolated systolic hypertension was defined as systolic blood pressure > or =140 mm Hg and diastolic blood pressure <90 mm Hg. Results showed that isolated systolic hypertension represented 76% and 45% of uncontrolled blood pressure in the older and middle-aged samples, respectively. Isolated systolic hypertension was often undiagnosed and untreated. Physicians reported treatment thresholds and goals that were significantly less aggressive for their patients > or =65 years of age. Physician awareness and treatment of isolated systolic hypertension have not yet caught up with consensus guidelines, and older patients may be affected most by this gap.
----P Editorial 
----M M_Diabetes_Mellitus_MeSH S_physiopathology_MeSH Diabetes_Mellitus_physiopathology_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus_prevention_&_control_MeSH M_Diet__Sodium-Restricted_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Kidney_Diseases_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH S_prevention_&_control_MeSH Kidney_Diseases_prevention_&_control_MeSH M_Obesity_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH M_Systole_MeSH 
****** 11937178
----K I
----T Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.
----A BACKGROUND: Blood pressure reduction achieved with beta-blockers and diuretics is the best recorded intervention to date for prevention of cardiovascular morbidity and death in patients with hypertension. Left ventricular hypertrophy (LVH) is a strong independent indicator of risk of cardiovascular morbidity and death. We aimed to establish whether selective blocking of angiotensin II improves LVH beyond reducing blood pressure and, consequently, reduces cardiovascular morbidity and death. METHODS: We did a double-masked, randomised, parallel-group trial in 9193 participants aged 55-80 years with essential hypertension (sitting blood pressure 160-200/95-115 mm Hg) and LVH ascertained by electrocardiography (ECG). We assigned participants once daily losartan-based or atenolol-based antihypertensive treatment for at least 4 years and until 1040 patients had a primary cardiovascular event (death, myocardial infarction, or stroke). We used Cox regression analysis to compare regimens. FINDINGS: Blood pressure fell by 30.2/16.6 (SD 18.5/10.1) and 29.1/16.8 mm Hg (19.2/10.1) in the losartan and atenolol groups, respectively. The primary composite endpoint occurred in 508 losartan (23.8 per 1000 patient-years) and 588 atenolol patients (27.9 per 1000 patient-years; relative risk 0.87, 95% CI 0.77-0.98, p=0.021). 204 losartan and 234 atenolol patients died from cardiovascular disease (0.89, 0.73-1.07, p=0.206); 232 and 309, respectively, had fatal or non-fatal stroke (0.75, 0.63-0.89, p=0.001); and myocardial infarction (non-fatal and fatal) occurred in 198 and 188, respectively (1.07, 0.88-1.31, p=0.491). New-onset diabetes was less frequent with losartan.Interpretation Losartan prevents more cardiovascular morbidity and death than atenolol for a similar reduction in blood pressure and is better tolerated. Losartan seems to confer benefits beyond reduction in blood pressure.
----P Clinical_Trial Comment Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11937179
----K I
----T Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.
----A BACKGROUND: The most suitable antihypertensive drug to reduce the risk of cardiovascular disease in patients with hypertension and diabetes is unclear. In prespecified analyses, we compared the effects of losartan and atenolol on cardiovascular morbidity and mortality in diabetic patients. METHODS: As part of the LIFE study, in a double-masked, randomised, parallel-group trial, we assigned a group of 1195 patients with diabetes, hypertension, and signs of left-ventricular hypertrophy (LVH) on electrocardiograms losartan-based or atenolol-based treatment. Mean age of patients was 67 years (SD 7) and mean blood pressure 177/96 mm Hg (14/10) after placebo run-in. We followed up patients for at least 4 years (mean 4.7 years [1.1]). We used Cox regression analysis with baseline Framingham risk score and electrocardiogram-LVH as covariates to compare the effects of the drugs on the primary composite endpoint of cardiovascular morbidity and mortality (cardiovascular death, stroke, or myocardial infarction). FINDINGS: Mean blood pressure fell to 146/79 mm Hg (17/11) in losartan patients and 148/79 mm Hg (19/11) in atenolol patients. The primary endpoint occurred in 103 patients assigned losartan (n=586) and 139 assigned atenolol (n=609); relative risk 0.76 (95% CI 0.58-.98), p=0.31. 38 and 61 patients in the losartan and atenolol groups, respectively, died from cardiovascular disease; 0.63 (0.42-0.95), p=0.028. Mortality from all causes was 63 and 104 in losartan and atenolol groups, respectively; 0.61 (0.45-0.84), p=0.002. INTERPRETATION: Losartan was more effective than atenolol in reducing cardiovascular morbidity and mortality as well as mortality from all causes in patients with hypertension, diabetes, and LVH. Losartan seems to have benefits beyond blood pressure reduction.
----P Clinical_Trial Comment Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11938776
----K E
----T [Efficacy of native carvedilol in patients with essential hypertension]
----A To compare the efficacy of native carvedilol(Cv) with native atenolol(At), we treated 80 cases of essential hypertension(stage I-II) for 4 weeks, using both open-test and double blind randomized imitative methods. The daily dose of carvedilol was 10 mg to 40 mg, and that of atenolol was 50 mg to 100 mg. Both drugs were given once daily. Out of 30 cases of Cv group, carvedilol showed significant efficiency in 20 cases, and was effective in 6 cases. The total therapeutic efficiency was 86.2% (26/30). In the double blind groups(25 patients in each group), those treated with carvedilol(Group A) had 21 effective cases(84.0%) while those treated with atenolol(Group B) had 18 effective cases(72.0%). A lower incidence of adverse effects was observed in carvedilol group. Dizziness occurred similarly in both drugs, but it lasted only a short time and could be tolerated. The recommended dose of 10-30 mg once daily would be appropriate. After treatment there was a significant reduction in blood pressure in both groups(P < 0.01). It suggests that native carvedilol is a safe and effective anti-hypertensive agent.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 11940545
----K E
----T Paradoxical pressor effects of beta-blockers in standing elderly patients with mild hypertension: a beneficial side effect.
----A BACKGROUND: Baroreflex sensitivity declines with age, creating a fall in systolic blood pressure and pulse pressure when standing. If, in addition, blood pressure is reduced as a result of antihypertensive medication, compensatory mechanisms may be inadequate and orthostatic problems may occur. This may be less true in patients on beta-blockers. beta-blockers cause pressor effects in standing patients with autonomic neuropathy, but their effects on standing pulse pressures in elderly subjects with mild hypertension have not been systematically studied. METHODS AND RESULTS: We studied 3741 patients with mild hypertension for 6 months who were being treated with the beta-blocker nebivolol 5 mg daily. Blood pressures were measured after 10 minutes in the supine position and after 1 minute in the standing position. Overall, systolic and diastolic blood pressures rose slightly while standing, whereas pulse pressures remained unchanged. When previously untreated patients (n=2085) >60 and <60 years of age were assessed separately, supine pulse pressures were consistently higher in the elderly group compared with those of the younger subjects by 6 to 11 mm Hg (P<0.001 to 0.0001). However, while standing, pulse pressures rose in the younger subjects, whereas they tended to fall in the elderly group. After 6 months of beta-blockade, this pattern was unchanged in the younger subjects but reversed into significant rise of pulse pressures in the elderly group by 4 (SD 1) mm Hg (P<0.001). In the patients previously treated with other classes of antihypertensive drugs (n=712), the effects were essentially the same. CONCLUSIONS: In elderly patients with mild hypertension, a depressor trend of pulse pressure while standing can be turned into a significant pressor response by treatment with a beta-blocker.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypotension__Orthostatic_MeSH S_prevention_&_control_MeSH Hypotension__Orthostatic_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Netherlands_MeSH P_Posture_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 11941903
----K 1
----T Gender differences in the treatment of hypertension: a community based study in Porto.
----A OBJECTIVES: To describe the use of antihypertensive drugs in a random sample of adults living in Porto, Portugal, and to identify gender differences in the treatment of hypertension. DESIGN: Observational, cross-sectional. PARTICIPANTS AND METHODS: Nine hundred and fifty-nine participants over 39 years of age, living in Porto, were selected by random digit dialing. For each subject, socioeconomic characterization, family and personal medical history, and information on antihypertensive treatment were obtained through a questionnaire. Blood pressure was measured on a single occasion, and a fasting blood sample was collected. Gender differences in the treatment of arterial hypertension and number and type of drugs were evaluated through the calculation of female:male proportion ratios and 95% confidence intervals (95% CI). RESULTS: Hypertension treatment was more frequent in women than in men (proportion ratio 1.40, 95% CI 1.15-1.72), although no differences were observed among hypertensives aware of their condition (proportion ratio 1.07, 95% CI 0.93-1.22). The female:male proportion ratios of treatment with one drug, fixed combination therapy and free combination therapy were 1.13 (95% CI 0.94-1.36), 0.83 (95% CI 0.34-2.01) and 0.76 (95% CI 0.49-1.19), respectively. In subjects treated with one drug the use of ACE inhibitors/AT-II antagonists was more frequent in men (proportion ratio 0.68, 95% IC 0.46-1.01) and treatment with diuretics higher in women (proportion ratio 1.83, 95% CI 1.04-3.23). In participants treated with combination therapy, ACE inhibitors/AT-II antagonists and diuretics were more frequently used by women and calcium channel blockers and beta-blockers by men (female:male proportion ratios were 1.27, 95% CI 0.96-1.68, 1.24, 95% CI 0.94-1.64, 0.61, 95% CI 0.37-1.02 and 0.74, 95% CI 0.31-1.79, respectively). CONCLUSIONS: Arterial hypertension tended to be more frequently treated among women and different therapeutic options were found according to gender. Gender differences in the awareness of hypertension, sexual specificity of the activity of antihypertensive drugs, and comorbidity may play a role in gender inequalities in the treatment of hypertension in Portugal.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portugal_MeSH M_Sex_Factors_MeSH 
****** 11950447
----K I
----T Comparison of effects of carvedilol versus metoprolol on cytokine levels in patients with idiopathic dilated cardiomyopathy.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_metabolism_MeSH Cardiomyopathy__Congestive_metabolism_MeSH M_Cytokines_MeSH S_blood_MeSH Cytokines_blood_MeSH S_drug_effects_MeSH Cytokines_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Interleukin-6_MeSH S_blood_MeSH Interleukin-6_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Tumor_Necrosis_Factor_MeSH S_drug_effects_MeSH Tumor_Necrosis_Factor_drug_effects_MeSH 
****** 11957798
----K 1
----T [Influence of therapy schedule on hospitalization frequency and prognosis in heart failure in 3 yrs. observations]
----A Patients with severe systolic heart left ventricle dysfunction determine a group loaded by high mortality. Continuous search for prognostic factors as well as treatment methods influencing a prognosis coming from clinical effects of applied prescriptions and survival in the mentioned group of patients can be observed in many published reports. In the presented work a retrospective analysis has been performed with regard to 106 patients with severe heart lesion: 72 cases with ischaemic disease, 20 cases with post-inflammation heart lesion, 7 cases with hypertension and 7 cases with idiopathic congestive cardiomyopathy. The main criterion including particular patient into the group under analysis was less or equal to 30% ejection fraction confirmed by echocardiographical examination and generally understand heart insufficiency in the clinical examination and laboratory tests. The observation period concerning patients qualified to the analyzed group incorporated 36 +/- 16.5 months. Influence of the parameters obtained from clinical, electrocardiographical, Holter monitoring, chest X-Ray, and serum concentration of both sodium (Na) and potassium (K) have been analyzed. Also the survival analysis has been performed for patients treated: according standard procedures, with addition of beta-adrenolytic drug, with addition of amiodaron, with addition of combination of both beta-adrenolytic drug and amiodaron. During the observation 64 patients have died (60%), 4 patients have had heart transplantation (Htx) performed (4%) and 38 patients survived without necessity of Htx (36%). Among investigated parameters there were following ones which proved their statistical significance in terms of prognosis evaluation: ejection fraction, features of pulmonary haemostasis, HR (heart rate), SBP (systolic blood pressure), serum concentration of both sodium (Na) and potassium (K). Much better therapy effects as well as longer survival have concerned patients with hypertension disease confirmed during the anamnesis. Comparison of the survival curves referring to the patients treated according to different schemes a positive trend in the direction of survival improvement has been observed. This trend however appeared in the group treated additionally with beta-blocker and only in the outpatient follow-up. On the other hand a combination of both beta-blocker and amiodaron has been connected with improved both early and outpatient follow-up survival. The survival curves for patients treated with amiodaron only has been quite similar as in the case of patients treated according standard procedures. Addition of beta-adrenolytic drug or amiodaron or eventually both of these medicines has a significant influence into decrease of repeated hospitalizations in the group under investigation.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Survival_Analysis_MeSH M_Thiazoles_MeSH S_administration_&_dosage_MeSH Thiazoles_administration_&_dosage_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH 
****** 11959051
----K E
----T Therapeutic options and heart failure survival score predictability in an academic heart failure center: an analysis of 120 consecutive patients during a 1-year period.
----A BACKGROUND: the incidence and prevalence of patients with advanced heart failure is increasing worldwide and the number of cardiac transplantations remains limited. AIMS: it was the aim of the study to describe our experience with the increasing number of available medical, interventional and cardiac surgery options, and to assess heart failure survival score predictability in an academic heart failure center within a 1-year follow-up. METHODS AND RESULTS: in all patients who were referred for cardiac transplant evaluation within a 12-month period between April 1998 and March 1999 at our Interdisciplinary Heart Failure and Transplant Program, our team assessed all medical interventions as well as interventional and surgical treatment options that were available, based on the clinical profile on initial presentation. In 92% of the 120 patients referred for cardiac transplantation evaluation, drug therapy could be optimized. A considerable number of patients could be subjected to an organ-preserving intervention or surgery, either PTCA (n=11), CABG (n=4), valve repair (n=7), multisite pacing (n=7), or partial ventricular resection (n=5). Only a small group of patients with the worst heart failure survival score were listed for heart transplantation (n=17) or received a ventricular assist device (n=3). CONCLUSIONS: within a contemporary cohort of advanced heart failure patients, only a small number of patients will undergo cardiac transplantation, which is predictable by the heart failure survival score. Most patients will undergo optimized medical therapy and a considerable number will be subjected to interventional or surgical treatment options.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Decision_Making_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Germany_MeSH S_epidemiology_MeSH Germany_epidemiology_MeSH M_Heart_Failure__Congestive_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Heart_Transplantation_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH 
****** 11959238
----K E
----T Effect of carvedilol therapy on functional mitral regurgitation, ventricular remodeling, and contractility in patients with heart failure due to left ventricular systolic dysfunction.
----A 
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Mitral_Valve_Insufficiency_MeSH S_drug_therapy_MeSH Mitral_Valve_Insufficiency_drug_therapy_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH S_physiology_MeSH Systole_physiology_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 11960591
----K I
----T The role of race in heart failure therapy.
----A Heart failure in blacks is a unique malady characterized by a different natural history, more worrisome prognosis, and potential variances in the response to current medical therapy for heart failure. The overwhelming burden of hypertension as a putative cause of left ventricular dysfunction identifies this illness. Although differences in the response to medical therapy have been described, angiotensin-converting enzyme inhibitors and beta-blockers remain the most appropriate therapy. Certain genetic polymorphisms may exist that explain the observed differences.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_African_Continental_Ancestry_Group_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Continental_Population_Groups_MeSH M_Coronary_Arteriosclerosis_MeSH S_complications_MeSH Coronary_Arteriosclerosis_complications_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH S_ethnology_MeSH Coronary_Arteriosclerosis_ethnology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Incidence_MeSH M_Prognosis_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_epidemiology_MeSH Ventricular_Dysfunction__Left_epidemiology_MeSH S_ethnology_MeSH Ventricular_Dysfunction__Left_ethnology_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 11967798
----K E
----T Reduction of resistance artery stiffness by treatment with the AT(1)-receptor antagonist losartan in essential hypertension.
----A In spontaneously hypertensive rats resistance artery structure, endothelial dysfunction and geometry-independent wall stiffness were reduced by an angiotensin AT(1)-receptor antagonist. In previous studies of human hypertension, interruption of the renin-angiotensin system corrected small artery structure and endothelial dysfunction, whereas the beta-blocker atenolol did not. We hypothesized that the AT(1)R antagonist losartan, but not the beta-blocker atenolol, would reduce stiffness of gluteal subcutaneous small arteries in essential hypertensive patients. Seventeen untreated mild essential hypertensive patients (47+/-2 years; 75% male) were randomly assigned in double-blind fashion to losartan or atenolol treatment for one year. Small, resistance size arteries were studied on pressurized myographs. Blood pressure (mmHg) was reduced (p<0.01) from 145 +/- 4/101 +/- 2 and 147 +/- 6/98 +/- 2 to 128 +/- 4/86 +/- 2 and 131 +/- 3/84 +/- 1 by losartan and atenolol, respectively. The media/lumen ratio of small arteries was unaffected by atenolol (8.3+/-0.3% before and 8.8+/-0.5% after treatment). In contrast, losartan reduced media/lumen ratio from 8.4+/-0.4% to 6.7+/-0.3% (p<0.01). Whereas isobaric elastic modulus was unaffected by either treatment, geometry-independent stiffness (slope of elastic modulus vs. stress) was reduced from 9.7+/-1.2 to 6.1+/-0.9 (P<0.05) under losartan treatment, but was unchanged by atenolol (8.2+/-1.3 to 7.8+/-0.6). In conclusion, treatment with losartan reduced stiffness and structural alterations of subcutaneous resistance arteries of previously untreated essential hypertensive patients, whereas atenolol failed to do so.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Buttocks_MeSH M_Elasticity_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Skin_MeSH S_blood_supply_MeSH Skin_blood_supply_MeSH M_Support__Non-U_S__Gov't_MeSH P_Vascular_Resistance_MeSH 
****** 11975770
----K I
----T Verapamil revisited: a transition in novel drug delivery systems and outcomes.
----A Verapamil, the oldest calcium-channel blocker, is now being rediscovered and reevaluated in the light of new novel drug delivery systems and new evidence-based trials. Verapamil, a phenylalkylamine, is useful in the treatment of hypertension, stable angina, and narrow QRS supraventricular arrhythmias. This calcium antagonist is effective in both young and old, and both black and white hypertensive patients, and is free of metabolic side effects. Verapamil has a well-documented history as an effective antianginal agent when directly compared with a beta-blocker, and is more effective in reducing myocardial ischemia compared with amlodipine monotherapy. Because of the short half-life of verapamil, drug delivery systems are used to prolong the duration of action. Novel drug delivery systems using encapsulated beads or a modified osmotic pump have been designed to be taken at nighttime to provide maximal blood pressure reduction in the early morning hours and effective 24-hour blood pressure control, and to avoid excessive blood pressure reduction during sleep. The Verapamil in Hypertension and Atherosclerosis Study has documented equivalent effectiveness of verapamil compared with chlorthalidone, but showed superior plaque regression and reduced events in subjects with the greatest plaques with verapamil treatment. The Angina Prognosis Study in Stockholm, comparing verapamil and metoprolol for stable angina, found no difference in total cardiovascular mortality or combined cardiovascular events. Other large ongoing randomized, multicenter trials, including Controlled-Onset Verapamil Investigation of Cardiovascular Endpoints and the International Verapamil-Trandolapril Study, will expand our knowledge of the role of verapamil in the treatment of hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Anti-Arrhythmia_Agents_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Double-Blind_Method_MeSH M_Drug_Delivery_Systems_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Multicenter_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 11975823
----K 4
----T Cardiovascular considerations in using topical, oral, and intravenous drugs for the treatment of glaucoma and ocular hypertension: focus on beta-adrenergic blockade.
----A Glaucoma and ocular hypertension are highly prevalent conditions in individuals over the age of 40 and are commonly seen together in patients with cardiovascular disease. Many of the antiglaucoma medications, when systemically absorbed, affect the sympathetic and parasympathetic nervous systems of patients and can cause cardiovascular toxicity. Such adverse effects are frequently associated with the long-term use of potentially toxic agents in elderly people, who are most prone to chronic eye disease. Moreover, patients may not associate their symptoms with the topical eye medications, and consequently may not report adverse drug effects. Drug-drug interactions can also occur when patients are taking medications for both cardiovascular disease and glaucoma. This review focuses on beta-adrenergic blockers as topical antiglaucoma medications and other topical antiglaucoma drugs. The systemic toxicity of these agents is reviewed, along with the possible drug interactions. Brief mention is also made of other antiglaucoma medications used alone and in combination with topical beta-blockers.
----P Journal_Article Review Review__Tutorial 
----M M_Administration__Topical_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Betaxolol_adverse_effects_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Carteolol_MeSH S_administration_&_dosage_MeSH Carteolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Carteolol_adverse_effects_MeSH M_Drug_Interactions_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Levobunolol_MeSH S_administration_&_dosage_MeSH Levobunolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Levobunolol_adverse_effects_MeSH M_Metipranolol_MeSH S_administration_&_dosage_MeSH Metipranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metipranolol_adverse_effects_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH 
****** 11975837
----K E
----T Medical resource use and costs of congestive heart failure after carvedilol use.
----A A retrospective cohort study based on claims and medical chart data was conducted to compare healthcare use and costs in congestive heart failure patients with and without carvedilol. Adult patients with a minimum of two claims with a valid congestive heart failure diagnosis from 1997 to 1999 were included. Patients receiving continuous carvedilol treatment for at least 4 months were considered study case patients. Case patients were matched based on age, gender, race, and concomitant medication. Healthcare use and costs were compared between the case and control groups. A total of 128 case and 147 control patients were identified. There were no significant differences in demographic characteristics, concomitant medication, or New York Heart Association classification between these two groups. Analysis of variance and chi-square analyses were conducted for continuous and categorical variables, respectively. Statistical adjustments were made using a multivariate model. Carvedilol had a significant economic reduction in the overall expenditures by approximately $14,530. Facility expenditures were approximately $9,000 lower for the carvedilol group than for the control group. Carvedilol-treated patients had less frequent hospital admissions and shorter lengths of stay compared with patients not receiving carvedilol. Congestive heart failure patients receiving carvedilol have significantly less healthcare use and costs than patients not receiving carvedilol.
----P Evaluation_Studies Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_economics_MeSH Carbazoles_economics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiology_MeSH S_economics_MeSH Cardiology_economics_MeSH M_Case-Control_Studies_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Cost_of_Illness_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Health_Expenditures_MeSH M_Health_Resources_MeSH S_economics_MeSH Health_Resources_economics_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Human_MeSH M_Length_of_Stay_MeSH S_economics_MeSH Length_of_Stay_economics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Patient_Admission_MeSH S_economics_MeSH Patient_Admission_economics_MeSH M_Propanolamines_MeSH S_economics_MeSH Propanolamines_economics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Sex_Factors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 11978956
----K E
----T Metoprolol treatment to prevent restenosis following percutaneous transluminal coronary angioplasty.
----A This study tested the hypothesis that metoprolol reduces the restenosis rate after percutaneous transluminal coronary angioplasty (PTCA) in native coronary arteries as compared to placebo. Apart from prognostic clinical effects in the treatment of patients with coronary heart disease, several in vivo and ex vivo studies have demonstrated antiproliferative and antiatherogenic effects of beta-blockers. In the present study, 192 male patients were randomized in a double-blind fashion to metoprolol sustained-release treatment or placebo starting at least 1 day before angioplasty. Lesion diameters and restenosis rates were evaluated using automatic edge detection systems. The study endpoint was the angiographic restenosis rate 4 months after PTCA. Ninety-seven randomized patients had a control angiography a mean of 4.5 months after PTCA. Dropouts were evenly distributed between the metoprolol and placebo groups. Lumen loss in the target lesion was 0.36 mm in the metoprolol group and 0.32 mm in the placebo group. Restenosis rates averaged 57.5% in the metoprolol group and 44.2% in the placebo group using conventional restenosis criteria. Taking metoprolol serum levels above 50 mmol/l as an indication of definite compliance with the metoprolol treatment, the restenosis rate was 58.3%. In conclusion, 95 mg of sustained-release metoprolol failed to reduce the restenosis rate following angioplasty in native coronary arteries.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Coronary_Disease_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Coronary_Restenosis_MeSH S_prevention_&_control_MeSH Coronary_Restenosis_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH M_Vascular_Patency_MeSH S_drug_effects_MeSH Vascular_Patency_drug_effects_MeSH 
****** 11981397
----K E
----T Migraine-associated dizziness: patient characteristics and management options.
----A OBJECTIVE: To determine patient characteristics and effectiveness of therapy for migraine-associated dizziness. STUDY DESIGN: Retrospective chart review. SETTING: Tertiary referral center. PATIENTS: Patients were identified through a code query of billing records for the diagnosis of migraine-associated vertigo or disequilibrium, based on the International Headache Society criteria. There were 81 patients (61 women, 20 men) with an average age of 36.6 years (range, 8-71 yr); all except four patients were evaluated between 1995 and 1999. Follow-up was obtained from chart review. Mean follow-up time was 54.5 weeks, with a range of 4 to 456 weeks. INTERVENTION: One or more treatment methods, including dietary manipulation, medication (tricyclic antidepressants, beta-blockers or calcium-channel blockers), and neurology consultation, were applied sequentially as necessary. MAIN OUTCOME MEASURE: Response to therapy was defined as greater than 75% reduction in symptom recurrence rate. RESULTS: Overall, 72% of patients experienced resolution or dramatic reduction of their attacks of vertigo or disequilibrium. Of the 13 patients treated with the introduction of dietary manipulation alone, 100% received significant relief. Of the 31 patients treated with dietary manipulation and the addition of a medication, 77% of these patients had significant relief. Of the final group of 37 patients treated with another medication or a neurology consultation, 57% received substantial relief. Of the responders, the majority (>95%) experienced an equal reduction in both vertigo or disequilibrium and headache symptoms. Interestingly, 100% of the patients in the migraine without active headache group received substantial relief of their vertigo or disequilibrium symptoms with migraine therapy. CONCLUSION: We conclude that there is effective therapy for the common problem of migraine-associated dizziness.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antidepressive_Agents__Tricyclic_MeSH S_therapeutic_use_MeSH Antidepressive_Agents__Tricyclic_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Child_MeSH M_Dizziness_MeSH S_diet_therapy_MeSH Dizziness_diet_therapy_MeSH S_drug_therapy_MeSH Dizziness_drug_therapy_MeSH S_etiology_MeSH Dizziness_etiology_MeSH S_physiopathology_MeSH Dizziness_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_complications_MeSH Migraine_complications_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 11984541
----K E
----T Discussion on randomized comparison of long-term losartan versus propranolol in lowering portal pressure in cirrhosis.
----A 
----P Letter 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 11986409
----K E
----T Myocardial gene expression in dilated cardiomyopathy treated with beta-blocking agents.
----A BACKGROUND: Beta-blocker therapy may improve cardiac function in patients with idiopathic dilated cardiomyopathy. We tested the hypothesis that beta-blocker therapy produces favorable functional effects in dilated cardiomyopathy by altering the expression of myocardial genes that regulate contractility and pathologic hypertrophy. METHODS: We randomly assigned 53 patients with idiopathic dilated cardiomyopathy to treatment with a beta-adrenergic-receptor blocking agent (metoprolol or carvedilol) or placebo. The amount of messenger RNA (mRNA) for contractility-regulating genes (those encoding beta1- and beta2-adrenergic receptors, calcium ATPase in the sarcoplasmic reticulum, and alpha- and beta-myosin heavy-chain isoforms) and of genes associated with pathologic hypertrophy (beta-myosin heavy chain and atrial natriuretic peptide) was measured with a quantitative reverse-transcription polymerase chain reaction in total RNA extracted from biopsy specimens of the right ventricular septal endomyocardium. Myocardial levels of beta-adrenergic receptors were also measured. Measurements were conducted at base line and after six months of treatment, and changes in gene expression were compared with changes in the left ventricular ejection fraction as measured by radionuclide ventriculography. RESULTS: Twenty-six of 32 beta-blocker-treated patients (those with complete mRNA measurements) had an improvement in left ventricular ejection fraction of at least 5 ejection-fraction (EF) units (mean [+/-SE] increase, 18.8+/-1.8). As compared with the six beta-blocker-treated patients who did not have a response (mean change, a decrease of 2.5+/-1.8 EF units), those who did have a response had an increase in sarcoplasmic-reticulum calcium ATPase mRNA and alpha-myosin heavy chain mRNA and a decrease in beta-myosin heavy chain mRNA. The change in sarcoplasmic-reticulum calcium ATPase was not present in the patients in the placebo group who had a spontaneous response. There were no differences between those who had a response and those who did not in terms of the change in mRNA or protein expression of beta-adrenergic receptors. CONCLUSIONS: In idiopathic dilated cardiomyopathy, functional improvement related to treatment with beta-blockers is associated with changes in myocardial gene expression.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Ca(2+)-Transporting_ATPase_MeSH S_drug_effects_MeSH Ca(2+)-Transporting_ATPase_drug_effects_MeSH S_genetics_MeSH Ca(2+)-Transporting_ATPase_genetics_MeSH S_metabolism_MeSH Ca(2+)-Transporting_ATPase_metabolism_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_genetics_MeSH Cardiomyopathy__Congestive_genetics_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Female_MeSH M_Gene_Expression_MeSH S_drug_effects_MeSH Gene_Expression_drug_effects_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Myosin_Heavy_Chains_MeSH S_drug_effects_MeSH Myosin_Heavy_Chains_drug_effects_MeSH S_genetics_MeSH Myosin_Heavy_Chains_genetics_MeSH S_metabolism_MeSH Myosin_Heavy_Chains_metabolism_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_RNA__Messenger_MeSH S_genetics_MeSH RNA__Messenger_genetics_MeSH S_metabolism_MeSH RNA__Messenger_metabolism_MeSH M_Receptors__Adrenergic__beta_MeSH S_genetics_MeSH Receptors__Adrenergic__beta_genetics_MeSH S_metabolism_MeSH Receptors__Adrenergic__beta_metabolism_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Ventricular_Myosins_MeSH S_drug_effects_MeSH Ventricular_Myosins_drug_effects_MeSH S_genetics_MeSH Ventricular_Myosins_genetics_MeSH S_metabolism_MeSH Ventricular_Myosins_metabolism_MeSH 
****** 11986110
----K 4
----T Comparison of travoprost 0.0015% and 0.004% with timolol 0.5% in patients with elevated intraocular pressure: a 6-month, masked, multicenter trial.
----A OBJECTIVE: To compare the safety and intraocular pressure (IOP)-lowering efficacy of once-daily travoprost (0.0015% and 0.004%) to twice-daily timolol 0.5%. DESIGN: Prospective, 6-month, randomized, controlled, multicenter, double-masked, phase III study. PARTICIPANTS: Six hundred five patients with open-angle glaucoma or ocular hypertension. METHODS: Patients with an 8 AM IOP between 24 to 36 mmHg in at least one eye (the same eye) at two eligibility visits received either travoprost 0.0015%, travoprost 0.004% (dosed every day), or timolol 0.5% (dosed twice daily). MAIN OUTCOME MEASURES: Mean IOP at 8 AM, 10 AM, and 4 PM in the patient's eye with the higher baseline IOP. RESULTS: The mean IOP was significantly lower for both concentrations of travoprost compared with timolol. Travoprost was statistically superior to timolol at 9 of 13 visits, with differences in IOP reductions ranging from 0.9 to 1.8 mmHg (0.0015%) and 10 of 13 visits with differences in IOP reductions from 0.9 to 2.4 mmHg (0.004%). Mean IOP changes from baseline ranged from -6.0 to -7.5 mmHg (0.0015%), -6.5 to -8.0 mmHg (0.004%), and -5.2 to -7.0 mmHg for timolol. Hyperemia was experienced at rates of 29.2% (59 of 202) for travoprost 0.0015%, 42.8% (86 of 201) for travoprost 0.004%, and 8.9% (18 of 202) for timolol. Iris pigmentation changes were observed in 1.0% (2 of 200) of patients receiving travoprost 0.004% with no changes noted in the travoprost 0.0015% group or the timolol group. A decrease in pulse and systolic blood pressure was observed in the timolol group. There were no other clinically relevant or statistically significant changes from baseline in ocular signs or laboratory values, and no serious, related, unexpected adverse events were reported for any group. CONCLUSIONS: Travoprost (0.0015% and 0.004%), dosed once daily in the evening, is statistically superior or equal to timolol 0.5% dosed twice daily at all treatment visits during this 6-month study. IOP reductions of up to 2.0 mmHg greater than timolol were found in the travoprost 0.004% pooled data group. Travoprost is safe and well tolerated in patients with open-angle glaucoma or ocular hypertension.
----P Clinical_Trial Clinical_Trial__Phase_III Evaluation_Studies Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cloprostenol_MeSH S_administration_&_dosage_MeSH Cloprostenol_administration_&_dosage_MeSH S_adverse_effects_MeSH Cloprostenol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Cloprostenol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Cloprostenol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 11992888
----K 4
----T Travoprost compared with latanoprost and timolol in patients with open-angle glaucoma or ocular hypertension.
----A 
----P Comment Letter 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Cloprostenol_MeSH S_adverse_effects_MeSH Cloprostenol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Cloprostenol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Cloprostenol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Evaluation_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 11992131
----K E
----T Biventricular pacing improves quality of life and exercise tolerance in patients with heart failure and intraventricular conduction delay.
----A Background: Biventricular pacing improves left ventricular dysynchrony, leading to improvement in congestive heart failure symptoms. The extent of placebo effect, the predictors of response and the long term benefits are unknown. Patients and Methods: Forty-five patients with symptomatic congestive heart failure underwent implantation of a biventricular pacing system over a 30-month period (age 65 10 years, 37 men). Patients underwent implantation of a biventricular pacemaker or implantable defibrillator one month or longer after stabilization of congestive heart failure on maximal medical therapy, including angiotensin-converting enzyme inhibitors in 84% of patients and beta-blockers in 56% of patients. Three patients had New York Heart Association (NYHA) class II heart failure, 34 had NYHA class III and eight had NYHA class IV. Cardiomyopathy was ischemic in 31 patients, dilated in 12 and the result of other causes in two. The left ventricular ejection fraction was 19 5%. Results: Implantation of the biventricular pacing system was successful in 38 of 45 patients (84%). Two patients had successful implantation with a second attempt, and one patient had an epicardial lead implant. Lead dislodgement occurred in four patients, with successful repositioning in all. During a mean follow-up of 10 7 months, the Minnesota Living with Heart Failure Questionnaire quality of life index score improved from 62 16 to 42 22 at one month (P<0.001), but subsequently returned to intermediate levels (55 26 at three months, 48 26 at six months and 56 34 at one year, P=0.50). In seven patients with deferred device activation, quality of life scores also improved by 10 15 points from baseline to one month with VDI 35 pacing, and improved a further 15 20 points with left ventricular lead activation. The mean NYHA class fell from 3.1 0.5 at baseline to 2.7 0.7 at one month (P=0.006) and remained stable thereafter (2.8 0.9 at three months, 2.8 0.9 at six months). Six patients died during follow-up, one patient had a cardiac transplantation and subsequently died, one patient had a successful cardiac transplantation and one patient underwent insertion of a left ventricular assist device. Death occurred due to progressive heart failure in five patients, sudden death occurred in one patient and a noncardiovascular cause resulted in the death of one patient. An analysis of NYHA responders (NYHA class improvement of 1 or more at last follow-up, 44% of patients) and quality of life responders (score improvement of 10 or more at last follow-up, 57% patients) did not show any difference in age, sex, heart failure etiology, QRS width, ejection fraction or baseline NYHA class. Conclusions: Biventricular pacing improves quality of life and NYHA class in patients with advanced heart failure and intraventricular conduction delay. The attenuated benefit seen over time may be related to initial placebo effect or simple dual- chamber pacing, or the natural history of the underlying disease. Identification of patients most likely to respond to biventricular pacing was not possible.
----P Evaluation_Studies Journal_Article 
----M M_Aged_MeSH M_Arrhythmia_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Cardiac_Pacing__Artificial_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH P_Exercise_Tolerance_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pacemaker__Artificial_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 11997407
----K E
----T Prognostic implications of autonomic function assessed by analyses of catecholamines and heart rate variability in stable angina pectoris.
----A OBJECTIVE: To assess the prognostic impact of autonomic activity, as reflected by catecholamines and heart rate variability (HRV), in patients with stable angina pectoris. DESIGN: Double blind, randomised treatment with metoprolol or verapamil. 24 hour ambulatory ECG, used for frequency domain analyses of HRV, and symptom limited exercise tests at baseline and after one month of treatment. Catecholamine concentrations were measured in plasma (rest and exercise) and urine. SETTING: Single centre at a university hospital. PATIENTS: 641 patients (449 men) with stable angina pectoris. MAIN OUTCOME MEASURES: Cardiovascular (CV) death, non-fatal myocardial infarction (MI). RESULTS: During follow up (median 40 months) there were 27 CV deaths and 26 MIs. Patients who died of CV causes had lower total power and high (HF), low (LF), and very low (VLF) frequency components of HRV. HRV was not altered in patients who suffered non-fatal MI. Catecholamines did not differ between patients with and those without events. Metoprolol increased HRV. Verapamil decreased noradrenaline (norepinephrine) excretion. Multivariate Cox analyses showed that total power, HF, LF, and VLF independently predicted CV death (also non-sudden death) but not MI. LF:HF ratios and catecholamines were not related to prognosis. Treatment effects on HRV did not influence prognosis. CONCLUSIONS: Low HRV predicted CV death but not non-fatal MI. Neither the LF:HF ratio nor catecholamines carried any prognostic information. Metoprolol and verapamil influenced LF, HF, and catecholamines differently but treatment effects were not related to prognosis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH S_urine_MeSH Angina_Pectoris_urine_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Autonomic_Nervous_System_Diseases_MeSH S_complications_MeSH Autonomic_Nervous_System_Diseases_complications_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH S_urine_MeSH Biological_Markers_urine_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH S_urine_MeSH Catecholamines_urine_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympatholytics_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12003701
----K I
----T Carcinogenicity of antihypertensive therapy.
----A Several studies have suggested that antihypertensive treatment may promote cancer through unknown mechanisms. Early retrospective studies implicated reserpine in breast cancer, but data from prospective studies and meta-analysis of several case-controlled studies showed only a weak association between reserpine and breast cancer which, although statistically significant, is of little clinical concern. Data from case-controlled studies and several cohort studies suggested an association between the use of a diuretic and the occurrence of renal cell cancer, particularly in women. A recent study showed an association between the use of a diuretic and the occurrence of colon cancer. Several prospective studies showed that treatment with atenolol may increase mortality from malignancy. However, other studies that analyzed data from several thousand patients could not confirm this association. In three prospective and a few case-controlled studies, angiotensin converting enzyme inhibitors were not associated with increased mortality from malignancy. In addition, a recent retrospective study showed that long-term use of angiotensin converting enzyme inhibitors had a protective effect against malignancy. Data from three large case-controlled studies and the combined data from eight randomized controlled studies and seven longitudinal studies showed a similar risk for malignancy among users and nonusers of calcium antagonists. Until further data from prospective clinical trials are available, we advise caution about long-term diuretic therapy in women. With regard to other antihypertensive drug classes, we suggest continuing the management of hypertension according to current treatment guidelines with little fear of any substantial cancer risk.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Breast_Neoplasms_MeSH S_chemically_induced_MeSH Breast_Neoplasms_chemically_induced_MeSH S_epidemiology_MeSH Breast_Neoplasms_epidemiology_MeSH M_Carcinogens_MeSH S_adverse_effects_MeSH Carcinogens_adverse_effects_MeSH S_therapeutic_use_MeSH Carcinogens_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Longitudinal_Studies_MeSH M_Neoplasms_MeSH S_chemically_induced_MeSH Neoplasms_chemically_induced_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH M_Neoplasms__Radiation-Induced_MeSH S_etiology_MeSH Neoplasms__Radiation-Induced_etiology_MeSH M_Randomized_Controlled_Trials_MeSH M_Reserpine_MeSH S_adverse_effects_MeSH Reserpine_adverse_effects_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH 
****** 12003704
----K E
----T Do angiotensin receptor antagonists have benefits beyond blood pressure lowering?
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 12007080
----K 5
----T What is the place of beta-blockade in patients who have experienced a myocardial infarction with preserved left ventricular function? Evidence and (mis)interpretation.
----A Beta blockers have long been used in patients who have experienced a myocardial infarction. However, many new therapies are available for this patient group, and as a result, the current role of beta blockers may have become uncertain. In this article we address a series of questions related to the important and continuing role of beta blockade after myocardial infarction.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12008178
----K E
----T Incidence of new coronary events in older persons with prior myocardial infarction and systemic hypertension treated with beta blockers, angiotensin-converting enzyme inhibitors, diuretics, calcium antagonists, and alpha blockers.
----A 
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Mass_Index_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH S_drug_effects_MeSH Lipoproteins__HDL_Cholesterol_drug_effects_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH S_drug_effects_MeSH Lipoproteins__LDL_Cholesterol_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 12007683
----K E
----T Induced ischemia detected by dobutamine stress echocardiography in coronary heart disease patients after myocardial re-vascularization. Experience in a District General Hospital.
----A Most episodes of myocardial ischemia in patients with known coronary artery disease (CHD) are asymptomatic. Silent myocardial ischemia (SMI) is an important predictor of adverse outcome in patients with proven coronary artery disease. beta-blockers are effective in suppressing ischemia, and improve clinical outcome in patients with coronary artery disease. At present, it is common practice to stop treatment with beta-blockers in clinically asymptomatic patients after coronary artery bypass graft (CABG) and/or myocardial re-vascularization (PTCA/Stent), although the possible presence of SMI/inducible ischemia after myocardial re-vascularization is not known. We examined 56 asymptomatic CHD patients after coronary artery bypass graft (n=36), percutaneous coronary angioplasty PTCA/stent (n=15), or both (n=5); therapy with beta-blockers was stopped in all of them after myocardial revascularization. All these patients underwent a dobutamine stress echocardiography test (DSE test). The DSE test was proposed to these asymptomatic CHD patients to investigate the possible presence of SMI/inducible ischemia after myocardial re-vascularization. All patients had history of myocardial infarction or evidence of mildly impaired left ventricular function at rest as assessed by cardiac catheterization. Abnormal DSE studies occurred in eight of the 56 patients (14%; 95% C.I.: 6-26%). Therapeutic approaches specifically targeted at reducing total ischaemic burden include pharmacologic therapy and myocardial revascularization. On the basis of these data, it can be concluded that asymptomatic CHD patients after myocardial re-vascularization must be re-evaluated to rule out SMI/inducible ischemia that can be treated (e.g. with beta-blockers) reducing cardiovascular morbidity and mortality.
----P Journal_Article 
----M M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_methods_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_methods_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Coronary_Artery_Bypass_MeSH S_methods_MeSH Coronary_Artery_Bypass_methods_MeSH M_Coronary_Disease_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Dobutamine_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Echocardiography_MeSH S_methods_MeSH Echocardiography_methods_MeSH M_Evaluation_Studies_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_ultrasonography_MeSH Myocardial_Ischemia_ultrasonography_MeSH M_Myocardial_Revascularization_MeSH S_methods_MeSH Myocardial_Revascularization_methods_MeSH M_Postoperative_Period_MeSH M_Prospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH M_Statistics__Nonparametric_MeSH M_Stents_MeSH 
****** 12012149
----K I
----T Incidence and determinants of migraine prophylactic medication in the Netherlands.
----A OBJECTIVE: To estimate and examine the incidence and determinants of initiation of migraine-prophylactic therapy as well as the corresponding drug of choice over a period of 5 years following the use of specific abortive migraine drugs.METHODS: By accessing data from a large prescription database, an identification of patients treated with ergotamine or a triptan from 1 January 1994 to 31 December 1998 was made. The cumulative incidence of initiation of migraine-prophylactic drugs (beta-blockers, serotonin antagonists, specific calcium antagonists, amitriptyline, clonidine and valproic acid) was estimated in patients following the use of ergotamine or a triptan. An assessment of the migraine-prophylactic drug of first choice was also performed. A few baseline determinants were analysed to highlight a possible association with the initiation of prophylactic therapy: age, gender, type of abortive migraine drug use and year of prophylaxis. Additional determinants included the analysis of drug-utilisation patterns, such as the consumption and switch patterns of abortive migraine drug use as well as co-medication use prior to prophylaxis. For this particular analysis a reference group (patients not having commenced prophylaxis) was selected from the initial study population.RESULTS: After having satisfied eligibility criteria, a total of 3999 first-time users of ergotamine and triptans were included of whom 479 (12%) had initiated migraine-prophylactic therapy. This corresponded to an incidence density of 6.0 per 100 person-years and was highest for patients younger than 45 years and for multiple abortive migraine drug users. The incidence fell considerably from 12.0 person-years in 1994 to 5.1 person-years in 1998. More than half of the patients had been prescribed a beta-blocker as the migraine-prophylactic drug of first choice by both general practitioners and neurologists. The use of antidepressants and/or benzodiazepines and oral contraceptives was significantly higher in patients starting prophylaxis compared with those who did not. The consumption of abortive migraine drug use (4.0 defined daily doses per month vs 3.7 defined daily doses per month), and switch patterns (27.1% vs 30.9%) were similar for patients starting and not starting prophylaxis.CONCLUSION: The overall incidence of initiation of migraine-prophylactic therapy following the use of abortive migraine analgesics was 6.0% per year and fell considerably during 5 years of the study. Beta-blockers were the migraine-prophylactic drugs of first choice for general practitioners and neurologists. In our study we could not determine any factors clearly associated with the initiation of migraine prophylaxis besides prior use of antidepressants and benzodiazepines. A future assessment of the usage patterns of migraine-prophylactic drugs may provide detailed information concerning the effectiveness and tolerability.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analgesics_MeSH S_administration_&_dosage_MeSH Analgesics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Databases__Factual_MeSH M_Drug_Utilization_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Ergotamine_MeSH S_administration_&_dosage_MeSH Ergotamine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ergotamine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_epidemiology_MeSH Migraine_epidemiology_MeSH M_Netherlands_MeSH S_epidemiology_MeSH Netherlands_epidemiology_MeSH M_Pharmacoepidemiology_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12010943
----K E
----T Dual chamber pacing in patients with severe heart failure on beta blocker and amiodarone treatment: preliminary results of a randomised study.
----A 
----P Clinical_Trial Letter Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Cardiac_Pacing__Artificial_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Heart_Transplantation_MeSH S_statistics_&_numerical_data_MeSH Heart_Transplantation_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Mitral_Valve_Insufficiency_MeSH S_prevention_&_control_MeSH Mitral_Valve_Insufficiency_prevention_&_control_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH 
****** 12015475
----K E
----T Levosimendan: a new era for inodilator therapy for heart failure?
----A Levosimendan is a new inotropic and vasodilator agent. The inotropic effect is mediated by calcium concentration-dependent conformational changes in troponin C during systole leading to sensitization of the contractile apparatus to calcium ions. The vasodilator effect is mediated by opening potassium channels on vascular smooth muscle. It has a complex pharmacokinetic profile, with a long-acting metabolite that has hemodynamic effects persisting for approximately 1 week. Although it is absorbed orally, it has been developed only for intravenous use thus far. The hemodynamic effects are not reduced and may be enhanced in the presence of beta-blockers, possibly an important attribute when dealing with exacerbation of heart failure caused by or in the presence of beta-blockers. More patients with heart failure have participated in randomized controlled trials of levosimendan than of any other intravenous inotropic agent. Experience with its use after cardiac surgery is limited. Preliminary observations suggest that hemodynamic changes are associated with symptomatic benefit and a reduction in morbidity and mortality in patients with severe heart failure caused by left ventricular systolic dysfunction, compared with placebo in one study and dobutamine in another. Levosimendan may be the first inotropic agent that it is both safe and effective in altering clinical outcomes relevant for patients. Part of this benefit may be achieved because levosimendan allows other inotropic agents that may have adverse effects on patient outcome to be avoided. Further research is required to confirm whether levosimendan reduces mortality and morbidity compared with a placebo and when administered repetitively. If it does, it may become routine therapy for the treatment of severe heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hydrazones_MeSH S_therapeutic_use_MeSH Hydrazones_therapeutic_use_MeSH M_Pyridazines_MeSH S_therapeutic_use_MeSH Pyridazines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 12016631
----K E
----T Concomitant beta-blocker therapy is associated with a lower occurrence of ventricular arrhythmias in patients with decompensated heart failure.
----A BACKGROUND: Ventricular arrhythmias are nearly universally present in patients with advanced congestive heart failure (CHF) and represent an important cause of mortality in these patients. One of the putative mechanisms for the salutary effects of beta-blockers on sudden death mortality in heart failure is their ability to suppress ventricular arrhythmias. However, supporting data in patients with CHF are sparse, especially in the setting of excessive neurohumoral activation associated with symptomatic decompensated heart failure. METHODS AND RESULTS: We studied 236 patients (159 men; mean age, 61 +/- 14 years) admitted for decompensated CHF. Fifty patients were receiving beta-blockers at the time of the study. The severity of ventricular arrhythmia was assessed by 24-hour Holter recordings by using several prospectively defined measures of ventricular ectopy. All measures of ventricular ectopy were lower in patients receiving beta-blockers. The average hourly total premature ventricular beats (PVCs), hourly ventricular couplets, repetitive PVCs, and frequency of ventricular tachycardia episodes were 15% (P =.02), 75% (P <.05), 72% (P <.05), and 87% (P =.01) lower in patient receiving beta-blockers, respectively. In a multivariate regression analysis, the negative relationship between beta-blockers and the average hourly PVCs (P =.03), the frequency of ventricular pairs (P =.03), repetitive PVCs (P <.05), and ventricular tachycardia episodes (P =.01) remained significant and independent. CONCLUSIONS: Concomitant beta-blocker therapy during heart failure decompensation is associated with a marked reduction in complex ventricular ectopy and episodes of ventricular tachycardia. This effect of beta-blockers may play an important protective role by preventing serious ventricular arrhythmias during transient increases in sympathetic activity.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analysis_of_Variance_MeSH M_Comparative_Study_MeSH M_Disease_Progression_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH M_Treatment_Outcome_MeSH 
****** 12019280
----K E
----T Resistant hypertension: comparing hemodynamic management to specialist care.
----A Although resistant hypertension affects a minority of all hypertensives, this group continues to experience disproportionately high cardiovascular event rates despite newer antihypertensive agents. Hypertension represents an imbalance of hemodynamic forces within the circulation, usually characterized by elevated systemic vascular resistance. We studied the utility of serial hemodynamic parameters in the selection and titration of antihypertensive medication in resistant hypertensive patients using highly reproducible noninvasive measurements by thoracic bioimpedance. Resistant hypertension patients (n=104) were randomized to drug selection based either on serial hemodynamic (HD) measurements and a predefined algorithm or on drug selection directed by a hypertension specialist (SC) in a 3-month intensive treatment program. Blood pressure was lowered by intensified drug therapy in both treatment groups (169+/-3/87+/-2 to 139+/-2/72+/-1 mm Hg HD versus 173+/-3/91+/-2 to 147+/-2/79+/-1 mm Hg SC, P<0.01 for systolic and diastolic BP), using similar numbers and intensity of antihypertensive medications. Blood pressures were reduced further for those treated according to hemodynamic measurements, resulting in improved control rates (56% HD versus 33% SC controlled to </=140/90 mm Hg, P<0.05) and incremental reduction in systemic vascular resistance measurements. Although the number of patients taking diuretics did not differ between groups, final diuretic dosage was higher in the hemodynamic cohort. Our results demonstrate superior blood pressure control using a treatment algorithm and serial hemodynamic measurements compared with clinical judgment alone in a randomized prospective study. Our measurements of thoracic fluid volume support occult volume expansion as a mediator of antihypertensive drug resistance and use of impedance measurements to guide advancing diuretic dose and adjustment of multidrug antihypertensive treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Nursing_Care_MeSH M_Treatment_Outcome_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 12021225
----K E
----T First experience with direct factor Xa inhibition in patients with stable coronary disease: a pharmacokinetic and pharmacodynamic evaluation.
----A BACKGROUND: Thrombin generation is critical to the formation of an arterial thrombus after rupture of an atherosclerotic plaque. In patients with stable coronary disease receiving standard medical therapy, we evaluated the pharmacokinetics, pharmacodynamics, and safety profile of DX-9065a, a novel small-molecule anticoagulant that directly, selectively, and reversibly inhibits factor Xa. METHODS AND RESULTS: In a double-blind trial, 73 patients (median age, 63 years; 29% women) were randomly assigned to receive a fixed-dose intravenous bolus, followed by a 72-hour infusion of placebo or 1 of 4 weight-adjusted regimens of DX-9065a. Plasma samples were collected during infusion and a 24-hour elimination period. Only minor bleeding occurred, predominantly ecchymoses at infusion sites, and its incidence did not differ significantly among the groups, including placebo. Median hemoglobin, platelet count, serum creatinine level, and liver function tests did not change significantly from baseline during infusion or elimination. Significant predictors of pharmacokinetic response included infusion dose and weight. At 60 hours into the DX-9065a infusion, plasma drug levels correlated strongly with anti-factor Xa activity (r=0.97), prothrombin time (r=0.77), and international normalized ratio (r=0.72) but less so with activated partial thromboplastin time (r=0.56; all P<0.001). CONCLUSIONS: This is the first study of a selective, reversible, and direct small-molecule factor Xa inhibitor in patients with stable coronary disease. These data lay the foundation for further investigation of factor Xa inhibitors in the treatment of patients with coronary atherothrombosis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anticoagulants_MeSH S_administration_&_dosage_MeSH Anticoagulants_administration_&_dosage_MeSH S_adverse_effects_MeSH Anticoagulants_adverse_effects_MeSH S_blood_MeSH Anticoagulants_blood_MeSH S_pharmacokinetics_MeSH Anticoagulants_pharmacokinetics_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Factor_Xa_MeSH S_analysis_MeSH Factor_Xa_analysis_MeSH S_antagonists_&_inhibitors_MeSH Factor_Xa_antagonists_&_inhibitors_MeSH M_Female_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Infusions__Intravenous_MeSH M_International_Normalized_Ratio_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Naphthalenes_MeSH S_administration_&_dosage_MeSH Naphthalenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Naphthalenes_adverse_effects_MeSH S_blood_MeSH Naphthalenes_blood_MeSH S_pharmacokinetics_MeSH Naphthalenes_pharmacokinetics_MeSH M_Partial_Thromboplastin_Time_MeSH M_Propionic_Acids_MeSH S_administration_&_dosage_MeSH Propionic_Acids_administration_&_dosage_MeSH S_adverse_effects_MeSH Propionic_Acids_adverse_effects_MeSH S_blood_MeSH Propionic_Acids_blood_MeSH S_pharmacokinetics_MeSH Propionic_Acids_pharmacokinetics_MeSH M_Prothrombin_Time_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 12020488
----K E
----T Impact of beta-blocker treatment on the prognostic value of currently used risk predictors in congestive heart failure.
----A OBJECTIVES: This prospective study tested the impact of beta-blocker treatment on currently used risk predictors in congestive heart failure (CHF). BACKGROUND: Given the survival benefit obtained by beta-blockade, risk stratification by factors established in the "pre-beta-blocker era" may be questioned. METHODS: The study included 408 patients who had CHF with left ventricular ejection fraction (LVEF) <45%, all treated with an angiotensin-converting enzyme inhibitor or angiotensin type 1 receptor antagonist, who were classified into those receiving a beta-blocker (n = 165) and those who were not (n = 243). In all patients, LVEF, peak oxygen consumption (peakVO(2)), plasma norepinephrine (NE) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were determined. RESULTS: Although the New York Heart Association functional class (2.2 +/- 0.7 vs. 2.3 +/- 0.7), peakVO(2) (14.4 +/- 5.2 ml/min per kg vs. 14.4 +/- 5.5 ml/min per kg) and NT-proBNP (337 +/- 360 pmol/l vs. 434 +/- 538 pmol/l) were similar in the groups with and without beta-blocker treatment, the group with beta-blocker treatment had a lower heart rate (68 +/- 30 beats/min vs. 76 +/- 30 beats/min), lower NE (1.7 +/- 1.2 nmol/l vs. 2.5 +/- 2.2 nmol/l) and higher LVEF (24 +/- 10% vs. 21 +/- 9%; all p < 0.05). Within one year, 34% of patients without beta-blocker treatment, but only 16% of those with beta-blocker treatment (p < 0.001), reached the combined end point, defined as hospital admission due to worsening CHF and/or cardiac death. A beneficial effect of beta-blocker treatment was most obvious in the advanced stages of CHF, because the end-point rates were markedly lower (all p < 0.05) in the group with beta-blocker treatment versus the group without it, as characterized by peakVO(2) <10 ml/min per kg (26% vs. 64%), LVEF < or = 20% (25% vs. 45%), NE >2.24 nmol/l (18% vs. 40%) and NT-proBNP >364 pmol/l (27% vs. 45%), although patients with beta-blocker treatment received only 37 +/- 21% of the maximal recommended beta-blocker dosages. CONCLUSIONS: The prognostic value of variables used for risk stratification of patients with CHF is markedly influenced by beta-blocker treatment. Therefore, in the beta-blocker era, a re-evaluation of the selection criteria for heart transplantation is warranted.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nerve_Tissue_Proteins_MeSH S_blood_MeSH Nerve_Tissue_Proteins_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Peptide_Fragments_MeSH S_blood_MeSH Peptide_Fragments_blood_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 12022239
----K E
----T Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: result from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial.
----A BACKGROUND: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. METHODS: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the beta1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured. RESULTS: After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (-21 +/- 19 SD mm Hg, n = 17) than both the TC (-14 +/- 18 mm Hg, n= 18) and CC (0 +/- 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level. CONCLUSIONS: The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Aldosterone_Synthase_MeSH S_genetics_MeSH Aldosterone_Synthase_genetics_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Base_Sequence_MeSH S_genetics_MeSH Base_Sequence_genetics_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Cytosine_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Polymorphism_(Genetics)_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Thymine_MeSH M_Treatment_Outcome_MeSH 
****** 12023696
----K E
----T Influence of age, sex and blood pressure on the principal endpoints of the Nordic Diltiazem (NORDIL) Study.
----A BACKGROUND : The aim of the Nordic Diltiazem (NORDIL) Study was to compare patients with essential hypertension receiving calcium-antagonist-based treatment with diltiazem and similar patients receiving conventional diuretic/beta-blocker-based treatment, with respect to cardiovascular morbidity and mortality. OBJECTIVE : To assess the influence of age, sex, severity of hypertension and heart rate on treatment effects, in a sub-analysis. METHODS : The NORDIL study was prospective, randomized, open and endpoint-blinded. It enrolled, at health centres in Norway and Sweden, 10 881 patients aged 50-74 years who had diastolic blood pressure (DBP) of 100 mmHg or more. Systolic blood pressure (SBP) and DBP were decreased by 20.3/18.7 mmHg in the diltiazem group and by 23.3/18.7 mmHg in the diuretic/beta-blocker group - a significant difference in SBP (P < 0.001). RESULTS : The incidence of the primary endpoint - a composite of cardiovascular death, cerebral stroke and myocardial infarction - was similar for the two treatments. Fatal and non-fatal stroke occurred in 159 patients in the diltiazem group and in 196 patients in the conventional treatment group [relative risk (RR) 0.80, 95% confidence interval (CI) 0.65 to 0.99; P = 0.040], whereas there was a non-significant inverse tendency with respect to all myocardial infarction. There were significantly fewer cerebral strokes in patients receiving diltiazem in the subgroups with baseline SBP > 170 mmHg (n = 5420, RR 0.75, 95% CI 0.58 to 0.98; P = 0.032), DBP >/= 105 mmHg (n = 5881, RR 0.74, 95% CI 0.57 to 0.97; P = 0.030) and pulse pressure >/= 66 mmHg (n = 5461, RR 0.76, 95% CI 0.58 to 0.99, P = 0.041), and more myocardial infarctions in those with heart rate less than 74 beats/min (n = 5303, RR 1.13, 95% CI 1.01 to 1.87; P = 0.040). However, the tendencies for fewer strokes and greater incidence of myocardial infarction were present across subgroups when results were analysed for age, sex, severity of hypertension and heart rate, and treatment-subgroup interaction analyses were not statistically significant. CONCLUSIONS : Compared with a conventional diuretic/beta-blocker-based antihypertensive regimen, there were additional 25% reductions in stroke in the diltiazem-treated patients with blood pressure or pulse pressure greater than the medians, and an increase in myocardial infarction in those with heart rate less than the median. Such findings may be attributable to chance, but the consistency of, in particular, the stroke findings may also suggest an ability of diltiazem, beyond conventional treatment, to prevent cerebral stroke in hypertensive patients with the greatest cardiovascular risk.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH P_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH P_Sex_Characteristics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 12027785
----K 5
----T Practical approaches to migraine management.
----A Migraine is a recurrent clinical syndrome characterised by combinations of neurological, gastrointestinal and autonomic manifestations. The exact pathophysiological disturbances that occur with migraine have yet to be elucidated; however, cervico-trigemino-vascular dysfunctions appear to be the primary cause. Despite advances in the understanding of the pathophysiology of migraine and new effective treatment options, migraine remains an under-diagnosed, under-treated and poorly treated health condition. Most patients will unsuccessfully attempt to treat their headaches with over-the-counter medications. Few well designed, placebo-controlled studies are available to guide physicians in medication selection. Recently published evidence-based guidelines advocate migraine-specific drugs, such as serotonin 5-HT(1B/1D) agonists (the 'triptans') and dihydroergotamine mesylate, for patients experiencing moderate to severe migraine attacks. Additional headache attack therapy options include other ergotamine derivatives, phenothiazines, nonsteroidal anti-inflammatory agents and opioids. Preventative medication therapy is indicated for patients experiencing frequent and/or refractory attacks.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Analgesics__Opioid_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Anesthetics__Local_MeSH S_therapeutic_use_MeSH Anesthetics__Local_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Dihydroergotamine_MeSH S_administration_&_dosage_MeSH Dihydroergotamine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Dihydroergotamine_therapeutic_use_MeSH M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Psychotropic_Drugs_MeSH S_therapeutic_use_MeSH Psychotropic_Drugs_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Serotonin_Agonists_MeSH S_administration_&_dosage_MeSH Serotonin_Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_administration_&_dosage_MeSH Sumatriptan_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Sumatriptan_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Vasoconstrictor_Agents_MeSH S_administration_&_dosage_MeSH Vasoconstrictor_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 12028187
----K 4
----T New glaucoma medications in the geriatric population: efficacy and safety.
----A Glaucoma can be considered a disease of the aging eye. Most medications used to treat glaucoma are in topical eyedrop form and may cause numerous untoward systemic effects in older persons. In recent years, several new ocular hypotensive medications have become available. These medications are being used more commonly because there is a growing trend by ophthalmologists to aggressively lower intraocular pressure. Therefore, geriatricians require a comprehensive knowledge of medications used to treat glaucoma, in addition to an understanding of their mechanism of action profiles of untoward effects and possible interactions with other diseases or medications. Therefore, we performed a review of the medications recently introduced into clinical practice. We selected drugs approved by the U.S. Food and Drug Administration between 1996 and September 2001. The safety profiles of these agents and their untoward side effects were reviewed by class: topical carbonic anhydrase inhibitors (brinzolamide: ocular tolerance, taste perversion), beta-adrenoceptor antagonists (timolol: bradycardia and bronchospasm), alpha-adrenergic agonists (brimonidine: oral dryness, headache, and fatigue), and prostaglandin analogs (latanoprost, bimatoprost, travoprost, and unoprostone isopropyl: ocular hyperemia, iris color changes). The function of this review is to make geriatricians more aware of the efficacy and untoward effects of medications recently introduced into clinical practice. We recommend that geriatricians perform a medication review on all medications their patients use, including eye drops.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_Agonists_MeSH S_adverse_effects_MeSH Adrenergic_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH P_Geriatrics_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Ophthalmic_Solutions_MeSH S_adverse_effects_MeSH Ophthalmic_Solutions_adverse_effects_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Prostaglandins__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12029205
----K E
----T Cardiac 123 I-MIBG imaging and clinical variables in risk stratification in patients with heart failure treated with beta blockers.
----A Both myocardial m-[123I]iodobenzylguanidine (123I-MIBG) uptake and plasma norepinephrine are markers of sympathetic activation in heart failure and have been shown to portend a poorer prognosis. However, these observations were noted before treatment with beta blockers became part of standard clinical practice. Fifty-eight patients with chronic heart failure (New York Heart Association functional class II and III, ejection fraction <35%; 53% ischaemic cardiomyopathy) were prospectively studied with a mean follow-up of 36 months. During the observational period, 17 patients (29.3%) had a predefined event (death and heart transplantation). All prognostic parameters were obtained before beta blocker therapy was initiated. In both uni- and multivariate analysis, the heart-mediastinum ratio of 123I-MIBG uptake did not correlate with cardiovascular mortality. In the multivariate Cox regression analysis, plasma norepinephrine, peak oxygen consumption, end-diastolic volume as measured by echocardiography and exercise performance during bicycling and walking had prognostic significance in patients with heart failure treated with beta blockers in addition to angiotensin-converting enzyme inhibitors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_3-Iodobenzylguanidine_MeSH S_diagnostic_use_MeSH 3-Iodobenzylguanidine_diagnostic_use_MeSH S_pharmacokinetics_MeSH 3-Iodobenzylguanidine_pharmacokinetics_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Aged_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Failure__Congestive_radionuclide_imaging_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Ventricles_radionuclide_imaging_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH S_diagnostic_use_MeSH Norepinephrine_diagnostic_use_MeSH M_Oxygen_Consumption_MeSH S_physiology_MeSH Oxygen_Consumption_physiology_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH S_methods_MeSH Radionuclide_Ventriculography_methods_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Risk_Assessment_MeSH S_methods_MeSH Risk_Assessment_methods_MeSH M_Risk_Factors_MeSH M_Sensitivity_and_Specificity_MeSH M_Stroke_Volume_MeSH 
****** 12031741
----K I
----T Comparison of the beta blocker bucindolol in younger versus older patients with heart failure.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12034151
----K E
----T Myocardial contractile reserve under low doses of dobutamine and improvement of left ventricular ejection fraction with treatment by carvedilol.
----A To examine the ability of myocardial contractile reserve (MCR) assessment to predict the improvement of left ventricular ejection fraction with treatment by carvedilol, a prospective study was undertaken in 85 patients with chronic heart failure and left ventricular ejection fraction < 45%. Low dose dobutamine echocardiography (DSE), a 6-min walk test and measured brain natriuretic peptide (BNP) were assessed in all the patients. Patients were separated into two groups. Group A were patients without any myocardial reserve and group B patients with a myocardial contractile reserve defined as an increment of more than 20% of the resting left ventricular ejection fraction during dobutamine infusion. The two groups differed for percentage of ischemic cardiomyopathy (67.8 in group A vs. 29.7% in group B P = 0.028), 6-min walk test performance (respectively, 343 vs. 415 meters P < 0.05) and BNP plasma levels (respectively, 184.5 vs. 70.1 P < 0.02) but not for left ventricular ejection fraction or NYHA class. During DSE, MCR and heart rate variation was higher in group B than in group A. At the end of the follow up, LVEF increased and NYHA class decreased in group B but not in group A. In multivariate analysis the existence of MCR could predict the improvement of LVEF with treatment by carvedilol. In our study, studying MCR could help to predict patients who will improve their LVEF with carvedilol prior to the administration of the treatment.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Echocardiography_MeSH M_Echocardiography__Stress_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_physiology_MeSH Myocardial_Contraction_physiology_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Predictive_Value_of_Tests_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Statistics_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12034158
----K I
----T Rationale and design of the carvedilol or metoprolol European trial in patients with chronic heart failure: COMET.
----A In large clinical trials both carvedilol and metoprolol have been shown to reduce mortality and morbidity in patients with chronic heart failure. Carvedilol is an adrenoceptor antagonist, which inhibits beta(1)-, beta(2)-, and alpha(1)-adrenergic receptors. Carvedilol has additional metabolic and antioxidant properties. Metoprolol is a selective antagonist of beta(1)-adrenergic receptors. The carvedilol or metoprolol European trial (COMET) is the first study to investigate whether beta-blocking agents with differing pharmacological profiles exert different effects on morbidity and mortality in patients with chronic heart failure. 3029 patients from 15 different European countries were enrolled into COMET and will be followed until 1020 fatal events have been observed, unless the data and safety monitoring committee (DSMC) recommends early termination. The target dose for carvedilol is 25 mg bid and for metoprolol tartrate 50 mg bid. This manuscript outlines the rationale, design and possible outcomes of COMET.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Europe_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Research_Design_MeSH 
****** 12035874
----K E
----T The effects of calcium channel blockers on cardiovascular outcomes: a review of randomised controlled trials.
----A The choice of antihypertensive treatment should be guided by evidence of a reduction in the risk of cardiovascular (CV) events and therefore improved long-term outcome. Using pre-determined criteria, ten randomised, controlled trials that assessed the effects of calcium channel blockers (CCBs) on CV events in patients with hypertension were identified. Six of them enrolled a relatively small number (< 1500) of hypertensive patients, whereas four of the studies were much larger (> 4500 patients). The smaller studies produced mixed findings, especially those trials where CCBs were compared with diuretics; this may reflect methodological limitations and the impact of random error. The results from the four larger studies produced a consistent message: long-acting CCBs such as nifedipine, administered in a gastro-intestinal-transport-system (GITS) formulation, nitrendipine and diltiazem, reduce CV morbidity and mortality in hypertensive patients. In the one study that specifically enrolled high-risk hypertensive patients, nifedipine GITS was as effective as diuretic therapy in reducing CV events, and in all four larger studies sub-group analyses showed that the benefits of these CCBs extend to hypertensive patients with diabetes. The available evidence supports the use of these long-acting CCBs as a first-line treatment option in hypertensive patients.
----P Journal_Article Review Review__Tutorial 
----M M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Outcome_Assessment_(Health_Care)_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12036665
----K 6
----T A comparison of once-daily morning vs evening dosing of concomitant latanoprost/timolol.
----A PURPOSE: To evaluate morning vs evening once daily concomitant latanoprost 0.005%/timolol maleate 0.5% therapy in ocular hypertensive or primary open-angle glaucoma patients. DESIGN: Prospective single-center double-masked crossover comparison. METHODS: Patients who responded to timolol maleate 0.5% given twice daily were randomized to either evening or morning dosing of concomitant latanoprost 0.005% and timolol maleate 0.5% therapy for 7 weeks. Twenty-four hour diurnal curve intraocular pressure (IOP) testing was performed following each period. RESULTS: Thirty-six patients completed this study. There was a significant reduction at each time point in the 24-hour diurnal curve of both evening (17.1 +/- 2.7 mm Hg) and morning (17.3 +/- 3.1 mm Hg) dosed latanoprost/timolol maleate compared with timolol maleate given twice daily (21.1 +/- 3.3 mm Hg) (P <.0001). When the morning and evening dosing groups were compared directly, the 06:00 time point was statistically lower with evening dosing (16.4 +/- 2.3 mm Hg) vs morning dosing (17.9 +/- 2.8 mm Hg) (P =.01). Overall, a trend existed for greater daytime reduction with night-time dosing of the concomitant therapy, whereas morning dosing tended to give lower night-time pressures. There was a significantly lower mean range of diurnal pressure with evening (3.6 mm Hg) vs morning (4.3 mm Hg) dosing (P =.02). No differences in adverse events existed between the treated arms. CONCLUSIONS: This study suggests that latanoprost and timolol maleate, both given once daily in the morning or evening, effectively reduce the IOP for the 24-hour diurnal curve when compared with timolol maleate twice daily.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Evaluation_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_ethnology_MeSH Glaucoma__Open-Angle_ethnology_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Greece_MeSH S_ethnology_MeSH Greece_ethnology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_ethnology_MeSH Ocular_Hypertension_ethnology_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Prospective_Studies_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH 
****** 12037702
----K E
----T Long-term persistence with antihypertensive drugs in new patients.
----A The objective of this study was to investigate stay-on-therapy patterns over 3 years among patients prescribed different classes of antihypertensive drugs for the first time. A retrospective analysis of information recorded in the drugs database of the Local Health Unit of Ravenna (Italy) was carried out on 7312 subjects receiving a first prescription for diuretics, beta-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin II antagonists between 1 January and 31 December 1997. Patients were followed up for 3 years. All prescriptions of antihypertensive drugs filled during the follow-up periods were considered. The patients continuing or discontinuing the initial treatment, the duration of treatment, and the doses taken were all calculated, as well as main factors influencing the persistence rate. The drugs prescribed were predominantly ACE-inhibitors, followed by calcium channel blockers, diuretics, beta-blockers and angiotensin II antagonists. A total of 57.9% of patients continued their initial treatment during the 3-year follow-up period, 34.5% discontinued the treatment, whilst 7.6% were restarted on a treatment in the third year. Persistence with treatment was influenced by: age of patient (persistence rate increasing proportionately with advancing years), type of drug first prescribed (persistence rate higher with angiotensin II antagonists, progressively lower with ACE-inhibitors, beta-blockers, calcium channel blockers and diuretics), gender of patient (persistence was better in males), age of general practitioner (GP) (the younger the GP, the better the persistence rate) and gender of GP (better stay-on-therapy rate with male GP prescribing). In the case of patients treated continuously, mean daily dose increased progressively over the 3 years. With adequate markers, helpful data can be collected from prescription claims databases for the purpose of monitoring the persistence of patients in continuing their medication, and the quality of antihypertensive treatment in a general practice setting.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Italy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH S_psychology_MeSH Patient_Compliance_psychology_MeSH M_Proportional_Hazards_Models_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 12040358
----K E
----T Carvedilol therapy in pediatric patients with congestive heart failure: a study investigating clinical and pharmacokinetic parameters.
----A OBJECTIVE: Our purpose was to evaluate the clinical effect of carvedilol among pediatric patients with congestive heart failure (CHF) who did not respond to standard therapy and to assess the pharmacokinetics of carvedilol among these children. METHODS: In this prospective, open intervention trial with blinded interpretation of selected end points, patients with CHF who did not improve on standard therapy, including digoxin, angiotensin-converting enzyme inhibitors, and diuretics, were treated with oral carvedilol in a ramped dosing scheme. Clinical parameters (ejection fraction, fractional shortening, and modified Ross score) were assessed before initiation of treatment and monthly for 6 months. Pharmacokinetic profiles of carvedilol were determined over the first 12-hour period after the initial dose in study patients, and for comparison, in 9 healthy adult volunteers. RESULTS: Fifteen patients (aged 6 weeks to 19 years) were enrolled in the study, including 10 patients with dilated cardiomyopathy and 5 with CHF secondary to congenital heart disease. All 15 patients tolerated carvedilol for the duration of the trial, and all achieved maximum target dosing. After 6 months of carvedilol therapy, ejection fraction increased (36% vs 54%; P <.05) and modified Ross Score improved (5 +/- 2 vs 3 +/- 3; P <.05). Elimination half-life was about 50% shorter in pediatric CHF patients compared with healthy adult volunteers (2.9 vs 5.2 hours; P <.05). CONCLUSIONS: Pediatric patients with CHF not responding to standard therapy may benefit from oral carvedilol treatment. The observed increased elimination of carvedilol in children suggests that optimal dosing strategies need to be further defined among the pediatric population.
----P Evaluation_Studies Journal_Article 
----M M_Administration__Oral_MeSH M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_pharmacokinetics_MeSH Carbazoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH M_Human_MeSH M_Infant_MeSH M_Male_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_pharmacokinetics_MeSH Propanolamines_pharmacokinetics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12042891
----K E
----T Beta-blocker/thiazide combination for treatment of hypertensive children: a randomized double-blind, placebo-controlled trial.
----A Antihypertensive medications are used extensively in children despite a paucity of randomized, placebo-controlled trials. This study was among the first randomized, controlled pediatric antihypertensive medication trials, in which the combination drug bisoprolol fumarate/hydrochlorothiazide (B/HT) was compared with placebo. The study comprised a 2-week single-blind placebo screening period, a 6-week double-blind dose titration period, a 4-week double-blind dose maintenance period, and a 2-week double-blind dose-tapering period. One hundred and forty subjects were enrolled to achieve 94 randomized subjects treated either with B/HT ( n=62) or placebo ( n=32). B/HT induced significant reductions compared with placebo for average sitting systolic blood pressure (SiSBP) (9.3 vs. 4.9 mmHg, P<0.05) and sitting diastolic blood pressure (SiDBP) (7.2 vs. 2.7 mmHg, P<0.05). The placebo-subtracted BP reductions were greater in younger children and those with more-severe baseline hypertension. The percentage of subjects with BP less than the 90th percentile at study completion was 45% for B/HT and 34% for placebo ( P=NS). Although the study demonstrated that B/HT reduced BP safely compared with placebo, the large placebo effect and failure of most subjects to achieve target BP control make it uncertain whether B/HT is appropriate first-line therapy for pediatric hypertension, particularly in adolescents with mild-to-moderate BP elevation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Child_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Placebos_MeSH M_Single-Blind_Method_MeSH M_Treatment_Failure_MeSH 
****** 12045161
----K E
----T Circulatory support for long-term treatment of heart failure: experience with an intraventricular continuous flow pump.
----A BACKGROUND: A lifetime mechanical solution for advanced heart failure must be reliable, with a low risk of life-threatening complications. After extensive laboratory testing, we began clinical trials with an axial flow pump for long-term treatment of New York Heart Association class IV, transplant-ineligible patients. METHODS AND RESULTS: The Jarvik 2000 is a continuous flow device that is implanted in the apex of the left ventricle with offloading to the descending thoracic aorta. Skull-based percutaneous power delivery was derived from cochlear implant technology. We used this system in 4 patients with end-stage dilated cardiomyopathy. Exercise capacity, quality of life, device parameters, and native heart function were monitored serially. One patient died from right heart failure at 3 months. The other patients were discharged from hospital between 3 and 8 weeks postoperatively and are currently New York Heart Association I or II. Follow-up lasted between 9 and 20 months. There has been no device failure or hemolysis. Native heart function and quality of life were markedly improved. CONCLUSIONS: The Jarvik 2000 is a true assist (rather than replacement) device that functions synergistically with the native left ventricle and provides excellent quality of life. Adverse events are infrequent. This blood pump may provide a mechanical solution for end-stage heart failure in the community.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Body_Weight_MeSH M_Cardiac_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiac_Surgical_Procedures_adverse_effects_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_therapy_MeSH Cardiomyopathy__Congestive_therapy_MeSH M_Echocardiography_MeSH M_Equipment_Design_MeSH M_Exercise_Tolerance_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Heart_Function_Tests_MeSH M_Heart_Ventricles_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_surgery_MeSH Heart_Ventricles_surgery_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH P_Heart-Assist_Devices_MeSH S_adverse_effects_MeSH Heart-Assist_Devices_adverse_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH M_Quality_of_Life_MeSH M_Recovery_of_Function_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Thrombosis_MeSH S_prevention_&_control_MeSH Thrombosis_prevention_&_control_MeSH M_Time_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction_MeSH S_complications_MeSH Ventricular_Dysfunction_complications_MeSH S_therapy_MeSH Ventricular_Dysfunction_therapy_MeSH 
****** 12045365
----K E
----T Omapatrilat provides long-term control of hypertension: a randomized trial of treatment withdrawal.
----A Omapatrilat simultaneously inhibits neutral endopeptidase and angiotensin-converting enzyme, increasing levels of vasodilatory peptides while decreasing production of angiotensin II. This study evaluated the clinical effects of withdrawal of omapatrilat after a patient's hypertension had been controlled (seated diastolic blood pressure <90 mm Hg) on omapatrilat for at least 6 months, with or without adjunctive antihypertensive medications. This double-blind study randomized 83 patients to receive either their established omapatrilat dose or placebo for 8 weeks; any concomitant antihypertensive medications were kept constant. Patients continuing on omapatrilat had no change in blood pressure. Patients whose chronic omapatrilat treatment was replaced by placebo had clinically important increases in both systolic (+16.5 mm Hg) and diastolic ((+9.6 mm Hg) blood pressures (both p<0.001). An increase in blood pressure was also seen in patients who were taking adjunctive antihypertensive medications prior to withdrawal of omapatrilat. This study demonstrates that when compared to withdrawal placebo, omapatrilat maintains clinically and statistically significant blood pressure reductions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Blood_Pressure_Determination_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pyridines_MeSH S_administration_&_dosage_MeSH Pyridines_administration_&_dosage_MeSH M_Reference_Values_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiazepines_MeSH S_administration_&_dosage_MeSH Thiazepines_administration_&_dosage_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Withholding_Treatment_MeSH 
****** 12047791
----K 5
----T Clinical management of the obese hypertensive patient.
----A Despite years of investigation our fundamental and clinical knowledge of the major public health problem, obesity-hypertension, is relatively meager and certainly inadequate. We are at a loss to explain why the pathophysiological mechanisms of obesity and hypertension are so inextricably intertwined. Adding to this frustration is the inadequacy of the treatment for obesity. Hemodynamically, we recognize that the expanded plasma volume caused by obesity imparts a significant volume overload on the heart, thereby increasing cardiac output, while the hypertension compounds this ventricular stress by an associated pressure overload. Thus, the ventricle has an eccentric as well as a concentric adaptive hypertrophy. Associated with obesity is an increased burden of pressor (e.g., catecholamine, angiotensin II); peptide (e.g., endothelin, insulin, leptin, natriuretic); hormonal (e.g., growth, steroids, thyroid); and neural mechanisms. Further complicating these alterations are electrolytic, lipid, uric acid, and other metabolic factors. Both diseases (obesity and hypertension) are exacerbated by frequently encountered comorbid pathophysiological disorders including atherosclerosis, ventricular dysfunction, diabetes mellitus, hyperlipidemias, and sleep apnea. To add to these issues, therapy for obesity-hypertension is suboptimal. Behavioral modification (of overweight and obesity) is commonly characterized by recidivism, and pharmacotherapy of obesity is woefully inadequate; the present agents either raise arterial pressure or are fraught with adverse effects. Fortunately, there are no contraindications imparted by obesity that complicate the drug treatment of the associated hypertension. Each of the lifestyle modifications and seven classes of antihypertensive therapy that is discussed herein is done in light of the coexistent hypertension and comorbid diseases.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Life_Style_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH S_therapy_MeSH Obesity_therapy_MeSH M_Risk_Factors_MeSH M_Weight_Loss_MeSH 
****** 12047461
----K I
----T Efficacy and tolerability in migraine prophylaxis of flunarizine in reduced doses: a comparison with propranolol 160 mg daily.
----A This was a phase-IV double-blind equivalence trial designed to assess the efficacy and tolerability of two doses of flunarizine (10 mg o.d.=FLU 10 mg and 5 mg o.d.=FLU 5 mg) in the prophylaxis of migraine, in comparison with slow-release propranolol (160 mg o.d.). A total of 808 subjects were treated in a treatment period of 16 weeks. 142 subjects discontinued the trial prematurely, mainly because of adverse events (n=58). The mean attack frequency in the double-blind period was 2.0 for the FLU 5 mg group, 1.9 for the FLU 10 mg group, and 1.9 for the propranolol group. The mean attack frequency in the last 28 days of the double-blind period was 1.8 for FLU 5 mg, 1.6 for FLU 10 mg, and 1.7 for propranolol. Both flunarizine groups were at least as effective as propranolol (P<0.001 in one-sided test). The percentage of responders (defined as subjects for whom attack frequency decreased by at least 50% compared to run-in) in the last 28 days of the double-blind period was 46% (118/259) for FLU 5 mg, 53% (141/264) for FLU 10 mg, and 48% (125/258) for propranolol. Statistical analysis showed that FLU 10 mg is at least as effective as propranolol (P<0.001) and showed a trend for noninferiority of FLU5 and propranolol (P=0.053). No statistically significant differences between the treatment groups were found for any of the secondary parameters. Overall, 190 subjects reported one or more adverse events during the run-in phase: 54 (20.5%) in the FLU 5 mg group, 76 (27.7%) in the FLU 10 mg group and 60 (22.3%) in the propranolol group. The results of this equivalence trial show that 10 mg flunarizine daily with a drug-free weekend is at least as effective as 160 mg propranolol in the prophylaxis of migraine for all evaluated parameters (one-sided equivalence tests) after 16 weeks of treatment. In addition, 5 mg flunarizine proves to be at least as effective as 160 mg propranolol when looking at the mean attack frequency for both the whole double-blind period and the last 28 days of treatment. However, in the analysis of responders, 160 mg propranolol seems to be slightly better than 5 mg flunarizine. In addition, no significant differences between the three treatments were found with regard to safety: all three treatments were generally well-tolerated and safe.
----P Clinical_Trial Clinical_Trial__Phase_IV Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Flunarizine_MeSH S_administration_&_dosage_MeSH Flunarizine_administration_&_dosage_MeSH S_adverse_effects_MeSH Flunarizine_adverse_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12049678
----K I
----T Randomized study of early intravenous esmolol versus oral beta-blockers in preventing post-CABG atrial fibrillation in high risk patients identified by signal-averaged ECG: results of a pilot study.
----A BACKGROUND: Patients with prolonged signal-averaged ECG have four times higher risk for development of atrial fibrillation (AF) after coronary artery bypass surgery (CABG). Incidence of AF is reduced, but not eliminated by prophylaxis with beta-blockers. The limitations of prophylaxis with oral beta-blockers may be related to the delayed effect of oral therapy. We performed a pilot study of the efficacy of early intravenous esmolol and an oral beta-blocker regimen for prevention of postoperative AF. METHODS: Fifty patients referred for CABG and considered to be at high risk for postoperative AF on the basis of prolonged signal-averaged ECG P wave duration > 140 ms were randomized to receive either a 24-hour infusion of esmolol 6-18 hours after CABG, at an average dose 67 +/- 7 microg/kg/min, followed by oral beta-blockers versus oral beta-blockers only beginning on postoperative day 1. RESULTS: Seven of 27 patients (26%) in the esmolol group and 6 of 23 patients (26%) in the oral beta-blocker group developed postoperative AF, P = NS. The mean time of onset of AF (2.7 +/- 0.5 vs 2.7 +/- 0.3 postoperative day, P = NS) and the median duration of AF (10 [2192] vs 7 [1.16] hours, P = NS) were similar between the two groups. Eleven (41%) patients treated with esmolol developed adverse events (hypotension: 8, bradycardia requiring temporary pacing: 2, left ventricular failure:1 patient) as compared to only one patient (4%) in the beta-blocker group who developed hypotension, P = 0.006. CONCLUSIONS: This randomized controlled pilot study suggests that intravenous esmolol is less well tolerated and offers no advantages to standard beta-blocker in preventing AF after CABG.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Bradycardia_MeSH S_chemically_induced_MeSH Bradycardia_chemically_induced_MeSH P_Coronary_Artery_Bypass_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH 
****** 12049684
----K E
----T Apnea-related heart rate variability and its clinical utility in congestive heart failure outpatients.
----A BACKGROUND: Cheyne-Stokes breathing (CSB) is an abnormal cyclical pattern of respiratory fluctuations observed during sleep in congestive heart failure (CHF) of poor prognosis. We examined the clinical usefulness of CSB screening using the heart rate variability (HRV) data from the ambulatory electrocardiogram. METHODS: We monitored ambulatory electrocardiograms and respiration simultaneously in 86 heart disease patients of both sexes, aged 57 +/- 1 years. HRV was analyzed by the maximum entropy method during the sleeping period (11 PM-5 AM). The 43 CHF patients underwent a 1-year follow-up study. RESULTS: In the power spectra of the HRV, peaks were observed within the CSB band (0.005 to 0.03 Hz). Statistically significant differences in HRV were observed between CSB patients and CSB-free patients in very low frequency (VLF) (P = 0.04), VLF/total frequency (TF) (P = 0.02), CSB (P = 0.01), CSB/TF (P = 0.003), and CSB/VLF (P < 0.0001). Cardiac events occurred in 23% of patients, including cardiac death in two, and rehospitalization for aggravated CHF in eight. In a multivariate Cox regression analysis in which age, sex, ejection fraction, NYHA functional class, beta blocker use, and basic heart disease were included, absence of ACE inhibitor use (RR 5.5, 95% CI 1.0-31) and CSB/VLF > or =80% (RR 4.2, 95% CI 1.1-17) remained significant predictors of cardiac events. CONCLUSIONS: HRV can act as an indicator of the presence of CSB in CHF patients, and could therefore be used, under outpatient conditions, to identify a CHF patients with a poor prognosis.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Apnea_MeSH S_physiopathology_MeSH Apnea_physiopathology_MeSH M_Cheyne-Stokes_Respiration_MeSH S_physiopathology_MeSH Cheyne-Stokes_Respiration_physiopathology_MeSH P_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 12053495
----K E
----T A time-to-treatment analysis in the medicine versus angiography in thrombolytic exclusion (MATE) trial.
----A Patients with acute coronary syndromes who are considered ineligible for thrombolytic therapy are at high risk of recurrent ischemia and death. This trial randomized 201 patients to triage angiography in the first 24 hours of hospital admission versus conventional medical care. Of the 165 patients who underwent angiography that was either protocol-driven or on the basis of physician preference, those who underwent angiography within 6 hours of symptom onset had a reduction in early and late adverse events. The rates of in-hospital recurrent ischemia were 15.4%, 15.4%, 17.5%, 32.4%, and 38.5%, respectively (P = 0.01 for trend), and rates of cumulative recurrent myocardial infarction or death were 0%, 12.8%, 10.0%, 11.8%, and 7.7%, respectively (P = 0.48 for trend) for patients who underwent angiography at 0-6, 6-12, 12-24, 24-48, and over 48 hours, respectively from symptom onset. Future trials of invasive versus conservative therapy should focus on performing angiography within 6 hours of symptom onset.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH P_Coronary_Angiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Patient_Selection_MeSH M_Prospective_Studies_MeSH P_Thrombolytic_Therapy_MeSH M_Time_Factors_MeSH 
****** 12060055
----K E
----T Prognosis following first acute myocardial infarction in Type 2 diabetes: a comparative population study.
----A AIMS: To estimate the incidence of death and macrovascular complications after a first myocardial infarction for patients with Type 2 diabetes. RESEARCH DESIGN: In a retrospective, incidence cohort study in the Tayside Region of Scotland we studied all patients hospitalized with a diagnosis of first acute myocardial infarction from 1 April 1993 to 31 December 1994. The primary endpoint was time to death. Secondary endpoints were 2-year incidence of hospital admission for angina, myocardial infarction, stroke, heart failure, coronary angiography, coronary artery bypass graft (CABG) and percutaneous transluminal coronary angioplasty (PTCA). RESULTS: The 147 patients with Type 2 diabetes had significantly worse survival with an increase in relative hazard of 67% compared with non-diabetic patients. After adjustment for age, sex, smoking status, prior heart failure, prior angina, delay to hospitalization, site of infarction, drug therapy with aspirin, beta-blockers, streptokinase and hyperlipidaemia and treated hypertension, Type 2 diabetes was still associated with a 40% higher death rate compared with people without diabetes (P < 0.05) There was no significant difference in death rates in those aged over 70 years, but an indication of a trend in younger individuals with a four-fold increase in death rate in those with diabetes aged < 60 years, compared with a rate ratio of 2.6 in those with diabetes aged 61-70 years. CONCLUSIONS: Among hospitalized patients with first acute myocardial infarction, Type 2 diabetes mellitus is consistently associated with increased mortality and increased hospital admission for heart failure. The estimated 4-year survival rate is only 50%. Our results indicate that younger subjects with Type 2 diabetes and acute myocardial infarction are a high-risk group deserving of special study, and support the argument for aggressive targeting of coronary risk factors among patients with Type 2 diabetes.
----P Journal_Article 
----M M_Aged_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Scotland_MeSH S_epidemiology_MeSH Scotland_epidemiology_MeSH M_Smoking_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 12062733
----K E
----T Effect of carvedilol on microcirculatory and glucose metabolic regulation in patients with congestive heart failure secondary to ischemic cardiomyopathy.
----A In a randomized (2:1), double-blinded design study, we studied 25 patients with congestive heart failure (66 +/- 9 years, ejection fraction 30 +/- 7%) before and after 23-week treatment with the beta blocker carvedilol 25 mg twice daily (n = 17) or placebo (n = 8) in addition to standard therapy. Using dynamic positron emission tomography, myocardial perfusion at rest and perfusion reserve after dipyridamole (0.56 mg/kg/min) were measured. Myocardial glucose uptake and plasma levels of catecholamines were also estimated. Carvedilol treatment reduced the rate-pressure product (8,781 +/- 2,672 vs 6,342 +/- 1,346, p <0.01) and improved ejection fraction (29 +/- 7% vs 37 +/- 11%, p <0.001), whereas no changes were observed in the control group. Perfusion at rest was unchanged in the placebo group (0.81 +/- 0.17 vs 0.86 +/- 0.23 ml/g/min, p = NS), whereas the carvedilol-treated group showed a significant reduction (0.88 +/- 0.26 vs 0.75 +/- 0.16 ml/g/min, p <0.05). Dipyridamole-induced hyperemia was significantly reduced after carvedilol treatment (1.51 +/- 0.45 vs 1.31 +/- 0.51 ml/g/min, p <0.001), whereas myocardial perfusion reserve was unaltered. Carvedilol did not alter myocardial glucose uptake (0.33 +/- 0.14 vs 0.32 +/- 0.12 micromol/g/min, p = NS) or the plasma catecholamines levels. We therefore conclude that in patients with congestive heart failure, carvedilol reduced resting and hyperemic perfusion. No effect on glucose uptake or catecholamine levels was observed. The reduced perfusion at rest must reflect reduced perfusion demand and thereby a higher threshold for myocardial ischemia and protection against myocardial damage or malignant arrhythmia. These effects may serve as a pathophysiologic explanation for the reduced mortality in patients with congestive heart failure who receive carvedilol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Coronary_Vessels_MeSH S_drug_effects_MeSH Coronary_Vessels_drug_effects_MeSH M_Dipyridamole_MeSH S_administration_&_dosage_MeSH Dipyridamole_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH S_radionuclide_imaging_MeSH Heart_Failure__Congestive_radionuclide_imaging_MeSH M_Human_MeSH M_Male_MeSH M_Microcirculation_MeSH S_drug_effects_MeSH Microcirculation_drug_effects_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tomography__Emission-Computed_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12067927
----K E
----T Patients with acute coronary syndrome should start a statin while still in hospital.
----A 
----P Comment Editorial 
----M M_Adult_MeSH M_Aged_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Female_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Physician's_Practice_Patterns_MeSH 
****** 12067934
----K E
----T Impact of availability and use of coronary interventions on the prescription of aspirin and lipid lowering treatment after acute coronary syndromes.
----A BACKGROUND: It has been suggested that patients undergoing acute intervention for coronary syndromes may not receive adequate secondary prevention. OBJECTIVE: To analyse the impact of availability and use of coronary interventions on the prescription of secondary prevention after acute coronary syndromes. DESIGN: Analysis of a prospective multicentre register of patients admitted to hospital for acute coronary syndromes. SETTING: A 1999 pan-European survey in 390 hospitals. PATIENTS: 3092 patients admitted to hospital with acute coronary syndromes (including 777 for ST elevation myocardial infarction within 12 hours of onset). MAIN OUTCOME MEASURES: Rates of prescription of aspirin and lipid lowering agents. RESULTS: Performance of coronary angiography and percutaneous coronary interventions (PCI) during the hospital stay were independent predictors of prescription of aspirin at discharge (odds ratio (OR) 1.29 and 1.89, p = 0.053 and p < 0.0001, respectively). Lipid lowering agents were prescribed more often on discharge in patients admitted to hospitals with catheterisation laboratories than without (for infarction with ST elevation, 45% v 40% (NS); for other acute coronary syndromes, 46% v 36%; p < 0.05). Prescription rates were higher among patients undergoing coronary angiography or PCI than in those treated conservatively (for infarction with ST elevation, 49%, 53%, and 39%, p < 0.05; for other acute coronary syndromes, 50%, 54%, and 34%, p < 0.05). Logistic regression analysis showed that PCI was an independent predictor of prescription of lipid lowering agents at discharge (OR 1.48, p < 0.0002). CONCLUSIONS: Contrary to expectations, invasive procedures for acute coronary syndromes are associated with higher rates of prescription of pharmacological secondary prevention.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_statistics_&_numerical_data_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_statistics_&_numerical_data_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Coronary_Angiography_MeSH S_statistics_&_numerical_data_MeSH Coronary_Angiography_statistics_&_numerical_data_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Discharge_MeSH S_statistics_&_numerical_data_MeSH Patient_Discharge_statistics_&_numerical_data_MeSH M_Prospective_Studies_MeSH M_Registries_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12075254
----K E
----T Baseline characteristics of patients with atrial fibrillation: the AFFIRM Study.
----A BACKGROUND: Although anticoagulation therapy is accepted for most patients with atrial fibrillation, 2 different strategies exist for management of the cardiac rhythm: atrial fibrillation is allowed to persist while the ventricular rate is controlled; and atrial fibrillation is converted, and an attempt is made to maintain sinus rhythm. METHODS: The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Study was a randomized clinical trial that compared these 2 strategies. We report the baseline characteristics of the patients enrolled in the AFFIRM Study. RESULTS: More than 7400 patients at more than 200 North American hospitals and clinics qualified for enrollment in the AFFIRM Study. A total of 4060 patients were enrolled in the AFFIRM Study. The average age of patients enrolled was 70 years, with 39% female and 89% white. Hypertension was present in 71%. Coronary artery disease was present in 38%. Echocardiography was performed in 3311 patients, and results showed normal ventricular function in 68% and normal left atrial size in 33%. Most patients with recurrent episodes had symptoms with atrial fibrillation. Approximately one third of patients were enrolled with a first episode of atrial fibrillation. CONCLUSION: The AFFIRM Study enrolled 4060 predominantly elderly patients with atrial fibrillation to compare ventricular rate control with rhythm control. The patients in the AFFIRM Study were representative of patients at high risk for complications from atrial fibrillation, which indicates that the results of this large clinical trial will be relevant to patient care.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Male_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Ventricular_Function_MeSH 
****** 12075713
----K E
----T Anesthesia for one-stage bilateral pheochromocytoma resection in a patient with MEN type IIa: attenuation of hypertensive crisis by magnesium sulfate.
----A Multiple endocrine neoplasia (MEN) type IIa, manifesting as an autosomal dominant trait, consists of medullary thyroid carcinoma, parathyroid adenoma or hyperplasia, and pheochromocytoma. We report our experience of a 42-year-old woman, MEN type IIa with a large bilateral pheochromocytoma, who underwent one-stage bilateral tumor resection under a combined continuous epidural technique with 0.25 per cent bupivacaine and general anesthesia using vecuronium, fentanyl, nitrous oxide, and isoflurane. An initial intra-operative hypertensive response was acceptably controlled by nitroprusside and a beta-blocker but during tumor handling the hypertensive crisis worsened and she developed acute pulmonary edema despite a continuing high dose of nitroprusside infusion. After receiving intermittent i.v. MgSO4 up to 3 g in 15 min, her condition gradually improved and the cardiovascular response was under control throughout the period of tumor handling. Hypotension encountered post-pheochromocytoma resection was treated by volume replacement, metaraminol, CaCl2, and dopamine infusion. The patient's post-operative course was uneventful.
----P Case_Reports Journal_Article 
----M M_Adrenal_Gland_Neoplasms_MeSH S_complications_MeSH Adrenal_Gland_Neoplasms_complications_MeSH S_diagnosis_MeSH Adrenal_Gland_Neoplasms_diagnosis_MeSH S_surgery_MeSH Adrenal_Gland_Neoplasms_surgery_MeSH M_Adrenalectomy_MeSH S_methods_MeSH Adrenalectomy_methods_MeSH M_Adult_MeSH M_Anesthesia_MeSH S_methods_MeSH Anesthesia_methods_MeSH M_Bupivacaine_MeSH S_administration_&_dosage_MeSH Bupivacaine_administration_&_dosage_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Intraoperative_Complications_MeSH S_diagnosis_MeSH Intraoperative_Complications_diagnosis_MeSH S_drug_therapy_MeSH Intraoperative_Complications_drug_therapy_MeSH M_Magnesium_Sulfate_MeSH S_administration_&_dosage_MeSH Magnesium_Sulfate_administration_&_dosage_MeSH M_Multiple_Endocrine_Neoplasia_Type_2a_MeSH S_complications_MeSH Multiple_Endocrine_Neoplasia_Type_2a_complications_MeSH S_diagnosis_MeSH Multiple_Endocrine_Neoplasia_Type_2a_diagnosis_MeSH M_Pheochromocytoma_MeSH S_complications_MeSH Pheochromocytoma_complications_MeSH S_diagnosis_MeSH Pheochromocytoma_diagnosis_MeSH S_surgery_MeSH Pheochromocytoma_surgery_MeSH M_Treatment_Outcome_MeSH 
****** 12082488
----K 5
----T The effect of antihypertensive drugs on the fetus.
----A A critical review of the literature on the effects of antihypertensive drugs on the fetus in pregnant women is presented. The survey covers the alpha-adrenergic receptor agonists, beta-blockers including topical eye medications, alpha-beta blockers, calcium antagonists, diuretics, and angiotensin-converting enzyme (ACE) inhibitors. The lack of data on angiotensin II receptor blockers is noted although effects are considered to be similar to those reported with ACE inhibitors and therefore to be avoided. Analysis of the literature underscores that some antihypertensive drugs can be used safely at certain stages of pregnancy, while others are suspect and to be avoided at all costs. The lack of placebo-controlled studies on the treatment of severe hypertension in pregnancy due to ethical considerations is discussed against the background of the pressing need to treat these women despite the possible deleterious effects of antihypertensive drugs.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Agonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Agonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Female_MeSH M_Fetus_MeSH S_drug_effects_MeSH Fetus_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Labetalol_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Methyldopa_MeSH S_therapeutic_use_MeSH Methyldopa_therapeutic_use_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH 
****** 12083978
----K 5
----T Beta-adrenergic blockers in systemic hypertension: pharmacokinetic considerations related to the current guidelines.
----A Beta-adrenergic blockade has provided one of the major pharmacotherapeutic advances of the 20th century. Beta-blockers are first-line drugs for the management of systemic hypertension, used alone and in combination with other antihypertensive agents. Drugs in the beta-blocking class have the common property of blocking the binding of catecholamines to beta-adrenergic receptor sites; however, there are significant pharmacodynamic and pharmacokinetic differences between the individual agents that are of clinical importance. Among these differences are the completeness of gastrointestinal absorption, the degree of hepatic first-pass metabolism, lipid solubility, protein binding, brain penetration, concentration within the cardiac tissue, rate of hepatic biotransformation, and renal clearance of drug and/or metabolites. Long-acting formulations of existing beta-blockers are currently in use, and ultra-short-acting agents are also available. Age, race, cigarette smoking and concomitant drug therapy can also influence the pharmacokinetics of beta-blocking drugs. The wide interpatient variability in plasma drug concentrations observed with beta-blockers makes this parameter unreliable in routine patient management. Despite the pharmacokinetic differences among beta-blockers, these drugs should always be titrated to achieve the desired individual patient response.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Biological_Availability_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Interactions_MeSH M_Half-Life_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Intestinal_Absorption_MeSH M_Protein_Binding_MeSH M_Structure-Activity_Relationship_MeSH 
****** 12084368
----K 1
----T [Effect of antihypertensive therapy on pulse pressure]
----A BACKGROUND: Pulse pressure (difference between systolic and diastolic pressure) is an important prognostic factor for cardiovascular mortality and morbidity in elderly hypertensives. However, data regarding the effect of antihypertensive treatment on pulse pressure (PP) are scarce. In the present study, we evaluate the effect of six classes of antihypertensive drugs on PP in an elderly hypertensive cohort. PATIENTS AND METHOD: It was an open, prospective and multicenter study performed by primary care physicians. 857 hypertensive patients (54% women) with a mean age of 68 years were included. Antihypertensive treatment (any antihypertensive drug used in monotherapy) was freely assigned by investigators and then grouped in classes for analysis. Blood pressure was measured by a validated oscillometric device using a standardized protocol. RESULTS: ACE inhibitors were the mostly used class of antihypertensive drugs (27.8%). We found no differences between drug classes in PP reduction. Likewise, no differences were observed regarding the effect on systolic, diastolic, and mean blood pressure. The percentage of adverse reactions was low (6.3%). When effects on PP reduction and adverse reactions were pooled together, angiotensin receptor blockers emerged as the antihypertensive drug class with the best profile. CONCLUSIONS: Antihypertensive drugs do not differ substantially in their ability to reduce PP. Although PP is considered as an important prognostic factor for cardiovascular mortality and morbidity, the present results do not strengthen its usefulness as a distinctive marker of antihypertensive drug classes.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_pharmacology_MeSH Diuretics_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Prospective_Studies_MeSH 
****** 12086238
----K 5
----T Management of common arrhythmias: Part II. Ventricular arrhythmias and arrhythmias in special populations.
----A In patients without established cardiac disease, the occurrence of premature ventricular complexes without sustained ventricular tachycardia is more an annoyance than a medical risk, and treatment is not required. In contrast, patients with established heart disease and premature ventricular complexes have a higher likelihood of developing ventricular tachycardia or fibrillation. These patients should be treated with a beta blocker or class I antiarrhythmic drug. Treatment of arrhythmias in pregnant women is rarely needed. When treatment is required, amiodarone should be avoided, and beta blockers should be used with caution, because these agents have been associated with fetal growth retardation. The most important rhythm abnormality in athletes is ventricular tachycardia associated with hypertrophic cardiomyopathy. If the presence of the disease is confirmed by echocardiography, beta-blocker therapy is necessary, and these patients should be limited to participation in nonstrenuous sports. Acute arrhythmias in children with Wolff-Parkinson-White syndrome can be treated with adenosine. Radiofrequency ablation of the accessory pathway can provide long-term control.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH M_Child_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Premature_Complexes_MeSH S_diagnosis_MeSH Ventricular_Premature_Complexes_diagnosis_MeSH S_therapy_MeSH Ventricular_Premature_Complexes_therapy_MeSH 
****** 12090102
----K 1
----T [Morbidity and mortality of treated essential arterial hypertension in a 26 years follow up]
----A BACKGROUND: Treatment has a definitive impact on mortality in hypertension. The magnitude of blood pressure reduction, the type of drug used and the associated risk factors may modulate the effect of treatment on mortality. AIM: To report the effects of treatment of essential hypertension, in a cohort followed for up to 26 years. PATIENTS AND METHODS: A cohort of 1,172 essential hypertensive patients followed up to 26 years. Patients were treated with different antihypertensive drugs, alone or in combination (diuretics, beta blockers, calcium channel blockers and angiotensin converting enzyme inhibitors) according to international rules and consensus. Subjects were followed until death or loss from follow-up. Blood pressure reduction was aimed to obtain figures near 140/90 mm Hg. Causes of death and complications were obtained from hospital records, phone and death certificates. Survival was studied using life tables (Kaplan Meier method and intention to treat analysis) and Cox proportional hazard analysis. RESULTS: Initial blood pressure dropped significantly from 181/109 to 154/92 mm Hg, p < 0.001. Mean follow-up time was 10.6 +/- 6.1 years. There were 143 cardiovascular deaths, 142 acute myocardial infarctions, 101 strokes, 83 subjects had cardiac failure and 49 had renal failure. The observed rates were 0.92% per year for cardiovascular mortality, 1.36% per year for coronary heart disease, 0.94% per year for stroke. CONCLUSIONS: Our mortality rate is lower than that found in classical randomized studies but similar or slightly higher than the more recent ones. Morbidity rates were also very similar. Except for mortality rate, frequency of complications did not change in comparison to our previous report after 15 year of follow up. Aging did not seem to negatively influence mortality rates in adequately treated hypertensive patients.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chile_MeSH S_epidemiology_MeSH Chile_epidemiology_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 12091004
----K E
----T Losartan for cardiovascular disease in patient's with and without diabetes in the LIFE study.
----A 
----P Comment Letter 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH M_Human_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12096962
----K 4
----T Latanoprost and timolol combination therapy vs monotherapy: one-year randomized trial.
----A OBJECTIVE: To compare the efficacy and safety of a fixed combination of 0.005% latanoprost and 0.5% timolol maleate administered once daily vs monotherapy with either 0.005% latanoprost once daily or 0.5% timolol twice daily. METHODS: Patients with either primary or secondary open-angle glaucoma or ocular hypertension participated in a 6-month, randomized, double-masked, multicenter study with 3 parallel treatment groups. The double-masked period was preceded by a 2- to 4-week "run-in" treatment with timolol. Subjects could receive fixed combination therapy during a 6-month open-label extension. MAIN OUTCOME MEASURE: The difference between groups in mean diurnal intraocular pressure reduction in study eye(s) from baseline through 6 months of treatment. RESULTS: Overall, 418 patients were enrolled in the study; 332 completed the open-label phase. Diurnal intraocular pressure levels were similar at baseline, but at week 26, they were 19.9 +/- 3.4 mm Hg in the fixed combination therapy group, 20.8 +/- 4.6 mm Hg in latanoprost-treated patients, and 23.4 +/- 5.4 mm Hg in timolol-treated patients (data are given as mean +/- SD). The mean change from baseline was greater among patients receiving fixed combination therapy compared with each monotherapy group (P<.01). Fixed combination therapy effectively lowered intraocular pressure levels for up to 1 year. All treatments were well tolerated. CONCLUSION: The combination of 0.005% latanoprost and 0.5% timolol administered once daily is effective and well tolerated for up to 12 months.
----P Clinical_Trial Evaluation_Studies Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12096985
----K 3
----T An accurate comparison of bimatoprost's efficacy and adverse effects.
----A 
----P Comment Letter 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lipids_MeSH S_administration_&_dosage_MeSH Lipids_administration_&_dosage_MeSH S_adverse_effects_MeSH Lipids_adverse_effects_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Safety_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH 
****** 12105139
----K E
----T Von Willebrand factor, soluble P-selectin, and target organ damage in hypertension: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT).
----A To investigate the relationship between soluble markers of platelet, endothelial and rheological function, and target organ damage and their response to intensified management in a population of middle-age hypertensive patients at high risk of cardiovascular complications, we studied 382 consecutive patients (308 men; mean age, 63 years, SD 8) along with 60 normotensive controls free of cardiovascular disease. Patients were divided into those with target organ damage (TOD; n=107) and those free of end-organ damage. Plasma levels of soluble P-selectin (sP-sel), a marker of platelet activation, and von Willebrand factor (vWF), an index of endothelial damage/dysfunction (both enzyme-linked immunosorbent assay), and the rheological indices fibrinogen, plasma viscosity, hematocrit, platelet, and white cell count were measured. In 53 patients, variables were further measured after 6 months of intensified cardiovascular risk management. Patients with TOD had significantly higher vWF, 137 (SD 33) versus 125 (SD 33) IU/dL (P=0.002,) and a greater proportion of smokers, 31% versus 16% (P=0.002). There were no statistically significant differences in plasma viscosity, fibrinogen, hematocrit, white blood cell count, platelet count, or sP-sel between the 2 subgroups. In multivariate analysis, vWF was a significant independent predictor for TOD. After 6 months of intensified management in 53 patients who entered the trial, there were significant reductions in systolic blood pressure, total cholesterol, hematocrit, plasma viscosity, sP-sel, and vWF (all P<0.01) but no significant change in fibrinogen. In conclusion, there is a relationship between TOD and endothelial damage/dysfunction in hypertension. Intensified management results in improvements in hemorheology, endothelial and platelet function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Sectional_Studies_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Hematocrit_MeSH M_Hemorheology_MeSH S_drug_effects_MeSH Hemorheology_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_P-Selectin_MeSH S_blood_MeSH P-Selectin_blood_MeSH S_drug_effects_MeSH P-Selectin_drug_effects_MeSH M_Perindopril_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Regression_Analysis_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_von_Willebrand_Factor_MeSH S_drug_effects_MeSH von_Willebrand_Factor_drug_effects_MeSH S_metabolism_MeSH von_Willebrand_Factor_metabolism_MeSH 
****** 12106847
----K E
----T Frequency of postprandial lipemia after a first acute coronary event (unstable angina pectoris or non-ST-segment elevation acute myocardial infarction) and the effects of atenolol on the lipemia.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angina__Unstable_MeSH S_blood_MeSH Angina__Unstable_blood_MeSH S_complications_MeSH Angina__Unstable_complications_MeSH M_Area_Under_Curve_MeSH M_Atenolol_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Fasting_MeSH S_blood_MeSH Fasting_blood_MeSH M_Female_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_blood_MeSH Hyperlipidemia_blood_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH P_Postprandial_Period_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 12107422
----K E
----T Antihypertensive persistence and drug class.
----A BACKGROUND: Noncompliance with antihypertensive therapy is a major problem that hinders successful hypertension management. OBJECTIVE: To study antihypertensive drug persistence for hypertensive patients in routine clinical settings. METHODS: Hypertensive patients were retrospectively studied (1994 through 1998) using databases managed by Saskatchewan Health. The study population (46,458 people) included all patients with an International Classification of Diseases-9 code of 401, 402, 403 or 404, or any four-digit code included in these categories, who received at least one antihypertensive therapy prescription during the first 4.5 years of the study and received no antihypertensive therapy 12 months before the dispensing of the first therapy. Prescriptions were placed into the following drug classes: angiotensin II antagonists, angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers and diuretics. Persistence was determined for four intervals in the patient's therapy at 180, 360, 540 and 720 days. RESULTS: Drug class had a statistically significant (P<0.001) effect on persistence. Angiotensin II antagonists had the highest persistence followed by angiotensin-converting enzyme inhibitors, calcium channel blockers, beta-blockers and diuretics. Persistence decreased as the time interval increased. Females were significantly more persistent than males (P<0.005), and elderly patients were significantly more persistent than younger patients (P<0.001) at each of the four time intervals. For angiotensin II antagonists, age and sex did not affect persistence. CONCLUSIONS: The consistently higher persistence associated with the use of angiotensin II antagonists may improve the management of hypertension.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Utilization_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH M_Saskatchewan_MeSH S_epidemiology_MeSH Saskatchewan_epidemiology_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12107602
----K I
----T Effect of antihypertensive treatment with valsartan or atenolol on sexual activity and plasma testosterone in hypertensive men.
----A OBJECTIVE: To compare the effects of valsartan and atenolol on sexual activity and plasma testosterone in newly diagnosed, previously untreated, essential hypertensive male subjects. METHODS: One hundred and ten hypertensive men, aged 40-49 years, homogeneous for marital status and without any previous sexual dysfunction were randomly treated with valsartan 80 mg daily (o.d.) or atenolol 50 mg o.d. for 16 weeks according to a double-blind, parallel-arm study design. After 8 weeks the dose was doubled in the non-responders (diastolic blood pressure > 90 mmHg). Clinical evaluation was performed after 8 weeks and 16 weeks of treatment and included blood pressure and plasma testosterone measurements and the compilation of a questionnaire about sexual activity (sexual intercourse episodes/month). RESULTS: Despite similar blood pressure lowering, atenolol significantly reduced sexual activity (from 6.0 sexual intercourse episodes/month to 4.2 sexual intercourse episodes/month, P < 0.01 vs placebo), whereas valsartan increased it, although not significantly (from 5.8 sexual intercourse episodes/month to 7.4 sexual intercourse episodes/month, P = 0.058), compared with placebo, but significantly compared with the atenolol group ( P < 0.05). Testosterone was reduced by atenolol (from 18.2 nmol/l to 13.8 nmol/l, P < 0.01 vs baseline) but was not affected by valsartan (from 17.6 nmol/l to 18.3 nmol/l). CONCLUSIONS: These results suggest that atenolol induces a worsening of sexual activity and a reduction of testosterone, whereas valsartan does not worsen sexual activity and does not change testosterone levels.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH P_Coitus_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Testosterone_MeSH S_blood_MeSH Testosterone_blood_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Valine_MeSH S_adverse_effects_MeSH Valine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 12107398
----K 1
----T Angiotensin converting enzyme inhibition and dihydropyridine calcium channel blockade in the treatment of left ventricular hypertrophy in arterial hypertension.
----A In arterial hypertension, left ventricular (LV) hypertrophy (H) is a prognostically relevant target organ damage associated with systolic and diastolic LV dysfunction. The level of LV dysfunction seems to be related to the degree of myocardial fibrosis. Prognosis of hypertensive patients who have LVH regression appears to be improved. Therefore, LVH regression is an important antihypertensive treatment goal. The renin-angiotensin-aldosterone system is implicated in LVH development and myocardial fibrosis in essential arterial hypertension. Early studies in the 80s and 90s have led expectations that angiotensin converting enzyme (ACE) inhibitors could induce greater LVH regression than other antihypertensive drugs at similar blood pressure reduction. In the late 90s, the double-blind randomized controlled PRESERVE trial (Prospective Randomize Enalapril Study Evaluating Reversal of Ventricular Enlargement) has been designed to evaluate whether the ACE inhibitor enalapril was more effective than nifedipine GITS in regressing LVH and improving LV diastolic dysfunction. The PRESERVE study demonstrated a mildly higher antihypertensive effect of nifedipine GITS than enalapril, which required more frequently association with hydrochlorothiazide to control blood pressure. However, at similar level of blood pressure reduction achieved with enalapril and long-acting nifedipine in association with hydrochlorothiazide or atenolol, both antihypertensive treatments showed similar efficacy in LVH regression and LV diastolic filling improvement.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dihydropyridines_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Disease_Models__Animal_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Meta-Analysis_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Rats_MeSH M_Rats__Inbred_SHR_MeSH M_Renin-Angiotensin_System_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Time_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH 
****** 12116987
----K E
----T Hypertension guidelines in elderly patients: is anybody listening?
----A PURPOSE: Previous guidelines for the management of uncomplicated hypertension in elderly patients have recommended diuretic agents and then beta-blockers. We examined trends in the initial treatment choice for elderly people with hypertension and the effects of a government-sponsored program to publish and disseminate a simplified version of the national guidelines for the treatment of hypertension to all physicians in Ontario, Canada. SUBJECTS AND METHODS: Linked administrative databases containing information on the more than 1.2 million elderly residents in Ontario were used. Time series analysis was performed to determine prescribing trends from 1993 to 1998 for patients who began antihypertensive medication for the treatment of hypertension and to examine the effects of the simplified guidelines that were distributed in July of 1995. RESULTS: Diuretic agents were the most commonly prescribed medications, with annual rates from 35% to 38% (P = 0.59) throughout the study. Beta-blocker prescribing rose from 12% to 16% (P <0.01), whereas angiotensin-converting enzyme (ACE) inhibitor prescribing rose from 27% to 32% (P <0.01). Prescriptions for calcium channel blockers dropped significantly, from 23% to 14% (P <0.01). However, the publication and dissemination of the Ontario hypertension guidelines had no statistically significant effects on the proportion of patients who began treatment with a diuretic agent (P = 0.55), beta-blocker, (P = 0.32), ACE inhibitor (P = 0.09), or calcium channel blocker (P = 0.07). CONCLUSION: The dissemination of simplified practice guidelines for hypertension did not have notable effects on prescribing patterns in Ontario.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comorbidity_MeSH M_Databases__Factual_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Ontario_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH P_Practice_Guidelines_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12114349
----K E
----T Noninvasive evaluation of pulmonary capillary wedge pressure by BP response to the Valsalva maneuver.
----A STUDY OBJECTIVES: To determine the BP response to the Valsalva maneuver (VM) at baseline and after changes in therapy and to compare this response to the invasively measured pulmonary capillary wedge pressure (PCWP). DESIGN: Comparison of the BP response to the VM with invasively measured PCWP. In a subset of patients, direct PCWP and pulse amplitude ratio (PAR) measurements were repeated (mean +/- SD) 3.2 +/- 4.5 months later after adjusting the therapy. SETTING: Tertiary-care center. PATIENTS: Forty-two stable patients (8 women; mean age, 58 +/- 13 years) undergoing right heart catheterization who were in sinus rhythm. MEASUREMENTS: PAR calculated between the end and the beginning of the VM using the last two beats and the first three beats of the straining phase and simultaneous measurement of PCWP. RESULTS: There was a highly significant correlation between the invasively measured PCWP (range, 2 to 32 mm Hg) and the PAR (range, 0.28 to 1.15; R(2) = 0.75; p < 0.001). In addition, changes of PCWP during follow-up (-16 to 13 mm Hg) were well-correlated (R(2) = 0.93; p < 0.001; n = 11) with changes in PAR (-0.44 to 0.47). The administration of medication (eg, beta-blockers, amiodarone, angiotensin-converting enzyme inhibitor, and digoxin) did not influence the results. CONCLUSIONS: PCWP and changes during therapy can be estimated noninvasively by measuring the PAR during the VM with acceptable accuracy in stable patients with cardiac conditions. Thus, this method may be a useful tool in detecting an elevated PCWP and hemodynamic response to therapy.
----P Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH P_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Female_MeSH P_Heart_Catheterization_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH P_Pulmonary_Wedge_Pressure_MeSH M_ROC_Curve_MeSH M_Supine_Position_MeSH P_Valsalva_Maneuver_MeSH 
****** 12113643
----K 4
----T Safety of unoprostone isopropyl as mono- or adjunctive therapy in patients with primary open-angle glaucoma or ocular hypertension.
----A This review summarises the safety of unoprostone isopropyl (both at the 0.12 and 0.15% concentrations) instilled twice daily in patients with primary open-angle glaucoma (POAG) or ocular hypertension (OH). For unoprostone 0.15%, combined data from two 12-month comparative monotherapy studies are reported, as well as data from three adjunctive therapy studies and two special population studies. With unoprostone monotherapy, most adverse events were mild or moderate and transient in nature. Less than 7% of unoprostone-treated patients discontinued therapy due to an adverse event. The most common adverse events associated with unoprostone were burning/stinging, burning/stinging directly upon drug instillation, ocular itching, and conjunctival hyperaemia. Unoprostone had no clinically notable effects on vital signs, laboratory profiles, or comprehensive ophthalmic examinations. One of 659 unoprostone 0.15%-treated patients had a change in iris colour after 12 months of monotherapy. Except for a higher incidence of burning/stinging and burning/stinging upon instillation, unoprostone was comparable to timolol 0.5% twice daily and betaxolol 0.5% twice daily. No safety concerns were raised with use of unoprostone as adjunctive therapy. Unoprostone had no significant effect on exercise-induced heart rate in healthy subjects or on pulmonary function in patients with mild-to-moderate asthma. The safety profile of unoprostone 0.15% was consistent with published information on the 0.12% formulation. In conclusion, unoprostone has an excellent safety profile in patients with POAG or OH.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Chemotherapy__Adjuvant_MeSH S_adverse_effects_MeSH Chemotherapy__Adjuvant_adverse_effects_MeSH M_Demography_MeSH M_Dinoprost_MeSH S_administration_&_dosage_MeSH Dinoprost_administration_&_dosage_MeSH S_adverse_effects_MeSH Dinoprost_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Dinoprost_analogs_&_derivatives_MeSH M_Drug_Therapy__Combination_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12116890
----K 5
----T Pharmacogenetics and cardiovascular disease: impact on drug response and applications to disease management.
----A The genetic polymorphisms that may affect individual responses to cardiovascular agents are reviewed, and the application of pharmacogenetics to cardiovascular disease management is discussed. Pharmacogenetics is the search for genetic polymorphisms that affect responses to drug therapy. Investigators have found many associations between genetic polymorphisms and responses to cardiovascular drugs. Some of these relationships have been demonstrated in large patient populations, such as patients with ischemic heart disease receiving statins. Study data consistently show a greater response to statins in ischemic heart disease patients with genotypes associated with worse prognoses. Studies of other polymorphisms, such as those in the genes encoding anglotensin-converting enzyme and beta 1-adrenergic receptors, have less consistently found relationships between these variations and cardiovascular drug responses. For gene-drug response associations for which the data are inconsistent, the interaction of multiple polymorphisms in multiple genes coding for proteins affected by drug therapy or influencing drug metabolism may prove to have a greater influence on drug responses than any one polymorphism. Once the polymorphisms that best determine the response to a particular drug are known and tests to rapidly identify these variations are available, individual patients may be screened for genetic polymorphisms before drug therapy is begun and the information used to choose agents with the greatest potential for efficacy and least potential for toxicity. Pharmacogenetics has many possible applications in the drug therapy of cardiovascular diseases. Much more must be learned, however, before pharmacogenetic factors can be routinely incorporated into therapeutic decisions.
----P Journal_Article Review Review__Tutorial 
----M M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH P_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_genetics_MeSH Cardiovascular_Diseases_genetics_MeSH M_Human_MeSH P_Pharmacogenetics_MeSH M_Polymorphism_(Genetics)_MeSH M_Receptors__Adrenergic__beta_MeSH S_genetics_MeSH Receptors__Adrenergic__beta_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH 
****** 12117453
----K E
----T Putting LIFE into hypertension.
----A 
----P Clinical_Trial Comment Journal_Article Randomized_Controlled_Trial 
----M 
****** 12117460
----K E
----T Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol.
----A 
----P Clinical_Trial Comment Journal_Article Randomized_Controlled_Trial 
----M 
****** 12117400
----K I
----T Beta-blocker therapy and symptoms of depression, fatigue, and sexual dysfunction.
----A CONTEXT: beta-Blocker therapy remains substantially underused in cardiac patients despite its proven mortality benefits. Reluctance to prescribe these agents may derive from concerns about their association with symptoms of depression, fatigue, and sexual dysfunction. OBJECTIVE: To determine the association of beta-blockers with depressive symptoms, fatigue, and sexual dysfunction by performing a quantitative review of randomized trials that tested beta-blockers in myocardial infarction, heart failure, and hypertension. DATA SOURCES: Randomized trials of beta-blockers used in the treatment of myocardial infarction, heart failure, or hypertension were identified by searching the MEDLINE database for English-language articles (1966-2001). In addition, we searched the reference lists of previously published trials and reviews of beta-blockers for additional studies. STUDY SELECTION: Criteria for inclusion of trials in the review were: random allocation of study treatments, placebo control, noncrossover design, enrollment of at least 100 patients, and a minimum of 6 months of follow-up. The initial search produced 475 articles, 42 of which met these criteria. Fifteen of these trials reported on depressive symptoms, fatigue, or sexual dysfunction and were selected for inclusion. DATA EXTRACTION: For each trial, 1 author abstracted the frequency of adverse events in the beta-blocker and placebo groups and the numbers of patients randomized to the treatment groups. Two other authors verified the counts of events, and all authors adjudicated any discrepancies. Two different types of information on adverse events were abstracted: patient-reported symptoms and withdrawal of therapy due to a specified symptom. We categorized the tested beta-blockers by generation (early vs late) and lipid solubility (high vs low to moderate). DATA SYNTHESIS: The 15 trials involved more than 35,000 subjects. beta-Blocker therapy was not associated with a significant absolute annual increase in risk of reported depressive symptoms (6 per 1000 patients; 95% confidence interval [CI], -7 to 19). beta-Blockers were associated with a small significant annual increase in risk of reported fatigue (18 per 1000 patients; 95% CI, 5-30), equivalent to 1 additional report of fatigue for every 57 patients treated per year with beta-blockers. beta-Blockers were also associated with a small, significant annual increase in risk of reported sexual dysfunction (5 per 1000 patients; 95% CI, 2-8), equivalent to one additional report for every 199 patients treated per year. None of the risks of adverse effects differed significantly by degree of beta-blocker lipid solubility. The risk associated with reported fatigue was significantly higher for early-generation than for late-generation beta-blockers (P =.04). CONCLUSION: The conventional wisdom that beta-blocker therapy is associated with substantial risks of depressive symptoms, fatigue, and sexual dysfunction is not supported by data from clinical trials. There is no significant increased risk of depressive symptoms and only small increased risks of fatigue and sexual dysfunction. The risks of these adverse effects should be put in the context of the documented benefits of these medications.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH M_Fatigue_MeSH S_chemically_induced_MeSH Fatigue_chemically_induced_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH 
****** 12118806
----K E
----T A comparison of two individual amiodarone regimens to placebo in open heart surgery patients.
----A BACKGROUND: This study compares the ability of two oral amiodarone regimens to reduce the risk of atrial fibrillation (AF) as compared with the placebo among elderly open heart surgery (OHS) patients receiving beta blockade. METHODS: This is a randomized, double-blinded, placebo-controlled trial of 220 patients undergoing OHS. Patients (average age, 73 years) received 7 g of oral amiodarone more than 10 days starting 5 days before OHS (slow load; n = 56), a 6 g oral amiodarone regimen more than 6 days starting 1 day before OHS (fast load; n = 64), or matching placebo in one of the two previously mentioned regimens (n = 100). RESULTS: Patients receiving the slow load amiodarone regimen had a significant reduction in the risk of AF (48.4%; p = 0.013), AF lasting more than 24 hours (76.5%; p = 0.003), symptomatic AF (90.0%; p = 0.002), and recurrent AF (64.5%; p = 0.025) as compared with the placebo. Patients receiving the fast load amiodarone regimen had significant reductions in the risk of AF lasting more than 24 hours (52.6%; p = 0.038) and symptomatic AF (65.0%; p = 0.024), but the incidence of any AF or any recurrence of AF only showed a trend toward significance (34.0% and 45.5%; p = 0.054 and 0.09, respectively). CONCLUSIONS: Oral amiodarone in a slow loading regimen provides significant suppression of all AF factors and can be used when a patient has started it at least 5 days before OHS. If a patient has less than 5 days before OHS, the fast loading regimen is an efficacious alternative as it provides significant benefits in preventing AF from lasting more than 24 hours and for preventing symptomatic AF. Both regimens were well tolerated and safe in elderly patients receiving beta blockade according to the hospital's standard protocol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH P_Cardiac_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiac_Surgical_Procedures_adverse_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12119608
----K 5
----T The genetic basis of variability in drug responses.
----A It is almost axiomatic that patients vary widely in their beneficial responses to drug therapy, and serious and apparently unpredictable adverse drug reactions continue to be a major public health problem. Here, we discuss the concept that genetic variants might determine much of this variability in drug response, and propose an algorithm to enable further evaluation of the benefits and pitfalls of this enticing possibility.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Genomics_MeSH M_Human_MeSH P_Pharmacogenetics_MeSH M_Pharmacokinetics_MeSH M_Polymorphism_(Genetics)_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12119800
----K 5
----T Clinical pharmacology of antihypertensive drugs.
----A Systemic hypertension is a major public health problem and is perhaps the most common chronic disorder in most societies. Most patients with vascular disease report hypertension in their medical history. Irrespective of the specialty that one practices, every physician will likely encounter patients with systemic hypertension. Unfortunately, an overwhelming number have so-called "primary" or "essential" hypertension for which a cure has yet to be found. Fortunately, excellent therapy is available to control this modern malady. The field of hypertension continues to evolve rapidly, particularly in the field of therapy. During the past two decades, the treatment of hypertension has moved from a cookbook approach to more scientifically based individualized management. This paradigm shift requires the practitioner to acquire sufficient knowledge about individual drugs and how they work in a given patient. Rapid expansion of available drugs has placed a burden on the clinician to keep up with these advances. We hope that the discussions contained herein will ease that burden somewhat and make the treatment options less cumbersome. This article addresses the practical issues related to selection of antihypertensive drugs and provides an overview of advantages and disadvantages of individual drug classes. The reader should also refer to the JNC VI document [1] to further understand the selection of drug therapy based upon compelling indications. The ultimate aim of hypertension management should always be to achieve target or goal blood pressure levels.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 12123401
----K E
----T The new definition of myocardial infarction: diagnostic and prognostic implications in patients with acute coronary syndromes.
----A BACKGROUND: The clinical implications of the recently revised criteria for diagnosis of acute myocardial infarction (AMI) in patients with suspected acute coronary syndromes are unknown. METHODS: To evaluate the prognostic implications of the new diagnostic criteria for AMI, we studied 493 consecutive patients with suspected acute coronary syndromes admitted to University of Michigan, Ann Arbor, between May 1, 1999, and January 1, 2000. Patients with positive cardiac enzymes and symptoms suggestive of coronary ischemia (n = 275) were divided into 2 groups: group A, with elevated peak creatine kinase-MB fraction and/or new electrocardiographic changes suggestive of AMI regardless of troponin status (diagnosed as AMI by old criteria), and group B, with normal peak creatine kinase-MB fraction but elevated troponin I level (additional patients diagnosed as having AMI by new criteria). RESULTS: As compared with group A (n = 224), patients in group B (n = 51) were older women, with increased comorbidities such as previous stroke or aortic stenosis, and had fewer in-hospital procedures. In-hospital adverse events (reinfarction, heart failure, shock, and mortality) were similar between the groups, whereas 6-month mortality was higher among group B patients (16.3% vs 5.8%; P =.03). This difference was not statistically significant after adjustment for differences in baseline characteristics between the groups (odds ratio, 1.6; 95% confidence interval, 0.5-5.9). CONCLUSIONS: The new criteria result in a substantial increase in the diagnosis of AMI. Furthermore, they help to identify patients with acute coronary syndromes who have greater comorbidities and worse 6-month outcomes who are otherwise missed by the old criteria. Additional studies are needed to confirm these preliminary findings and to determine the financial implications of the new criteria.
----P Evaluation_Studies Journal_Article 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Isoenzymes_MeSH S_blood_MeSH Isoenzymes_blood_MeSH M_Length_of_Stay_MeSH M_Male_MeSH M_Michigan_MeSH S_epidemiology_MeSH Michigan_epidemiology_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Platelet_Glycoprotein_GPIIb-IIIa_Complex_MeSH S_antagonists_&_inhibitors_MeSH Platelet_Glycoprotein_GPIIb-IIIa_Complex_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Glycoprotein_GPIIb-IIIa_Complex_therapeutic_use_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Syndrome_MeSH 
****** 12123409
----K E
----T Successful blood pressure control in the African American Study of Kidney Disease and Hypertension.
----A BACKGROUND: The African American Study of Kidney Disease and Hypertension (AASK) is an ongoing trial to evaluate the effect of blood pressure and choice of antihypertensive drug on the rate of decline of renal function. OBJECTIVE: To present the success of the AASK in achieving the trial's rigorous blood pressure goals in an extremely challenging patient population. METHODS: The AASK participants included African American patients with hypertension (n = 1094), aged 18 to 70 years, with glomerular filtration rates between 20 and 65 mL/min per 1.73 m(2) and no other identified causes of renal insufficiency. Participants were randomized to a goal mean arterial blood pressure (MAP) of either 102 to 107 mm Hg (usual MAP goal) or 92 mm Hg or less (low MAP goal). Participants in each of these groups were also randomized (double-blind) to a regimen containing metoprolol succinate, ramipril, or amlodipine besylate. Additional agents were added, if required, in the following recommended order: furosemide, doxazosin mesylate, clonidine hydrochloride, or hydralazine hydrochloride (or minoxidil, if needed). RESULTS: In participants randomized to the low MAP goal, the percentage of participants who achieved a blood pressure of less than 140/90 mm Hg increased from a baseline of 20.0% to 78.9% by 14 months after randomization. For usual MAP goal participants, the corresponding percentages increased from 21.5% to 41.8%. The difference in median levels of MAP between the 2 MAP goal groups increased and remained at approximately 12 mm Hg. Blood pressure reduction was similar regardless of age, sex, body mass index, education, insurance or employment status, income, or marital status. CONCLUSION: The blood pressure goals set and achieved in AASK participants clearly demonstrate that adequate blood pressure control can be achieved even in hypertensive populations whose blood pressure is the most difficult to control.
----P Clinical_Trial Evaluation_Studies Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH S_physiology_MeSH Glomerular_Filtration_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Diseases_MeSH S_complications_MeSH Kidney_Diseases_complications_MeSH S_drug_therapy_MeSH Kidney_Diseases_drug_therapy_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12135934
----K 5
----T Beta-blockers in the post-myocardial infarction patient.
----A 
----P Case_Reports Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_African_Americans_MeSH M_Aged_MeSH M_Clinical_Trials_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Peripheral_Vascular_Diseases_MeSH S_complications_MeSH Peripheral_Vascular_Diseases_complications_MeSH M_Pulmonary_Disease__Chronic_Obstructive_MeSH S_complications_MeSH Pulmonary_Disease__Chronic_Obstructive_complications_MeSH M_Treatment_Outcome_MeSH 
****** 12140804
----K E
----T African-American Heart Failure Trial (A-HeFT): rationale, design, and methodology.
----A BACKGROUND: Hydralazine and isosorbide dinitrate combination (H+ISDN), angiotensin-converting enzyme inhibitors, and beta-blockers have improved outcomes in heart failure (HF). Analysis of previous trials has shown that H+ISDN appears especially beneficial in African American patients. METHODS AND RESULTS: The African-American Heart Failure Trial (A-HeFT) is double-blind, placebo-controlled, and includes African American patients with stable New York Heart Association Class III-IV HF on standard therapy. Patients must have prior HF-related events and left ventricular ejection fraction (LVEF) < or = 35% or LVEF <45% with left ventricular internal diastolic dimension >2.9 cm/m(2). Randomization to addition of placebo or BiDil (Nitro Med, Inc., Bedford, MA), a fixed combination of H+ISDN, is stratified for beta-blocker usage. All patients are treated and followed until the last patient entered completes 6 months of follow-up. The primary efficacy endpoint is a composite score including quality of life, death, and hospitalization for HF. At least 600 patients will be randomized; the first was randomized in June 2001. CONCLUSIONS: In addition to providing additional information on BiDil efficacy in HF, A-HeFT is the first HF trial aimed at a selected subgroup of patients and the first to use a new composite HF score as its primary efficacy endpoint.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hydralazine_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Informed_Consent_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Selection_MeSH M_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 12142116
----K E
----T Dose of metoprolol CR/XL and clinical outcomes in patients with heart failure: analysis of the experience in metoprolol CR/XL randomized intervention trial in chronic heart failure (MERIT-HF).
----A OBJECTIVES: We performed a post-hoc subgroup analysis in the Metoprolol CR/XL Randomized Intervention Trial in Chronic Heart Failure (MERIT-HF) with the aim of reporting on the heart rate (HR) response during the titration phase and clinical outcomes from the three-month follow-up visit to end of study in two dosage subgroups: one that had reached more than 100 mg of metoprolol CR/XL once daily (high-dose group; n = 1,202; mean 192 mg) and one that had reached 100 mg or less (low-dose group; n = 412; mean 76 mg). BACKGROUND: Clinicians have questioned whether patients need to reach the target beta-blocker dose to receive benefit. METHODS; Outcome (Cox-adjusted) was compared with all placebo patients with dose available at the three-month visit (n = 1,845). RESULTS: Data indicated somewhat higher risk in the low-dose group compared with the high-dose group. Heart rate was reduced to a similar degree in the two dose groups, indicating higher sensitivity for beta-blockade in the low-dose group. The reduction in total mortality with metoprolol CR/XL compared with placebo was similar: 38% (95% confidence interval [CI], 16 to 55) in high-dose group (p = 0.0022) and also 38% (95% CI, 11 to 57) in the low-dose group (p = 0.010). CONCLUSIONS: Risk reduction was similar in the high- and low-dose subgroups, which, at least partly, may be the result of similar beta-blockade as judged from the HR response. The results support the idea of an individualized dose-titration regimen, which is guided by patient tolerability and the HR response. Further research is needed to shed light on why some patients respond with a marked HR reduction and reduced mortality risk on a relatively small dose of a beta-blocker.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH M_Aged_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_blood_MeSH Metoprolol_blood_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Withholding_Treatment_MeSH 
****** 12147929
----K I
----T Essential hypertension of Caribbean Hispanics: sodium, renin, and response to therapy.
----A Little is known about essential hypertension in Hispanic Americans, despite the fact that they are the fastest-growing minority in the United States and have a disproportionate degree of hypertensive target organ damage. The authors studied 89 Caribbean Hispanic hypertensive patients who participated in six double-blind, randomized trials of antihypertensive agents. Demographics, laboratory data, sodium excretion, plasma renin activity, and atrial natriuretic peptide were obtained after 3-4 weeks on placebo. Blood pressure responses to angiotensin-converting enzyme (ACE) inhibitors, beta blockers, calcium channel blockers, hydrochlorothiazide (HCTZ), and fixed combinations of ACE inhibitors and HCTZ, were compared to the placebo values after 8-12 weeks of treatment. Patients had a multiple risk factor profile (obesity and diabetes) and a wide spectrum of blood pressure elevation, left ventricular hypertrophy, and hypertensive renal damage. Urine sodium excretion rates indicated inability to comply with salt restriction in 65% of patients. Plasma renin activity was lower than that of Hispanic normotensive controls, and 62% of patients had low-renin essential hypertension by renin profiling to sodium excretion. On analysis of variance, blood pressure reductions by calcium channel blockers, HCTZ, and ACE inhibitor/HCTZ combinations were significantly greater than that with placebo, while those of ACE inhibitors and beta blockers as monotherapy were not. The authors conclude that essential hypertension of Caribbean Hispanics is associated with multiple risk factors and is largely of the low-renin type. Responses to therapy are consistent with those observed in other populations with the low-renin phenotype and suggest salt-sensitivity of blood pressure in this population. Confirmation of the latter has implications for prevention and treatment of essential hypertension in Hispanics.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH P_Hispanic_Americans_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_New_York_City_MeSH S_epidemiology_MeSH New_York_City_epidemiology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Risk_Factors_MeSH M_Sodium_MeSH S_urine_MeSH Sodium_urine_MeSH M_West_Indies_MeSH S_ethnology_MeSH West_Indies_ethnology_MeSH 
****** 12147937
----K I
----T The Losartan Intervention for Endpoint Reduction (LIFE) trial-have angiotensin-receptor blockers come of age?
----A The Losartan Intervention for Endpoint Reduction trial is one of several end-point trials that are now available with angiotensin-receptor blockers. This trial compared two regimens-losartan-based therapy to atenolol-based therapy-in 9193 hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy. In the instance of each of these therapeutic groups, hydrochlorothiazide add-on therapy was permitted as per protocol. Although blood pressures were comparably reduced in both the losartan and the atenolol-based treatment groups, stroke rate was notably less in the losartan-treatment group. The 1195 patient diabetic cohort in this trial also experienced a substantial reduction in total and cardiovascular mortality favoring losartan. An additional finding in this trial was that new-onset diabetes developed 25% less frequently in the losartan-treated group. The results of this trial are both interesting and relevant to what is an expanding use of angiotensin-receptor blockers in the hypertensive population.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Treatment_Outcome_MeSH M_Uric_Acid_MeSH S_blood_MeSH Uric_Acid_blood_MeSH 
****** 12149663
----K E
----T A population-based European cohort study of persistence in newly diagnosed hypertensive patients.
----A This study assessed the percentage of patients after 1 year who persisted on initially prescribed antihypertensive therapy. Medical records of 2416 patients with newly diagnosed hypertension who were prescribed initial antihypertensive monotherapy by general practitioners in Germany, France, and the United Kingdom were evaluated. Comparisons were made among the angiotensin II receptor antagonist (AIIRA) irbesartan, all other antihypertensive classes (including AIIRAs other than irbesartan), and the AIIRA losartan. Patients initiated on the AIIRA irbesartan scored highest with a persistence rate of 60.8%, followed by patients who received all other AIIRA agents with a persistence rate of 51.3%. Angiotensin-converting enzyme inhibitors, calcium channel blockers, beta-blockers, and losartan were associated with comparable persistence rates, between 42.0% and 49.7%. Patients who received diuretics scored lowest with a persistence rate of 34.4%. Persistence has emerged as an essential factor for blood pressure control. Prescribing an antihypertensive agent that provides a favourable efficacy and tolerability profile may provide greater persistence with therapy and hence a higher level of blood pressure control.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Europe_MeSH S_epidemiology_MeSH Europe_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Receptors__Angiotensin_therapeutic_use_MeSH M_Retreatment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH P_Treatment_Failure_MeSH 
****** 12149666
----K E
----T A blood pressure independent association between glomerular albumin leakage and electrocardiographic left ventricular hypertrophy. The LIFE Study. Losartan Intervention For Endpoint reduction.
----A In the Losartan Intervention For Endpoint reduction (LIFE) study left ventricular (LV) hypertrophy was associated with increased urine albumin/creatinine ratio (UACR) at baseline. To evaluate whether this association was due only to parallel blood pressure (BP)-induced changes we re-examined the patients after 1 year of antihypertensive treatment to investigate whether changes in LV hypertrophy and UACR were related independently of changes in BP. In 7,142 hypertensive patients included in the LIFE study, we measured UACR, LV hypertrophy by electrocardiography, plasma glucose and BP after 2 weeks of placebo treatment and again after 1 year of antihypertensive treatment with either an atenolol or a losartan based regime. At baseline and still after 1 year of treatment logUACR (R = 0.28, P < 0.001) was still correlated to LV hypertrophy (beta = 0.05) assessed by ECG independently of systolic BP (beta = 0.16), plasma glucose (beta = 0.19) and age (beta = 0.08). Change in logUACR (R = 0.19, P < 0.001) during treatment was correlated to change in LV hypertrophy (beta = 0.10) independently of reduction in systolic BP (beta = 0.13) and change in plasma glucose (beta = 0.06). After 1 year of antihypertensive treatment UACR was still related to LV hypertrophy independently of systolic BP, and the reduction in UACR during that first year of treatment was related to regression of LV hypertrophy independently of reduction in systolic BP. This suggests that the relationship between LV hypertrophy and glomerular albumin leakage is not just due to parallel BP-induced changes. As glomerular albumin leakage may represent generalised vascular damage we hypothesise a vascular relationship between cardiac and glomerular damage.
----P Journal_Article 
----M M_Aged_MeSH M_Albuminuria_MeSH S_drug_therapy_MeSH Albuminuria_drug_therapy_MeSH S_ultrasonography_MeSH Albuminuria_ultrasonography_MeSH S_urine_MeSH Albuminuria_urine_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Creatinine_MeSH S_urine_MeSH Creatinine_urine_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH S_urine_MeSH Hypertrophy__Left_Ventricular_urine_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 12151907
----K E
----T Weight and blood pressure change during clozapine treatment.
----A We examined whether clozapine-related weight gain is associated with an increase in mean arterial blood pressure. Weight gain and mean arterial blood pressure changes were assessed in 61 outpatients with schizophrenia who were randomly assigned to either clozapine or haloperidol in a 10-week parallel group, double-blind study and in 55 patients who chose to continue to receive clozapine in a subsequent 1-year open-label prospective study. Clozapine treatment was associated with significant weight gain in the double blind and open-label trials. Haloperidol treatment was not associated with significant weight gain. Neither clozapine nor haloperidol treatment were associated with significant changes in mean arterial blood pressure. There were no significant correlations between weight gain and mean arterial blood pressure change with either medication. Although clozapine treatment is associated with weight gain, the correlation between this weight gain and increases in arterial blood pressure during the first year of treatment appears to be low.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antipsychotic_Agents_MeSH S_pharmacology_MeSH Antipsychotic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antipsychotic_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH S_physiology_MeSH Body_Weight_physiology_MeSH M_Clozapine_MeSH S_pharmacology_MeSH Clozapine_pharmacology_MeSH S_therapeutic_use_MeSH Clozapine_therapeutic_use_MeSH M_Confidence_Intervals_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Haloperidol_MeSH S_pharmacology_MeSH Haloperidol_pharmacology_MeSH S_therapeutic_use_MeSH Haloperidol_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Schizophrenia_MeSH S_drug_therapy_MeSH Schizophrenia_drug_therapy_MeSH S_physiopathology_MeSH Schizophrenia_physiopathology_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12152252
----K 1
----T [The effect of aspirin on rheological properties of erythrocytes in essential hypertension]
----A Essential hypertension is one of the most important risk factors for cardiovascular diseases. Its pathophysiological mechanism is unknown. Recent data suggests that deformability and aggregation of red blood cells may play an important role in the regulation of blood rheology in hypertension. Simultaneously there are reports suggesting that antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) could be counteracted by high doses of aspirin. We postulate that these effects could be related to the changes in blood rheology. Accordingly we designed a study to evaluate the effect of low or high dose of aspirin on deformability and aggregability of red blood cells from patients with essential hypertension. Deformability and aggregability of red blood cells were measured by laser diffractometer (Rheodyn SSD, Myrenne GmbH) and computerized automatic aggregometer (MA1 Myrenne GmbH, Germany), respectively. The effects of aspirin on deformability and aggregation of red blood cells were studied ex vivo in whole blood from three groups of patients with essential hypertension (group I: 10 patients receiving placebo, group II: 23 patients receiving 75 mg/day p.o. aspirin for 3 days, and group III: 23 patients receiving 300 mg/day p.o. aspirin for 3 days). Subjects in all groups received the same combination of antihypertensive agents consisting of: one of ACEI (enalapril or perindopril), one of beta-antagonists (metoprolol or bisoprolol), and diuretic agent (indapamid). In patients receiving high dose of aspirin (300 mg/day) we observed that erythrocyte aggregability was 25% higher than in the placebo group (MEA = 25.8 +/- 6 SD, vs MEA = 20.6 +/- 3 SD, p < 0.05). Aspirin had no effects on deformability of erythrocytes or on arterial blood pressure. High doses of aspirin or possibly also other nonsteroidal anti-inflammatory drugs (NSAID) in patients receiving antihypertensive therapy can directly affect rheological properties of the blood due to the activation of red blood cell aggregation. Increased aggregation of red blood cells during antihypertensive therapy may be an important indicator of the worsening of organ perfusion.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_administration_&_dosage_MeSH Anti-Inflammatory_Agents__Non-Steroidal_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_English_Abstract_MeSH M_Erythrocyte_Aggregation_MeSH S_drug_effects_MeSH Erythrocyte_Aggregation_drug_effects_MeSH M_Erythrocyte_Deformability_MeSH S_drug_effects_MeSH Erythrocyte_Deformability_drug_effects_MeSH M_Female_MeSH M_Hemorheology_MeSH S_drug_effects_MeSH Hemorheology_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 12167382
----K I
----T Carvedilol does not alter the insulin sensitivity in patients with congestive heart failure.
----A BACKGROUND: Congestive heart failure (CHF) has previously been shown to be associated with insulin resistance and hyperinsulinemia. A beneficial effect of the non-selective beta-blocker carvedilol has been demonstrated in patients with CHF. However, whether the drug affects the insulin sensitivity (S(i)) is unknown. AIMS: To investigate whether treatment with carvedilol alters the S(i) in patients with CHF during a prospective, double-blinded, placebo-controlled study. METHODS AND RESULTS: The patients were randomized to receive either carvedilol (n=29) or matched placebo (n=17). Insulin and glucose responses were measured during a 0.3 g/kg intravenous glucose tolerance test, and S(i) was calculated according to Bergman's Minimal Model. Baseline S(i) values correlated significantly with body mass index (r=-0.42, P=0.002), plasma urate (r=-0.42, P=0.002), plasma HDL-cholesterol (r=0.39, P=0.003), maximal oxygen uptake (r=0.35, P=0.009), plasma triglycerides (r=-0.34, P=0.01) and weight (r=-0.29, P=0.03). During the study the insulin sensitivity was unchanged in the carvedilol group compared with placebo (2.63+/-1.45 to 2.38+/-1.64 vs. 2.81+/-2.36 to 2.48+/-1.84x10(-4) min(-1)/mUl(-1), P=0.83). CONCLUSION: Additional treatment with carvedilol is neutral with regard to influence the insulin sensitivity in patients with mild to moderate CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Insulin_Resistance_MeSH S_physiology_MeSH Insulin_Resistance_physiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12167389
----K 5
----T Is beta-blockade useful in heart failure patients with atrial fibrillation? An analysis of data from two previously completed prospective trials.
----A BACKGROUND: Beta-adrenergic blockade is of proven value in chronic heart failure. It is uncertain, however, if beta-blockade provides a similar degree of clinical benefit for heart failure patients with atrial fibrillation (AF) as those in sinus rhythm (SR). AIMS: To compare the effectiveness of beta blockade in patients with heart failure and AF. METHODS: Patients with chronic heart failure were randomized to treatment (double blind) with metoprolol 50 mg twice daily or carvedilol 25 mg twice daily in addition to standard therapy. Response was assessed after 12 weeks by a quality of life questionnaire, New York Heart Association class, exercise capacity (6-min walk test), radionucleotide ventriculography for LVEF, 2-D echocardiography measurement of left ventricular (LV) dimensions and diastolic filling and 24-h electrocardiograph monitoring to assess heart rate changes. RESULTS: Both beta-blockers produced significant improvements in LVEF in both the SR group: (+6+/-10% at 12-week, P<0.001) and the AF group: (+11+/-9% at 12-week, P<0.05). However, significant improvement in symptoms (P<0.001) and exercise capacity (P<0.001) were observed only in the SR group but not in the AF group despite a significant improvement in LVEF. CONCLUSION: Beta-blockers were effective in improving LV ejection fraction in chronic heart failure patients in either SR or AF but had less effect on symptoms and exercise capacity in those with AF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comorbidity_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 12167390
----K E
----T The incomplete bucindolol evaluation in acute myocardial infarction Trial (BEAT).
----A The aim of this study was to evaluate the efficacy of adding the beta-blocker bucindolol to standard therapy shortly after a myocardial infarction in a high-risk population with reduced left ventricular function. METHODS: The study was planned to include 2000 patients with an enzyme confirmed myocardial infarction and severely reduced left ventricular function determined by echocardiography (corresponding to ejection fraction < or =0.35). The primary endpoint was all cause mortality and the secondary endpoints were time to first event of death, progression of heart failure or reinfarction-and the components. The study was closed early due to discontinuation of development of bucindolol by the manufacturer. Therefore, 170 patients were randomised to receive bucindolol and 173 to receive placebo. RESULTS: There were 27 deaths in the bucindolol group and 30 in the placebo group, hazard ratio of bucindolol 0.88 (95% confidence limits 0.5-1.5; P=0.6). There were 9/4 (bucindolol/placebo, P=0.16) heart failure events and 5/17 (P=0.01) reinfarctions in the bucindolol/placebo groups. CONCLUSION: Due to early closure it is unknown whether bucindolol changes mortality in high-risk post myocardial infarct patients when added to best medical therapy. The frequency of reinfarction was significantly reduced.
----P Clinical_Trial Evaluation_Studies Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Survival_Rate_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 12167391
----K 5
----T The effect of carvedilol in patients with impaired left ventricular systolic function following an acute myocardial infarction. How do the treatment effects on total mortality and recurrent myocardial infarction in CAPRICORN compare with previous beta-blocker trials?
----A In previous beta-blocker trials, post-myocardial infarction (MI) patients were essentially treated with a beta-blocker or placebo. In the CAPRICORN trial, patients were selected on the basis of a left ventricular (LV) ejection fraction (EF) <40% following the index MI and randomised to carvedilol or placebo, in addition to modern secondary prophylaxis with ACE inhibitors, aspirin and statins. In 1959 patients with a mean LVEF of 33%, treatment with carvedilol over a mean follow-up period of 15 months reduced total mortality from 15.3% with placebo to 11.9% with carvedilol [relative risk reduction (RRR) =23%, absolute risk reduction (ARR) =3.4%]. The incidence of recurrent MI was reduced from 5.8 to 2.3% (RRR 41%, ARR 2.3%). The number needed to treat (NNT) to prevent one death was 28 for the entire study period and 43 for 1 year of treatment. The results of the CAPRICORN trial are compared with three previous beta-blocker post-MI trials: the Gothenburg metoprolol trial (GMT), the Norwegian timolol trial (NTT) and the beta-blocker heart attack trial (BHAT). The RRRs for total mortality were 36% in the GMT and NTT, and 27% in BHAT. The respective NNTs for total mortality were 32, 18 and 38. NNT for 1 year of treatment was 25 in NTT and 80 in BHAT. The RRR for recurrent MIs were 28% in NTT and 16% in BHAT. The reduction of mortality and recurrent MIs in CAPRICORN is within the range of previous post-MI beta-blocker studies. In post-MI patients with LVEF<40%, add-on treatment with a beta-blocker should be given >48 h after initiation with an angiotensin-converting enzyme inhibitor (ACEI) and then with a slow dose escalation as applied in CAPRICORN.
----P Clinical_Trial Evaluation_Studies Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH S_physiology_MeSH Myocardial_Contraction_physiology_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Recurrence_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Survival_Rate_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH S_physiology_MeSH Systole_physiology_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12169866
----K E
----T Labetalol-induced hyperkalemia in renal transplant recipients.
----A BACKGROUND: Labetalol is a commonly used agent for perioperative hypertension in renal transplant recipients. A previous report suggested that labetalol may cause life-threatening hyperkalemia after renal transplantation. METHODS: We performed a retrospective review of 103 consecutive renal transplants to determine whether labetalol was an independent predictor of hyperkalemia treatment. Thirty-eight patients (36.9%) received labetalol, and 65 patients (63.1%) had no labetalol medication. RESULTS: Of the 103 patients, 24 (23.3%) required treatment for hyperkalemia. Thirteen (34.2%) of the patients who had labetolol medication and 11 (16.9%) of the patients who did not receive labetalol were treated for hyperkalemia (p = 0.045). Factors considered for a logistic regression model included: the use of labetalol, cold ischemia time, diabetes, and dialysis method; intake of tacrolimus, beta blockers, angiotensin-converting enzyme inhibitors, or other antihypertensives prior to admission; the mannitol dose given intraoperatively, and the 24-hour urine output postoperatively. Intravenous labetalol (odds ratio OR = 4.52, confidence interval CI = 1.33-15.28; p = 0.02), 24- hour urine output (OR = 4.4, CI = 0.97-20.1: p = 0.47), increasing cold ischemia time (OR = 1.09, CI = 1.01-1.17; p = 0.02), and continuous ambulatory peritoneal dialysis (OR = 0.17, CI = 0.29-0.98; p = 0.036) were independent predictors. CONCLUSION: Labetalol appears to increase the risk of hyperkalemia in patients after renal transplantation.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Chi-Square_Distribution_MeSH M_Female_MeSH M_Human_MeSH M_Hyperkalemia_MeSH S_chemically_induced_MeSH Hyperkalemia_chemically_induced_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Kidney_Transplantation_MeSH M_Labetalol_MeSH S_adverse_effects_MeSH Labetalol_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Perioperative_Care_MeSH M_Postoperative_Complications_MeSH S_chemically_induced_MeSH Postoperative_Complications_chemically_induced_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH M_Retrospective_Studies_MeSH M_Risk_MeSH 
****** 12172356
----K E
----T Pharmacologic efficacy in gastric variceal rebleeding and survival: including multivariate analysis.
----A BACKGROUND: Therapy with beta-blocker and nitrate has been reported to improve survival of patients with bleeding esophageal varices and to decrease esophageal rebleeding. However, there is little information available concerning the efficacy of these medications on rebleeding risk and survival in gastric variceal bleeding after initial hemostasis. METHODS: We conducted an open trial to observe the roles of beta-blocker and nitrate in the long-term outcome of bleeding gastric varices. Eighty-three patients were included and evaluated on the basis of age, gender, gastric variceal size, associated esophageal variceal size, Child-Pugh classification, existence of hepatoma and portal vein thrombosis, beta-blocker or nitrate therapy, and follow-up histoacryl injection. Survival analysis and multivariate analysis with the Cox proportional hazards model were performed to evaluate independent risk factors. RESULTS: Larger gastric varices have been shown to be the only risk factor for rebleeding (adjusted odds ratio, 4.50; 95% CI, 1.30-15.59). beta-Blocker and nitrate did not significantly reduce the incidence of rebleeding (adjusted odds ratio, 0.37; 95% CI, 0.08-1.66). Although medical treatment was shown to improve the overall survival by Kaplan-Meier method (p < 0.01), multivariate analysis showed Child-Pugh class B or C and advanced hepatoma with portal vein thrombosis to be the real independent risk factors that influence survival (Child-Pugh class B or C odds ratio, 2.72; 95% CI, 1.53-4.84; portal vein thrombosis odds ratio, 6.99; 95% CI, 2.42-20.16). beta-Blocker and nitrate did not significantly prolong survival independently. CONCLUSIONS: beta-Blocker and nitrate did not decrease the risk of rebleeding and did not improve the overall survival independently. The poor prognosis was correlated with Child-Pugh class B or C, and the advance hepatoma, with portal vein thrombosis.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Carcinoma__Hepatocellular_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_classification_MeSH Esophageal_and_Gastric_Varices_classification_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_classification_MeSH Gastrointestinal_Hemorrhage_classification_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH M_Liver_Neoplasms_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Portal_Vein_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Venous_Thrombosis_MeSH 
****** 12175444
----K E
----T Anti-hypertensive drugs in pregnancy and fetal growth: evidence for "pharmacological programming" in the first trimester?
----A OBJECTIVES: To determine the timing and exact nature of the effect of the drug atenolol upon fetal growth. Also to discover if the reduction in fetal growth is due to superimposed pre-eclampsia or any other confounding variable. DESIGN: A retrospective cohort study of prospectively collected data in a hypertensive pregnancy database. SETTING: Two district general hospitals in the midlands of England. Both hospitals have specialised medical antenatal clinics for pregnant women with chronic hypertension. PARTICIPANTS: 491 pregnancies in 380 women with essential or secondary hypertension. OUTCOME MEASURES: The outcome measures used were the infant birth weight, birth weight standardized for gestational age, and the ponderal index at birth, a surrogate measure for in utero growth restriction. RESULTS: The babies of women taking atenolol at conception or during the first trimester had significantly lower birth weights (by 139-512 g, p<0.01) than women on calcium channel blockers or no medication. Likewise the ponderal index was also significantly reduced, p<0.01. In addition most of these babies were small for gestational age (SGA) with 70% on or below the 10th centile and 40% below the third centile. No such independent association was seen with anti-hypertensives taken in the second trimester. CONCLUSIONS: Atenolol taken at the time of conception and/or during the first trimester of pregnancy was associated with low birth weight. This finding was independent of the development of superimposed pre-eclampsia. Other anti-hypertensives were not found to be associated with low birth weight. Use of atenolol in the second trimester of pregnancy did not produce the same effect and was not materially different in its effects from the other anti-hypertensive drugs. In the second trimester, the development of superimposed pre-eclampsia is the over-riding effect in the reduction of infant birth weight. Atenolol used in the first trimester could be pharmacologically programming these infants to restricted growth patterns.
----P Journal_Article Multicenter_Study 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Embryo_and_Fetal_Development_MeSH S_drug_effects_MeSH Embryo_and_Fetal_Development_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant__Newborn_MeSH M_Infant__Small_for_Gestational_Age_MeSH M_Multivariate_Analysis_MeSH M_Pre-Eclampsia_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Pregnancy_Outcome_MeSH M_Pregnancy_Trimester__First_MeSH M_Retrospective_Studies_MeSH 
****** 12195325
----K E
----T Endoscopic variceal ligation plus propranolol vs. transjugular intrahepatic portosystemic stent shunt: a long-term randomized trial.
----A BACKGROUND AND STUDY AIMS: After a first variceal bleeding episode in patients with cirrhosis of the liver, treatment with transjugular intrahepatic portosystemic stent shunt (TIPS) and endoscopic variceal ligation (EVL) plus propranolol were compared, with regard to prevention of variceal rebleeding, complications, and mortality. PATIENTS AND METHODS: 85 patients were randomly allocated to receive TIPS (n = 43) or EVL (n = 42). The groups were comparable regarding age, sex, etiology of liver cirrhosis, and liver function. RESULTS: The mean observation times were 4.1 years in the TIPS group and 3.6 years in the EVL group. Although the probability of rebleeding was higher in the EVL group (29.9%) than in the TIPS group (19.4%), the difference was not statistically significant. Three of five patients of the EVL group successfully underwent TIPS placement after treatment failure. The probability of TIPS dysfunction requiring shunt revision was 89 %. Hepatic encephalopathy was observed more often in the TIPS group (40.5%) than in the EVL group (20.5%; P < 0.05). The probability of survival was similar in both groups (TIPS group 75.9%, EVL group 82.2%; n.s.). CONCLUSIONS: In view of its good efficacy and the lower cost of treatment, endoscopic ligation plus propranolol may be recommended as initial procedure for prevention of recurrent variceal hemorrhage, whereas TIPS seems to be the preferable procedure in patients with recurrent bleeding after adequate endoscopic and pharmacological treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Female_MeSH M_Hepatic_Encephalopathy_MeSH S_epidemiology_MeSH Hepatic_Encephalopathy_epidemiology_MeSH S_etiology_MeSH Hepatic_Encephalopathy_etiology_MeSH M_Human_MeSH M_Ligation_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH S_adverse_effects_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_adverse_effects_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12198699
----K E
----T Banding ligation versus nadolol and isosorbide mononitrate for the prevention of esophageal variceal rebleeding.
----A BACKGROUND & AIMS: beta-blockers and banding ligation are effective in the prevention of variceal rebleeding. However, the relative efficacy and safety remains unresolved. METHODS: One hundred twenty-one patients with a history of esophageal variceal bleeding were enrolled. Patients were randomized to undergo regular endoscopic variceal ligation (EVL group, 60 patients) until variceal obliteration, or drug therapy by using nadolol plus isosorbide mononitrate (N+I group, 61 patients) during the study period to prevent rebleeding. RESULTS: After a median follow-up period of 25 months, recurrent upper gastrointestinal bleeding developed in 23 patients in the EVL group and 35 patients in the N+I group (P = 0.10). Recurrent bleeding from esophageal varices occurred in 12 patients (20%) in the EVL group and 26 patients (42%) in the N+I group (relative risk = 0.45; 95% confidence interval, 0.24-0.85). The actuarial probability of rebleeding from esophageal varices was lower in the EVL group (P = 0.01). The multivariate Cox analysis indicated that the treatment was the only factor predictive of rebleeding. Treatment failure occurred in 8 patients (13%) in the EVL group and 17 patients (28%) in the N+I group (P = 0.01). Fifteen patients in the EVL group and 8 patients of the N+I group died (P = 0.06). Complications occurred in 17% of the EVL group and in 19% of the N+I group (P = 0.6). CONCLUSIONS: Our trial showed that ligation was more effective than nadolol plus isosorbide-5-mononitrate in the prevention of variceal rebleeding, with similar complications in both treatment modalities. However, there is no significant difference in the survival rate between the 2 groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Ligation_MeSH S_adverse_effects_MeSH Ligation_adverse_effects_MeSH S_methods_MeSH Ligation_methods_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_adverse_effects_MeSH Nadolol_adverse_effects_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Failure_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12198700
----K E
----T Primary prophylaxis of variceal hemorrhage: a randomized controlled trial comparing band ligation, propranolol, and isosorbide mononitrate.
----A BACKGROUND & AIMS: This randomized controlled trial compared variceal band ligation (VBL), propranolol (PPL), and isosorbide-5-mononitrate (ISMN) in the prevention of first esophageal variceal bleed. METHODS: Over a 6-year period, 172 patients with cirrhosis, grade II or III esophageal varices that had never bled, were recruited; 44 into VBL, 66 into PPL, and 62 into ISMN. Baseline patient characteristics: age, 55 +/- 11 years; Child-Pugh score, 8 +/- 2; 65% alcohol-induced cirrhosis; follow-up period, 19.7 +/- 17.6 months (range, 0.13-72.1 months), were comparable in the 3 groups. RESULTS: On intention-to-treat analysis, variceal bleeding occurred in 7% of patients randomized to VBL, 14% to PPL, and 23% to ISMN. The 2-year actuarial risks for first variceal bleed were 6.2% (95% confidence interval [CI], 0.0%-15.0%) for VBL, 19.4% (95% CI, 0.1%-32.4%) for PPL, and 27.7% (95% CI, 14.2%-41.2%) for ISMN. A significant number of patients reported side effects with drug treatment (45% PPL and 42% ISMN vs. 2% VBL; P = 0.00), resulting in withdrawal from treatment in 30% of PPL and 21% of ISMN patients. There were no statistically significant differences in mortality rates in the 3 groups. In as-treated analysis, there was a statistically significant difference in actuarial risk for bleeding at 2 years between VBL and ISMN (7.5%, 95% CI, 2.5%-10.6% vs. 33.0%, 95% CI, 15%-49%, respectively, log rank test P = 0.03) but not between VBL and PPL. CONCLUSIONS: VBL was equivalent to PPL and superior to ISMN in preventing first variceal bleed. The side-effect profile for pharmacotherapy was considerable.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Ligation_MeSH S_adverse_effects_MeSH Ligation_adverse_effects_MeSH S_methods_MeSH Ligation_methods_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12201792
----K 4
----T Cost effectiveness of implantable cardioverter defibrillator therapy versus drug therapy for patients at high risk of sudden cardiac death.
----A The implantable cardioverter defibrillator (ICD) is a therapy for patients at risk of sudden cardiac death due to ventricular tachycardia (VT) or ventricular fibrillation (VF). But the apparent high cost of ICD therapy relative to antiarrhythmic drugs such as amiodarone has raised questions about the cost effectiveness of ICD therapy versus drug therapy. To inform this debate we reviewed the literature on ICD cost effectiveness. An electronic and manual search was conducted for articles published since 1980 reporting original data on the cost effectiveness of ICD versus drug therapy for patients at risk of VT/VF. Data on costs and life-years gained were abstracted and studies were grouped into those that used decision-analysis models and those that were trial-based analyses. Cost-effectiveness ratios were inflated to 2001 US dollars. Nine studies were included in the review; five studies were modelling studies and four were part of randomised trials of ICD therapy. Studies varied in time horizon, but all except one indicated that ICD therapy was more costly than drug therapy. Early decision models assumed larger survival benefits than those observed in subsequent trials and therefore had attractive incremental cost-effectiveness ratios in the range of dollars US 27000 to dollars US 60000 per life-year gained. Trial-based studies, with the exception of one small trial, indicated cost per life-year gained in the range dollars US 44000 to dollars US 144000. Stratified analysis shows clearly that patients with a greater risk of mortality due to structural heart disease (e.g. left ventricular ejection fraction < or =35%) benefit more from ICD therapy and therefore have a more attractive cost effectiveness ratio than patients at lower risk. ICD therapy is still evolving over time with implant costs declining and device technology improving. Current evidence is that, in selected patients who are at high risk of VT/VF, ICD therapy can be a cost-effective option. Future research should focus on (i) patient selection to optimise benefits for available resources; and (ii) more comprehensive outcome measures to include health-related quality of life.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_economics_MeSH Anti-Arrhythmia_Agents_economics_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Cost-Benefit_Analysis_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH S_economics_MeSH Defibrillators__Implantable_economics_MeSH M_Drug_Therapy_MeSH S_economics_MeSH Drug_Therapy_economics_MeSH M_Human_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12204014
----K E
----T Relationship of antihypertensive treatment regimens and change in blood pressure to risk for heart failure in hypertensive patients randomly assigned to doxazosin or chlorthalidone: further analyses from the Antihypertensive and Lipid-Lowering treatment to prevent Heart Attack Trial.
----A BACKGROUND: The Antihypertensive and Lipid-Lowering treatment to prevent Heart Attack Trial reported that treatment initiated with doxazosin compared with chlorthalidone doubled the risk for heart failure in high-risk hypertensive patients (relative risk, 2.04 [95% CI, 1.79 to 2.32]). Patients assigned to doxazosin therapy had a mean in-trial systolic/diastolic blood pressure 3/0 mm Hg higher than that in patients assigned to chlorthalidone. Sixty-eight percent (6167 of 9061) of the former patients and 59% (9081 of 15 256) of the latter patients were given additional medications to achieve a target blood pressure of less than 140/90 mm Hg. OBJECTIVE: To ascertain the influence of open-label antihypertensive drugs and subsequent blood pressure on relative risk for heart failure. DESIGN: Randomized, double-blind, active-controlled clinical trial. SETTING: 623 sites in the United States and Canada. PATIENTS: Hypertensive patients 55 years of age or older with at least one additional risk factor for cardiovascular disease. INTERVENTION: Chlorthalidone (12.5 to 25 mg/d) or doxazosin (2 to 8 mg/d) for a planned follow-up of 4 to 8 years. MEASUREMENTS: Data on blood pressure, medication, and incident heart failure (treated outside hospital, hospitalized, or fatal) from February 1994 through December 1999. RESULTS: After the treatment groups were categorized as having no exposure to open-label medications (monotherapy) or exposure to open-label therapy, the relative risk for heart failure with doxazosin versus chlorthalidone was 3.10 (CI, 2.51 to 3.82) and 1.42 (CI, 1.20 to 1.69), respectively. After adjustment for follow-up systolic/diastolic blood pressure, the overall relative risk was 2.00 (CI, 1.72 to 2.32). CONCLUSION: In high-risk patients with hypertension, the higher risk for heart failure while taking doxazosin compared with chlorthalidone is attenuated but not eliminated by adding other antihypertensive drugs. The small observed difference in systolic blood pressure does not explain this increased risk.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output__Low_MeSH S_etiology_MeSH Cardiac_Output__Low_etiology_MeSH S_prevention_&_control_MeSH Cardiac_Output__Low_prevention_&_control_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_administration_&_dosage_MeSH Doxazosin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 12204730
----K I
----T The effect of preoperative digitalis and atenolol combination on postoperative atrial fibrillation incidence.
----A PURPOSE: The most frequent arrhythmia after coronary artery bypass surgery is atrial fibrillation (AF). The prevention and treatment of this type of arrhythmia is subobtimal. Digitalis, beta-blockers, diltiazem and amiodarone are the preferred drugs for the treatment. This study was designed to compare the effects of preoperatively started digitalis and atenolol in combination and separately, on the incidence of AF that occurs within 7 days following the operation. MATERIALS AND METHOD: One-hundred and sixty patients who had similar demographic properties were randomly grouped as group I, that preoperatively received combined drug therapy (n=40), group II preoperatively used digitalis (n=40), group III atenolol (n=40), and group IV was the control group (n=40). RESULTS: Postoperative AF incidence was 25, 15,4, and 17,9% in groups IV, III, and II, respectively, whereas it was 5% in group I which was lower than all other groups, but the difference was only significant between groups I and IV (P=0.012). CONCLUSION: The combined use of atenolol and digitalis preoperatively was considered as an efficient treatment for lowering the incidence of AF following coronary artery bypass surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Premedication_MeSH 
****** 12204496
----K E
----T Mortality benefit of beta-blockade after successful elective percutaneous coronary intervention.
----A OBJECTIVES: The goal of this study was to evaluate the mortality benefit of beta-blockers after successful percutaneous coronary intervention (PCI). BACKGROUND: Beta-blockers reduce mortality after myocardial infarction (MI), though limited data are available regarding their role after successful PCI. METHODS: Each year from 1993 through 1999, the first 1,000 consecutive patients undergoing PCI were systematically followed up. Patients presenting with acute or recent MI, shock, or unsuccessful revascularization procedures were excluded from the analysis. Clinical, procedural, and follow-up data of beta-blocker-treated and non-beta-blocker-treated patients were compared. A multivariate survival analysis model using propensity analysis was used to adjust for heterogeneity between the two groups. RESULTS: Of the 4,553 patients, 2,056 (45%) were treated with beta-blockers at the time of the procedure. Beta-blocker therapy was associated with a mortality reduction from 1.3% to 0.8% at 30 days (p = 0.13) and a reduction from 6.0% to 3.9% at one year (p = 0.0014). This survival benefit of beta-blockers was independent of left ventricular function, diabetic status, history of hypertension, or history of MI. Using propensity analysis, beta-blocker therapy remained an independent predictor for one-year survival after PCI (hazard ratio, 0.63; 95% confidence interval, 0.46 to 0.87; p = 0.0054). CONCLUSIONS: Within this large prospective registry, beta-blocker use was associated with a marked long-term survival benefit among patients undergoing successful elective percutaneous coronary revascularization.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Prospective_Studies_MeSH M_Surgical_Procedures__Elective_MeSH M_Survival_Analysis_MeSH 
****** 12204500
----K E
----T Augmentation of myocardial blood flow in hypertensive heart disease by angiotensin antagonists: a comparison of lisinopril and losartan.
----A OBJECTIVES: The goal of this study was to compare myocardial perfusion reserve (MPR) before and after long-term treatment with lisinopril and losartan in patients with hypertension and left ventricular hypertrophy (LVH). BACKGROUND: Studies have suggested that treatment with angiotensin-converting enzyme inhibitors (ACEIs) improves MPR in patients with hypertension by potentiating endogenous bradykinins. Because angiotensin receptor blockers (ARBs) lack a direct effect on bradykinins, we hypothesized that they may not improve MPR. METHODS: We measured pre- and post-treatment myocardial blood flow (MBF) by positron emission tomography in 17 patients (lisinopril: 9 patients, losartan: 8 patients) with hypertension and LVH at baseline and after coronary vasodilation with intravenous dipyridamole. In addition, we measured rest and hyperemic blood flow in eight normotensive controls. RESULTS: Post-treatment maximal coronary blood flow and MPR in the lisinopril group increased significantly compared with pretreatment values (3.5 +/- 1.2 vs. 2.6 +/- 1.1 ml/min/g, p = 0.02; 3.7 +/- 1.1 vs. 2.4 +/- 1 ml/min/g, respectively, p = 0.002, respectively). Post-treatment hyperemic flow in the patients treated with lisinopril was not significantly different from corresponding measurements in controls (3.5 +/- 1.2 vs. 3.9 +/- 1 ml/min/g, respectively, p = NS). In the patients treated with losartan, there was no difference between pre- and post-treatment MBF values and MPR. CONCLUSIONS: Myocardial perfusion reserve and maximal coronary flow improved in asymptomatic patients with hypertension-induced LVH after long-term treatment with lisinopril but not with losartan. Thus, ACEIs, but not ARBs, might be effective in repairing the coronary microangiopathy associated with hypertension-induced LVH.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Ventricles_radionuclide_imaging_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Lisinopril_MeSH S_pharmacology_MeSH Lisinopril_pharmacology_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Tomography__Emission-Computed_MeSH 
****** 12204508
----K E
----T Acute effects of vasoactive drug treatment on brachial artery reactivity.
----A OBJECTIVES: The goal of this study was to investigate whether concomitant therapy with vasoactive medications alters the results of noninvasive assessment of endothelial function. BACKGROUND: Ultrasound assessment of brachial artery flow-mediated dilation is emerging as a useful clinical tool. The current practice of withholding cardiac medications before ultrasound studies has unknown utility and would limit the clinical use of the methodology. METHODS: To determine whether a single dose of a vasoactive drug influences brachial reactivity, we examined flow-mediated dilation and nitroglycerin-mediated dilation in 73 healthy subjects (age 27 +/- 6 years). Studies were completed at baseline and 3 h after randomized treatment with a single oral dose of placebo, felodipine (5 mg), metoprolol (50 mg), or enalapril (10 mg). To determine if holding vasoactive therapy for 24 h before study yields different results than continuation of clinically prescribed medications, we examined vascular function in 72 patients (age 57 +/- 10 years) with coronary artery disease. Ultrasound studies were performed 24 h after the last dose and again 3 h after patients took their clinically prescribed medications. RESULTS: In healthy subjects one dose of all three drugs lowered blood pressure, and metoprolol also lowered heart rate. However, there was no significant effect of treatment on brachial artery dilation. In patients with coronary artery disease on chronic treatment, taking prescribed medications reduced blood pressure and heart rate, but had no significant effect on brachial artery dilation. CONCLUSIONS: Recent administration of commonly used nonnitrate vasoactive drugs has no significant effect on brachial reactivity. These findings suggest that current practice of withholding cardiac medications before testing endothelial function may not be necessary, making this methodology more practical for clinical use.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Brachial_Artery_MeSH S_drug_effects_MeSH Brachial_Artery_drug_effects_MeSH S_physiology_MeSH Brachial_Artery_physiology_MeSH M_Cardiovascular_Agents_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiology_MeSH Endothelium__Vascular_physiology_MeSH M_Felodipine_MeSH S_pharmacology_MeSH Felodipine_pharmacology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Models__Cardiovascular_MeSH M_Reference_Values_MeSH M_Reproducibility_of_Results_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 12208417
----K E
----T Status of glucose metabolism in patients with heart failure secondary to coronary artery disease.
----A 
----P Evaluation_Studies Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Comparative_Study_MeSH M_Coronary_Arteriosclerosis_MeSH S_complications_MeSH Coronary_Arteriosclerosis_complications_MeSH S_mortality_MeSH Coronary_Arteriosclerosis_mortality_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_mortality_MeSH Diabetes_Mellitus__Type_II_mortality_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glucose_MeSH S_metabolism_MeSH Glucose_metabolism_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Predictive_Value_of_Tests_MeSH M_Prevalence_MeSH M_Survival_Analysis_MeSH M_Time_Factors_MeSH 
****** 12209278
----K E
----T Short-term treatment of severe hypertension of pregnancy: prospective comparison of nicardipine and labetalol.
----A OBJECTIVES: To assess the efficacy and safety of nicardipine in comparison to labetalol in the initial management of severe hypertension in pregnancy. DESIGN. Randomized prospective study. SETTING: The obstetric ward of the teaching hospital of Monastir Tunisia. PATIENTS: Sixty consecutive pregnant women admitted beyond the 24th week of pregnancy with severe hypertension. INTERVENTION: Patients were randomly assigned to receive intravenously for 1 h either labetalol ( n=30) or nicardipine ( n=30). Treatment was titrated to achieve a 20% lowering of blood pressure (BP). MEASUREMENTS: Maternal BP and heart rate were measured at inclusion and repeatedly during the first hour following the drugs administration. Fetal heart rate was recorded throughout the study period. The main outcome endpoints were the success rate and the length of time needed to achieve the therapeutic goal. The rate of maternal and fetal adverse events and dose adjustments were also analyzed. RESULTS: Labetalol and nicardipine achieved the 20% lowering in BP in the same proportion (63% and 70% success rates, respectively). Overall nicardipine caused a significantly greater decrease in systolic and diastolic BP. No patient had any episode of hypotension. The length of time to achieve the BP goal was also similar (12 vs. 11 min, respectively). Both drugs were well tolerated except for a moderate tachycardia observed with the use of nicardipine. CONCLUSION: Nicardipine and labetalol are effective and safe in the initial treatment of severe hypertension of pregnancy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Labetalol_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Nicardipine_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Pre-Eclampsia_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Tunisia_MeSH 
****** 12225716
----K E
----T Medical treatment of myocardial ischemia in coronary artery disease: effect of drug regime and irregular dosing in the CAPE II trial.
----A OBJECTIVES: The Circadian Anti-ischemia Program in Europe (CAPE II) compared the efficacy of amlodipine and diltiazem (Adizem XL) and the combination of amlodipine/atenolol and diltiazem (Adizem XL)/isosorbide 5-mononitrate on exercise and ambulatory myocardial ischemia during regular therapy and after omission of medication. BACKGROUND: The optimal medical therapy for ischemia suppression and the impact of irregular dosing using agents with different pharmacologic properties has not been established in patients with coronary disease. METHODS: Patients with > or = 4 ischemic episodes or > or = 20 min of ST segment depression on 72-h electrocardiogram were randomized to amlodipine 10 mg once daily or diltiazem (Adizem XL) 300 mg once daily in a 14-week double-blind randomized multicountry study. In the second phase, atenolol 100 mg was added to amlodipine and isosorbide 5-mononitrate 100 mg to diltiazem (Adizem XL). Ambulatory monitoring (72 h) and exercise testing were repeated after both phases, on treatment and after a 24-h drug-free interval. RESULTS: Both monotherapy with amlodipine and diltiazem (Adizem XL) were effective on symptoms and ambulatory and exercise ischemia. Combination therapy reduced ischemia further, with amlodipine/atenolol superior to diltiazem (Adizem XL)/isosorbide 5-mononitrate. Amlodipine/atenolol was significantly superior during the drug-free interval with maintenance of ischemia reduction. CONCLUSIONS: Amlodipine, with its intrinsically long half-life alone or together with beta-blocker, is likely to produce superior ischemia reduction in clinical practice when patients frequently forget to take medication or dose irregularly.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_MeSH S_administration_&_dosage_MeSH Isosorbide_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12225725
----K E
----T Valsartan benefits left ventricular structure and function in heart failure: Val-HeFT echocardiographic study.
----A OBJECTIVES: The objective of the study was to evaluate the effect of an angiotensin receptor blocker on left ventricular (LV) structure and function when added to prescribed heart failure therapy. BACKGROUND: The clinical benefit derived from heart failure therapy is attributed to the regression of LV remodeling. METHODS: At 302 multinational sites, 5,010 patients in New York Heart Association (NYHA) classification II to IV heart failure taking angiotensin-converting enzyme inhibitor (ACEI) and/or beta-blocker (BB) were randomized into valsartan and placebo groups and followed for a mean of 22.4 months. Serial echocardiographic measurements of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were recorded. Total study reproducibility calculated to 90% power at 5% significance defined detectable differences of 0.09 cm for LVIDd and 0.86% for EF. RESULTS: Baseline LVIDd and EF for valsartan and placebo groups were similar: 3.6 +/- 0.5 versus 3.7 +/- 0.5 (cm/m(2)) and 26.6 +/- 7.3 versus 26.9 +/- 7.0 (%). Mean group changes from baseline over time were compared. Significant decrease in LVIDd and increase in EF began by four months, reached plateau by one year, and persisted to two years in valsartan compared with placebo patients, irrespective of age, gender, race, etiology, NYHA classification, and co-treatment therapy. Changes at 18 months were -0.12 +/- 0.4 versus -0.05 +/- 0.4 (cm/m(2)), p < 0.00001 for LVIDd, and +4.5 +/- 8.9 versus +3.2 +/- 8.6 (%), p < 0.00001 for EF. The exception occurred in patients taking both ACEI and BB as co-treatment, in whom the decrease in LVIDd and increase in EF were no different between valsartan and placebo groups. CONCLUSIONS: The Val-HeFT echocardiographic substudy of 5,010 patients with moderate heart failure demonstrated that valsartan therapy taken with either ACEI or BB reversed LV remodeling.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_pharmacology_MeSH Tetrazoles_pharmacology_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_pharmacology_MeSH Valine_pharmacology_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 12228773
----K E
----T The Pediatric Randomized Carvedilol Trial in Children with Heart Failure: rationale and design.
----A BACKGROUND: Carvedilol is a medication with both beta-receptor and alpha-receptor blocking properties that has been approved for the treatment of heart failure in adults. Little is known about its safety, efficacy, pharmacokinetics, and dosing profile in children. METHODS: The primary objective of this study is to evaluate the efficacy of carvedilol administered twice daily for 8 months in terms of its effect compared with placebo on a composite measure of clinical outcomes in children with symptomatic systemic ventricular systolic dysfunction and heart failure. The secondary objectives are to determine the effect of carvedilol on individual components of a composite of clinical outcomes (hospitalizations for worsening heart failure, all-cause mortality and cardiovascular hospitalizations, all cause mortality, heart failure symptoms, and patient and physician global assessment); determine the effect of carvedilol on echocardiographic indices of ventricular function and remodeling; characterize the pharmacokinetics of carvedilol in pediatric patients with heart failure; characterize the effects carvedilol on neurohormonal systems; and provide data for the selection of an optimal titration schedule and daily dose of carvedilol in children with heart failure. This study will enroll 150 children between birth and 17 years of age with chronic symptomatic heart failure caused by systemic ventricular systolic dysfunction. CONCLUSION: This study will determine whether carvedilol improves symptoms in children with heart failure as a result of systemic ventricular systolic dysfunction. The study also will provide information on echocardiographic changes of ventricular performance and neurohormonal levels in children with heart failure before and after treatment with carvedilol, in addition to pharmacokinetics of carvedilol in children.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Adrenergic_alpha-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Infant_MeSH M_Infant__Newborn_MeSH M_Male_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Placebos_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction_MeSH S_blood_MeSH Ventricular_Dysfunction_blood_MeSH S_complications_MeSH Ventricular_Dysfunction_complications_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction_drug_therapy_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 12228778
----K I
----T Overview of randomized trials of antiarrhythmic drugs and devices for the prevention of sudden cardiac death.
----A BACKGROUND: Sudden cardiac death is a prominent feature of the natural history of heart disease. The efficacy of antiarrhythmic drugs and devices in preventing sudden death and reducing total mortality is uncertain. METHODS: We reviewed randomized trials and quantitative overviews of type I and type III antiarrhythmic drugs. We also reviewed the randomized trials of implantable cardioverter defibrillators and combined these outcomes in a quantitative overview. RESULTS: Randomized trials of type I antiarrhythmic agents used as secondary prevention after myocardial infarction show an overall 21% increase in mortality rate. Randomized trials of amiodarone suggest a 13% to 19% decrease in mortality rate, and sotalol has been effective in several small trials. Trials of pure type III agents, however, have shown no mortality benefit. An overview of implantable defibrillator trials shows a 24% reduction in mortality rate (CI 15%-33%) compared with alternative therapy, most often amiodarone. CONCLUSION: Amiodarone is effective in reducing the total mortality rate by 13% to 19%, and the implantable defibrillator reduces the mortality rate by a further 24%.
----P Journal_Article Meta-Analysis 
----M M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH S_utilization_MeSH Defibrillators__Implantable_utilization_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12229255
----K 1
----T [Beta blockers in post-infarction state]
----A In the 80s, randomized clinical studies and overviews have shown that adjunctive therapy with beta blockers can be beneficial post-myocardial infarction (MI). Despite this evidence, the use of beta blockers in the post-MI setting is far from uniform and now lags considerably behind the routine use of angiotensin-converting enzyme inhibitors (ACEIs) in this clinical setting. Given the major advances in the management of myocardial infarction and its sequelae that have occurred in the last two decades (including the use of percutaneous transluminal coronary angioplasty [PTCA], thrombolysis, aspirin, ACEIs, and statins), there was clearly a need to revisit the issue of beta blocker therapy in patients with beta blockers in the setting of post-MI heart failure. For all these reasons, the CAPRICORN trial of carvedilol in post-MI left ventricular dysfunction was an important and eagerly awaited trial, which could show that carvedilol treatment post-MI on top of the so-called modern post-MI therapy reduces mortality. Further studies have to show whether this results can be repeated with other beta blockers.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 12230635
----K 5
----T Acute atrial fibrillation.
----A 
----P Journal_Article Review Review_Literature 
----M M_Acute_Disease_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_adverse_effects_MeSH Digoxin_adverse_effects_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diltiazem_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Fibrinolytic_Agents_MeSH S_adverse_effects_MeSH Fibrinolytic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Thromboembolism_MeSH S_prevention_&_control_MeSH Thromboembolism_prevention_&_control_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12230638
----K I
----T Heart failure.
----A 
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Defibrillators__Implantable_MeSH M_Digoxin_MeSH S_adverse_effects_MeSH Digoxin_adverse_effects_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Exercise_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Patient_Care_Team_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Spironolactone_MeSH S_adverse_effects_MeSH Spironolactone_adverse_effects_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 12230735
----K E
----T Essential tremor.
----A 
----P Journal_Article Review Review_Literature 
----M M_Botulinum_Toxin_Type_A_MeSH S_administration_&_dosage_MeSH Botulinum_Toxin_Type_A_administration_&_dosage_MeSH S_adverse_effects_MeSH Botulinum_Toxin_Type_A_adverse_effects_MeSH M_Comparative_Study_MeSH M_Essential_Tremor_MeSH S_diagnosis_MeSH Essential_Tremor_diagnosis_MeSH S_drug_therapy_MeSH Essential_Tremor_drug_therapy_MeSH S_etiology_MeSH Essential_Tremor_etiology_MeSH M_Human_MeSH M_Phenobarbital_MeSH S_administration_&_dosage_MeSH Phenobarbital_administration_&_dosage_MeSH S_adverse_effects_MeSH Phenobarbital_adverse_effects_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12231591
----K E
----T Management and outcome of patients with atrial fibrillation during acute myocardial infarction: the GUSTO-III experience. Global use of strategies to open occluded coronary arteries.
----A OBJECTIVE: To investigate the use of antiarrhythmic agents and electrical cardioversion in the management of patients with atrial fibrillation complicating acute myocardial infarction, and their relation to 30 day and one year mortality. DESIGN: Prospective study of 1138 patients with atrial fibrillation from the GUSTO-III trial. INTERVENTIONS: Of the 1138 study patients, 317 (28%) received antiarrhythmic treatment, including class I antiarrhythmic agents (12%), sotalol (5%), and amiodarone (15%); electrical cardioversion was attempted in 116 (10%). RESULTS: Sinus rhythm was restored in 72% of patients receiving class I antiarrhythmic agents, 67% of those receiving sotalol, 79% of those receiving amiodarone, and 64% of those having electrical cardioversion. After adjusting for baseline characteristics and complications occurring before the onset of atrial fibrillation, there was no difference among the treatment groups in the incidence of sinus rhythm at the time of discharge or before deterioration to hospital death. However, the use of class I antiarrhythmic drugs or sotalol was associated with a lower unadjusted 30 day and one year mortality. After adjustment for baseline factors and pre-atrial fibrillation complications, the odds ratios for 30 day and one year mortality were 0.42 (95% confidence interval (CI) 0.19 to 0.89) and 0.58 (95% CI 0.33 to 1.04) with class I agents, and 0.31 (95% CI 0.07 to 1.32) and 0.31 (95% CI 0.09 to 1.02) with sotalol. In contrast, there was no association between the use of amiodarone or electrical cardioversion and 30 day or one year mortality. CONCLUSIONS: There was a strong trend towards lower mortality associated with the use of class I antiarrhythmic agents or sotalol in managing patients with atrial fibrillation after acute myocardial infarction. Randomised trials are indicated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Electric_Countershock_MeSH S_methods_MeSH Electric_Countershock_methods_MeSH M_Female_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12243852
----K E
----T Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors with Heart Failure (SENIORS). Rationale and design.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Clinical_Trials__Phase_III_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Multicenter_Studies_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12243636
----K I
----T Effects of losartan on cardiovascular morbidity and mortality in patients with isolated systolic hypertension and left ventricular hypertrophy: a Losartan Intervention for Endpoint Reduction (LIFE) substudy.
----A CONTEXT: Drug intervention in placebo-controlled trials has been beneficial in isolated systolic hypertension. OBJECTIVE: To test the hypothesis that losartan improves outcome better than atenolol in patients with isolated systolic hypertension and electrocardiographically documented left ventricular hypertrophy (ECG-LVH). DESIGN: Double-blind, randomized, parallel-group study conducted in 1995-2001. SETTING AND PARTICIPANTS: A total of 1326 men and women aged 55 through 80 years (mean, 70 years) with systolic blood pressure of 160 to 200 mm Hg and diastolic blood pressure of less than 90 mm Hg (mean, 174/83 mm Hg) and ECG-LVH, recruited from 945 outpatient settings in the Nordic countries, the United Kingdom, and the United States. INTERVENTIONS: Patients were randomly assigned to receive once-daily losartan (n = 660) or atenolol (n = 666) with hydrochlorothiazide as the second agent in both arms, for a mean of 4.7 years. MAIN OUTCOME MEASURE: Composite end point of cardiovascular death, stroke, or myocardial infarction. RESULTS: Blood pressure was reduced by 28/9 and 28/9 mm Hg in the losartan and atenolol arms. The main outcome was reduced by 25% with losartan compared with atenolol, 25.1 vs 35.4 events per 1000 patient-years (relative risk [RR], 0.75; 95% confidence interval [CI], 0.56-1.01; P =.06, adjusted for risk and degree of ECG-LVH; unadjusted RR, 0.71; 95% CI, 0.53-0.95; P =.02). Patients receiving losartan had reductions in the following without a difference in the incidence of myocardial infarction: cardiovascular mortality (8.7 vs 16.9 events per 1000 patient-years; RR, 0.54; 95% CI, 0.34-0.87; P =.01), nonfatal and fatal stroke (10.6 vs 18.9 events per 1000 patient-years; RR, 0.60; 95% CI, 0.38-0.92; P =.02), new-onset diabetes (12.6 vs 20.1 events per 1000 patient-years; RR, 0.62; 95% CI, 0.40-0.97; P =.04), and total mortality (21.2 vs 30.2 events per 1000 patient-years; RR, 0.72; 95% CI, 0.53-1.00; P =.046). Losartan decreased ECG-LVH more than atenolol (P<.001) and was better tolerated. CONCLUSION: These data suggest that losartan is superior to atenolol for treatment of patients with isolated systolic hypertension and ECG-LVH.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH M_Proportional_Hazards_Models_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 12269863
----K E
----T Spotlight on rizatriptan in migraine.
----A Rizatriptan is an orally active serotonin 5-HT(1) receptor agonist that potently and selectively binds to 5-HT(1B/1D) subtypes. Earlier clinical trials demonstrated that rizatriptan 5 or 10mg is more effective than placebo at providing pain relief and a pain-free state, relieving associated symptoms of migraine, normalising functional ability and improving patient quality of life, and showed that rizatriptan provides faster freedom from pain and reduces nausea to a greater extent than oral sumatriptan. More recently, rizatriptan 10mg was shown to be more effective than zolmitriptan 2.5mg or naratriptan 2.5mg at producing a pain-free state 2 hours postdose. Furthermore, compared with naratriptan, significantly more patients who received rizatriptan were pain free or had pain relief from 1 hour onwards. The number of patients with normal functional ability at 2 hours was significantly higher after rizatriptan than after naratriptan or zolmitriptan. Rizatriptan was also generally more effective than zolmitriptan or naratriptan at relieving migraine-associated symptoms. Rizatriptan is generally well tolerated, and adverse events are usually mild and transient. The most common adverse events associated with rizatriptan in recent randomised trials were asthenia/fatigue, dizziness, somnolence and nausea. There was a trend towards a lower incidence of adverse events with rizatriptan compared with zolmitriptan (31.2 vs 38.8%). However, rizatriptan was associated with a significantly higher incidence of adverse events than naratriptan (39 vs 29%). The incidence of chest pain was similar after the administration of rizatriptan, zolmitriptan or naratriptan (2-4%). In conclusion, rizatriptan is an effective drug for the acute treatment of moderate or severe migraine. Oral rizatriptan 5 and 10mg have shown greater efficacy than placebo in providing pain relief, an absence of pain, relief from associated symptoms, normal functional ability and an improvement in patient quality of life. Earlier results showed that rizatriptan provides faster freedom from pain and reduces nausea to a greater extent than oral sumatriptan. More recent studies have shown that rizatriptan 10mg provides faster pain relief and a higher percentage of patients with an absence of pain and normal functional ability at 2 hours than naratriptan 2.5mg or zolmitriptan 2.5mg. The efficacy of rizatriptan is retained when used in the long term, and the drug is generally well tolerated. Although well designed studies comparing rizatriptan with almotriptan, eletriptan and frovatriptan would further define the position of rizatriptan, current data suggest that rizatriptan should be considered as a first-line treatment option in the management of migraine.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Serotonin_Agonists_MeSH S_pharmacology_MeSH Serotonin_Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Triazoles_MeSH S_pharmacology_MeSH Triazoles_pharmacology_MeSH S_therapeutic_use_MeSH Triazoles_therapeutic_use_MeSH 
****** 12296615
----K 3
----T The effect of doxazosin on sexual function in patients with benign prostatic hyperplasia, hypertension, or both.
----A The prevalence of both benign prostatic hyperplasia (BPH) and hypertension increases with advancing age. These conditions coexist in almost 25% of men aged 60 years and older. The use of transurethral prostatectomy, a common surgical therapy for BPH, alleviates symptoms but results in erectile dysfunction (ED) in up to 35% of patients. Pharmacological intervention for BPH, including androgen-suppressing agents, has resulted in an increased incidence of sexual adverse experiences compared with the incidence observed in patients receiving placebo. Patients with hypertension also frequently experience problems with sexual function; in addition, antihypertensive medications used to treat this disease may increase problems with sexual function. ED is an age-related phenomenon, with estimated prevalence rates of 39% among men 40 years old and 67% among those 70 years old. Doxazosin, an alpha1-adrenoceptor antagonist indicated for the treatment of patients with BPH and/or hypertension, is not associated with the occurrence of ED compared with other antihypertensive treatments.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Doxazosin_MeSH S_adverse_effects_MeSH Doxazosin_adverse_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Impotence_MeSH S_chemically_induced_MeSH Impotence_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prostatic_Hyperplasia_MeSH S_drug_therapy_MeSH Prostatic_Hyperplasia_drug_therapy_MeSH M_Quality_of_Life_MeSH 
****** 12357261
----K I
----T Ventricular arrhythmia: role of the implantable cardioverter defibrillator and radiofrequency ablation in addition to drugs.
----A The control of life-threatening arrhythmias in the prevention of sudden cardiac death has been a long-standing challenge to clinicians. Large-scale, randomized, controlled trials have contributed immensely to our understanding of the management of life-threatening arrhythmias. There are many causes of life-threatening ventricular arrhythmias, which they occur mostly in the setting of healed myocardial infarction. Available treatments for the management of ventricular arrhythmias include antiarrhythmic drugs, implantable cardioverter defibrillators and catheter ablation. Each therapy provides unique advantages for selected patients with life-threatening arrhythmias. Because the goal of arrhythmia management is not only to provide the single best therapy but to provide the greatest assurance of symptomatic arrhythmia control, the use of combined therapy has become a standard treatment strategy for patients with sustained ventricular arrhythmias. This review will discuss the different modes of treatment available for the treatment of life-threatening ventricular arrhythmias, and their potential risks and benefits. The rationale for using hybrid or combination therapy will be presented. Finally, some of the better-known primary and secondary prevention trials for treatment of ventricular tachycardias will be reviewed.
----P Journal_Article Review Review__Academic 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH P_Catheter_Ablation_MeSH M_Combined_Modality_Therapy_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH P_Defibrillators__Implantable_MeSH M_Human_MeSH M_Tachycardia__Ventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH 
****** 12358202
----K 5
----T The 2001 Canadian hypertension recommendations: take-home messages.
----A 
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Chemical_Analysis_MeSH M_Blood_Pressure_Determination_MeSH M_Canada_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Life_Style_MeSH M_Practice_Guidelines_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12360462
----K E
----T A randomized, controlled trial of medical therapy versus endoscopic ligation for the prevention of variceal rebleeding in patients with cirrhosis.
----A BACKGROUND & AIMS: Patients who have had one variceal bleed are at high risk of rebleeding. Since its introduction, endoscopic variceal banding has been shown to be superior to needle sclerotherapy. Banding has not been compared with hepatic venous pressure-guided medical therapy (beta-blockers and nitrates). METHODS: One hundred two patients with cirrhosis and a recent esophageal variceal bleed were randomized to either endoscopic banding (51 patients) or medical therapy (51 patients). The hepatic venous pressure gradient was measured in all patients at baseline, at 3 months (drug therapy arm), and at yearly intervals (all patients). Primary end points were death or rebleeding. RESULTS: The 2 groups were well matched. Fifty-one percent were Pughs C, with a median Pughs score of 9.5. Nineteen patients rebled in the drug arm (median time, 24 days) and 27 patients in the banding arm (median time, 24 days). At 1 year, 43.7% of patients had bled in the drug arm compared with 53.8% in the banding arm (P = 0.25). Thirty-two percent of patients on medical therapy had died at 1 year, 22.5% on banding (P = 0.97). CONCLUSIONS: In the prevention of variceal rebleeding, beta-blockers +/- nitrates are as effective as endoscopic banding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH P_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH M_Ligation_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH M_Venous_Pressure_MeSH 
****** 12365089
----K E
----T [Uncontrolled arterial hypertension: pharmaco-economic interest of hospital diagnostic work-up]
----A The aim of this study was to assess both the clinical usefulness and the economical efficiency of an in-hospital workup for patients with uncontrolled arterial hypertension. PATIENTS AND METHODS: Eligible patients were hospitalized in a specialized unit between 1st January 1998 and 30th June 2000 for management of an uncontrolled arterial hypertension, to general practitioners (GPs) request. A questionnaire was sent to each of these GPs in May 2001. RESULTS: The cohort consisted of 214 patients (107 male, 107 female, mean age: 58 +/- 16 years). Pre-hospitalisation therapy was precisely identified in 178 patients. Forty-nine patients (28%) were given more than 3 antihypertensive drugs. The most frequently administered drugs were the following: diuretics (n = 93), beta-blockers (n = 85), and ACE-inhibitors (n = 78). Mean therapy cost was 1.71 +/- 1.05 [symbol: see text]. An etiology was found in 30 patients (14%). Plasma renin was measured in 140 out of the 184 patients with essential hypertension: it was found as low (< or = 7 ng/L) in 96 patients, with 50 of them (36%) having a very low plasma renin (< or = 3 ng/L). One hundred and fifty-four questionnaires were fulfilled by the GPs. Median follow-up was 23 months. Seventeen patients were lost of follow-up. Nine cardiovascular events were listed. Mean clinic BP was < 160/95 mmHg in 86 out of the 108 patients with both an essential hypertension and a fulfilled questionnaire, including 38 patients (35%) with a clinic BP < 140/90 mmHg. Eleven patients only, were given more than 3 antihypertensive drugs. The most frequently administered drugs were: calcium antagonists (73%), followed by diuretics (50%) and beta-blockers (34%). Mean therapy cost was 1.39 +/- 0.76 [symbol: see text] (p < 0.002 vs pre-hospitalization therapy cost); 84% of the GPs answered that the in-hospital workup resulted in an useful help in managing their patients. CONCLUSION: The in-hospital workup of patients with uncontrolled hypertension turned out to be both clinically useful and economically efficient: an aetiology has been found in 14% of the cases; an appropriate therapy, based on the hormonal profile, allowed for a lowering of BP below 160/95 in 80% of the cases, and below 140/90 in one thirds of the patients; the mean therapy cost has been reduced by 19%.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Cost_Control_MeSH M_Drug_Costs_MeSH S_statistics_&_numerical_data_MeSH Drug_Costs_statistics_&_numerical_data_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Inpatients_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Care_Planning_MeSH 
****** 12365906
----K 4
----T One-year, randomized study comparing bimatoprost and timolol in glaucoma and ocular hypertension.
----A OBJECTIVE: To compare bimatoprost with timolol maleate in patients with glaucoma or ocular hypertension. METHODS: In 2 identical, multicenter, randomized, double-masked, 1-year clinical trials, patients were treated with 0.03% bimatoprost once daily (QD) (n = 474), 0.03% bimatoprost twice daily (BID) (n = 483), or 0.5% timolol maleate BID (n = 241). MAIN OUTCOME MEASURES: Diurnal intraocular pressure (IOP) at 8 AM, 10 AM, and 4 PM and safety variables (IOP was also measured at 8 PM at selected sites). RESULTS: Bimatoprost QD provided significantly lower mean IOP than timolol at every time of the day at each study visit (P<.001). This was also true for bimatoprost BID at most time points, but the efficacy was not as good as that of the QD regimen. At 10 AM (peak timolol effect) at month 12, the mean reduction in IOP from baseline was 7.6 mm Hg (30%) with bimatoprost and 5.3 mm Hg (21%) with timolol (P<.001). A significantly higher percentage of patients receiving bimatoprost QD (58%) than timolol (37%) achieved IOPs at or below 17 mm Hg (10 AM, month 12; P<.001). The most common adverse effect with bimatoprost was hyperemia (significantly higher with bimatoprost QD than timolol; P<.001). CONCLUSIONS: Bimatoprost QD provides sustained IOP lowering superior to timolol or bimatoprost BID and achieves low target IOPs in significantly more patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma_physiopathology_MeSH M_Human_MeSH M_Hyperemia_MeSH S_chemically_induced_MeSH Hyperemia_chemically_induced_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lipids_MeSH S_administration_&_dosage_MeSH Lipids_administration_&_dosage_MeSH S_adverse_effects_MeSH Lipids_adverse_effects_MeSH S_therapeutic_use_MeSH Lipids_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12368928
----K E
----T The prevalence of cardiac risk factors in women 45 years of age or younger undergoing angiography for evaluation of undiagnosed chest pain.
----A BACKGROUND: Relatively little is known about the prevalence of cardiac risk factors, the use of noninvasive testing and the medical management of younger women (younger than 45 years of age) undergoing evaluation for chest pain. OBJECTIVES: To determine the rate of angiographically critical coronary artery disease (CAD) in women under the age of 45 years who were sent for first-time evaluation of chest pain requiring cardiac catheterization, and to determine the prevalence of cardiac risk factors, the role of noninvasive testing and the quality of medical management in these patients. PATIENTS AND METHODS: A retrospective chart review was performed on all female patients aged 45 years or younger from February 1997 to December 2000 (n=187) without prior known CAD referred for diagnostic cardiac catheterization. Chart information was studied, including catheterization results, cardiac risk factors, noninvasive testing done before catheterization (within six months) and medications at discharge. RESULTS: Angiographically critical CAD was found in 55 of 187 patients (29%), of whom 52% had single-vessel disease. One hundred twenty-one patients (65%) had completely normal coronary arteries. The most prominent cardiac risk factor for all study patients was a family history of premature CAD (67%), followed by smoking (55%) and dyslipidemia (55%). When compared with people without CAD, women with CAD had a higher prevalence of dyslipidemia (72% versus 47%, P=0.002), diabetes (29% versus 9%, P<0.001) and smoking (67% versus 50%, P=0.03). Noninvasive testing including exercise stress testing (calculated sensitivity of 44% and a specificity of 73%), and stress sestamibi scintigraphy (sensitivity of 67%, specificity of 30%) were both found to be poor predictors of those with CAD. Of all patients diagnosed as having critical CAD (n=55), 40% were discharged on an angiotensin-converting enzyme inhibitor, 73% on acetylsalicylic acid and 69% on a beta-blocker. CONCLUSIONS: The present study implies that younger women with CAD may have a higher prevalence of dyslipidemia, diabetes and smoking. The high percentage of women with minimally diseased or normal coronary arteries emphasizes the importance of confirmatory testing and poor use of noninvasive testing. The medical management of young women diagnosed with CAD is seemingly suboptimal, which may have important implications in later years of life.
----P Journal_Article 
----M M_Adult_MeSH M_Chest_Pain_MeSH S_radiography_MeSH Chest_Pain_radiography_MeSH P_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH 
****** 12372580
----K E
----T Utility of immediate exercise treadmill testing in patients taking beta blockers or calcium channel blockers.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chest_Pain_MeSH S_etiology_MeSH Chest_Pain_etiology_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Diagnosis__Differential_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH P_Emergencies_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Predictive_Value_of_Tests_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 12381236
----K I
----T Optimising the use of beta-blockers in older patients with heart failure.
----A Heart failure is predominantly a disease of the older person with half of all patients with the condition aged >75 years. Diuretics are the first-line symptomatic treatment for heart failure. beta-blockers should be initiated on an outpatient basis once the patient is stable, euvolaemic (by means of a diuretic) and established on an angiotensin converting enzyme (ACE) inhibitor. Large trials have demonstrated the beneficial effects of the beta-blockers carvedilol, metoprolol and bisoprolol in patients with heart failure, most of whom were also receiving ACE inhibitors. However, the mean age of patients in these trials was generally 60 to 65 years, with very few patients aged >75 years being recruited. It is, thus, not immediately clear how to apply these trial results to older patients with heart failure. Subgroup analyses from these large beta-blocker heart failure trials suggest that older patients gain similar benefit from beta-blocker treatment to younger patients. The trials, however, give no guidance as to whether older patients should receive the same target dosage or titration regimen as younger patients. It is suggested that a less aggressive titration regimen may be more appropriate for older patients while still attempting to achieve the trial target dosages. Titration can be safely achieved on an outpatient basis. In particular, a period of observation in the clinic after initiation of treatment does not appear to be necessary. The survival benefit resulting from the use of a beta-blocker in patients with heart failure is modest (months rather than years). It is, thus important not to neglect the effects of treatment on quality of life. A proportion of patients experience adverse effects with a beta-blocker. For such patients a balance needs to be made between the adverse effects on quality of life and the likely extension of life from the use of a beta-blocker. For patients who can tolerate a beta-blocker, the available evidence suggests that it can improve quality of life. The evidence currently available does not support the use of an angiotensin II receptor blocker (ARB) in addition to an ACE inhibitor and beta-blocker. For patients unable to tolerate an ACE inhibitor or beta-blocker, the use of an ARB may confer some advantage.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12383572
----K I
----T Beta-blocker therapy influences the hemodynamic response to inotropic agents in patients with heart failure: a randomized comparison of dobutamine and enoximone before and after chronic treatment with metoprolol or carvedilol.
----A OBJECTIVE: We compared the hemodynamic effects of dobutamine and enoximone administration before and after long-term beta-blocker therapy with metoprolol or carvedilol in patients with chronic heart failure (HF). BACKGROUND: Patients with HF on beta-blocker therapy may need hemodynamic support with inotropic agents, and the hemodynamic response may be influenced by both the inotropic agent and the beta-blocker used. METHODS: The hemodynamic effects of dobutamine (5 to 20 microg/kg/min intravenously) and enoximone (0.5 to 2 mg/kg intravenously) were assessed by pulmonary artery catheterization in 29 patients with chronic HF before and after 9 to 12 months of treatment with metoprolol or carvedilol at standard target maintenance oral doses. Hemodynamic studies were performed after >/=12 h of wash-out from all cardiovascular medications, except the beta-blockers that were administered 3 h before the second study. RESULTS: Compared with before beta-blocker therapy, metoprolol treatment decreased the magnitude of mean pulmonary artery pressure (PAP) and pulmonary wedge pressure (PWP) decline during dobutamine infusion and increased the cardiac index (CI) and stroke volume index (SVI) response to enoximone administration, without any effect on other hemodynamic parameters. Carvedilol treatment abolished the increase in heart rate, SVI, and CI and caused a rise, rather than a decline, in PAP, PWP, systemic vascular resistance, and pulmonary vascular resistance during dobutamine infusion. The hemodynamic response to enoximone, however, was maintained or enhanced in the presence of carvedilol. CONCLUSIONS: In contrast with its effects on enoximone, carvedilol and, to a lesser extent, metoprolol treatment may significantly inhibit the favorable hemodynamic response to dobutamine. No such beta-blocker-related attenuation of hemodynamic effects occurs with enoximone.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Dobutamine_MeSH S_pharmacology_MeSH Dobutamine_pharmacology_MeSH S_therapeutic_use_MeSH Dobutamine_therapeutic_use_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Enoximone_MeSH S_pharmacology_MeSH Enoximone_pharmacology_MeSH S_therapeutic_use_MeSH Enoximone_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Radionuclide_Angiography_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 12384991
----K E
----T Pathophysiologic role of myocardial apoptosis in post-infarction left ventricular remodeling.
----A Left ventricular (LV) remodeling and heart failure (HF) complicate acute myocardial infarction (AMI) even weeks to months after the initial insult. Apoptosis may represent an important pathophysiologic mechanism causing progressive myocardiocyte loss and LV dilatation even late after AMI. This review will discuss the role of apoptosis according to findings in animal experimental data and observational studies in humans in order to assess clinical relevance, determinants, and mechanisms of myocardial apoptosis and potential therapeutic implications. More complete definition of the impact of myocardiocyte loss on prognosis and of the mechanisms involved may lead to improved understanding of cardiac remodeling and possibly improved patients' care. Mitochondrial damage and bcl-2 to bax balance play a central role in ischemia-dependent apoptosis while angiotensin II and beta(1)-adrenergic-stimulation may be major causes of receptor-mediated apoptosis. Benefits due to treatment with ACE-inhibitors and beta-blockers appear to be in part due to reduced myocardial apoptosis. Moreover, infarct-related artery patency late after AMI may be a major determinant of myocardial apoptosis and clinical benefits deriving from an open artery late post AMI (the "open artery hypothesis") may be, at least in part, due to reduced myocardiocyte loss.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH P_Apoptosis_MeSH M_Caspases_MeSH S_metabolism_MeSH Caspases_metabolism_MeSH M_Heart_Failure__Congestive_MeSH S_pathology_MeSH Heart_Failure__Congestive_pathology_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Myocardial_Ischemia_MeSH S_enzymology_MeSH Myocardial_Ischemia_enzymology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH P_Ventricular_Remodeling_MeSH 
****** 12386502
----K E
----T Management of acute coronary syndromes.
----A Acute coronary syndromes represent the acute, life-threatening phases of coronary heart disease. Patients with acute coronary syndromes are at high risk of major adverse cardiac events. Treatment of these patients remains controversial because of the heterogeneous nature of these conditions and recent advances in their management options. The older standbys of aspirin, heparins, nitrates, beta-blockers, and thrombolytic therapy have given way to vastly improved interventional capabilities (with improved adjunctive pharmacotherapy), low molecular weight heparins, glycoprotein IIb/IIIa antagonists, safer theinopyridines, thrombin inhibitors, and newer generation fibrinolytics. Despite these substantial advances, a great deal of confusion remains. Clinicians know that there are better forms of therapy but are not sure how to use them, when to use them, or even what to use. They do not have all the answers at present and probably have more questions than answers.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Angina__Unstable_MeSH S_diagnosis_MeSH Angina__Unstable_diagnosis_MeSH S_mortality_MeSH Angina__Unstable_mortality_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_methods_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_methods_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Critical_Care_MeSH S_methods_MeSH Critical_Care_methods_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Analysis_MeSH M_Thrombolytic_Therapy_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 12390940
----K E
----T Carvedilol prospective randomized cumulative survival (COPERNICUS) trial: carvedilol as the sun and center of the beta-blocker world?
----A 
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Analysis_MeSH 
****** 12390947
----K I
----T Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study.
----A BACKGROUND: Beta-blocking agents improve functional status and reduce morbidity in mild-to-moderate heart failure, but it is not known whether they produce such benefits in severe heart failure. METHODS AND RESULTS: We randomly assigned 2289 patients with symptoms of heart failure at rest or on minimal exertion and with an ejection fraction <25% (but not volume-overloaded) to double-blind treatment with either placebo (n=1133) or carvedilol (n=1156) for an average of 10.4 months. Carvedilol reduced the combined risk of death or hospitalization for a cardiovascular reason by 27% (P=0.00002) and the combined risk of death or hospitalization for heart failure by 31% (P=0.000004). Patients in the carvedilol group also spent 27% fewer days in the hospital for any reason (P=0.0005) and 40% fewer days in the hospital for heart failure (P<0.0001). These differences were as a result of both a decrease in the number of hospitalizations and a shorter duration of each admission. More patients felt improved and fewer patients felt worse in the carvedilol group than in the placebo group after 6 months of maintenance therapy (P=0.0009). Carvedilol-treated patients were also less likely than placebo-treated patients to experience a serious adverse event (P=0.002), especially worsening heart failure, sudden death, cardiogenic shock, or ventricular tachycardia. CONCLUSION: In euvolemic patients with symptoms at rest or on minimal exertion, the addition of carvedilol to conventional therapy ameliorates the severity of heart failure and reduces the risk of clinical deterioration, hospitalization, and other serious adverse clinical events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Disease-Free_Survival_MeSH M_Double-Blind_Method_MeSH M_Health_Resources_MeSH S_utilization_MeSH Health_Resources_utilization_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 12392039
----K E
----T The African-American Heart Failure Trial: background, rationale and significance.
----A New treatments have improved outcomes in heart failure (HF), but applicability of these advances may be limited in African Americans. Analysis of previous trials has shown that a combination of hydralazine (H) plus isosorbide dinitrate (ISDN) may be especially beneficial in African Americans with HF. The African American Heart Failure Trial (A-HeFT) is a double-blind, randomized, and placebo-controlled trial in African American patients with stable NYHA Class III-IV HF while on standard therapy. Randomization to addition of BiDil, a fixed combination of H+ISDN, or placebo, will be stratified for beta-blocker usage, and all patients will be treated and followed until the last patient entered has completed six months of follow-up. The primary efficacy endpoint will be a composite score including quality of life, deaths, and hospitalizations for HF. At least 600 patients will be randomized. The first patient was randomized in June, 2001. Besides additional testing of H+ISDN in HF, A-HeFT will be the first HF trial aimed at a subgroup of African American patients, as well as the first to use a new composite HF score as its primary efficacy endpoint.
----P Clinical_Trial Randomized_Controlled_Trial 
----M P_African_Americans_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH M_Human_MeSH M_Hydralazine_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH P_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12398962
----K E
----T Effects of celecoxib and rofecoxib on blood pressure and edema in patients > or =65 years of age with systemic hypertension and osteoarthritis.
----A Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs), including the cyclooxygenase-2 (COX-2) specific inhibitors, with antihypertensive medication is common practice for many patients with arthritis. This study evaluated the effects of celecoxib 200 mg/day and rofecoxib 25 mg/day on blood pressure (BP) and edema in a 6-week, randomized, parallel-group, double-blind study in patients > or =65 years of age with osteoarthritis who were treated with fixed antihypertensive regimens. One thousand ninety-two patients received study medication (celecoxib, n = 549; rofecoxib, n = 543). Significantly more patients in the rofecoxib group compared with the celecoxib group developed increased systolic BP (change >20 mm Hg plus absolute value > or =140 mm Hg) at any time point (14.9% vs 6.9%, p <0.01). Rofecoxib caused the greatest increase in systolic BP in patients receiving angiotensin-converting enzyme inhibitors or beta blockers, whereas those on calcium channel antagonists or diuretic monotherapy receiving either celecoxib or rofecoxib showed no significant increases in BP. Clinically significant new-onset or worsening edema associated with weight gain developed in a greater percentage of patients in the rofecoxib group (7.7%) compared with the celecoxib group (4.7%) (p <0.05). Thus, in patients with controlled hypertension on a fixed antihypertensive regimen, careful monitoring of BP is warranted after the initiation of celecoxib or rofecoxib therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cyclooxygenase_Inhibitors_MeSH S_therapeutic_use_MeSH Cyclooxygenase_Inhibitors_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Edema_MeSH S_complications_MeSH Edema_complications_MeSH S_drug_therapy_MeSH Edema_drug_therapy_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lactones_MeSH S_therapeutic_use_MeSH Lactones_therapeutic_use_MeSH M_Male_MeSH M_North_America_MeSH M_Osteoarthritis_MeSH S_complications_MeSH Osteoarthritis_complications_MeSH S_drug_therapy_MeSH Osteoarthritis_drug_therapy_MeSH M_Sulfonamides_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Weight_Gain_MeSH S_drug_effects_MeSH Weight_Gain_drug_effects_MeSH 
****** 12398977
----K E
----T Effectiveness of amiodarone therapy in patients with severe congestive heart failure and intolerance to metoprolol.
----A 
----P Evaluation_Studies Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Drug_Tolerance_MeSH S_physiology_MeSH Drug_Tolerance_physiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH 
****** 12401122
----K E
----T Influence of drugs and gender on the arterial pulse wave and natriuretic peptide secretion in untreated patients with essential hypertension.
----A Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure are the same. We studied 30 untreated hypertensive patients, aged 28-55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5 mg, doxazosin 4 mg, lisinopril 10 mg, bisoprolol 5 mg, bendrofluazide 2.5 mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP). The Sphygmocor derivation of the central aortic pulse wave was used to measure time for transmission of the reflected wave (T(R)) and the augmentation index (AI), which is the proportional increase in systolic pressure due to the reflected wave. There was a dissociation between the effects of the drugs on blood pressure and pulse wave analysis. Bisoprolol caused the greatest falls in blood pressure and T(R), but was the only drug to increase AI. This paradoxical response to bisoprolol was associated with a 3-fold increase in plasma BNP levels. There was a smaller elevation of BNP in women compared with men, as described previously, and this elevation also was associated with significantly higher values of AI. Other drugs reduced AI, and this was associated with a significant decrease in BNP by amlodipine. In conclusion, antihypertensive drugs differ in their short-term effects on augmentation of the systolic pulse wave and secretion of BNP from the heart, regarded as a sensitive measure of strain on cardiomyocytes. These differences may help to explain cause-specific differences in outcome in recent trials.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Aorta_MeSH S_physiopathology_MeSH Aorta_physiopathology_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Determination_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH S_drug_effects_MeSH Natriuretic_Peptide__Brain_drug_effects_MeSH M_Pulsatile_Flow_MeSH S_drug_effects_MeSH Pulsatile_Flow_drug_effects_MeSH M_Radial_Artery_MeSH S_physiopathology_MeSH Radial_Artery_physiopathology_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12401144
----K E
----T Beta-blocker survival benefit outweighs side-effect risks.
----A 
----P Comment Journal_Article 
----M 
****** 12417537
----K I
----T Calcium antagonist lacidipine slows down progression of asymptomatic carotid atherosclerosis: principal results of the European Lacidipine Study on Atherosclerosis (ELSA), a randomized, double-blind, long-term trial.
----A BACKGROUND: Most cardiovascular events associated with hypertension are complications of atherosclerosis. Some antihypertensive agents influence experimental models of atherosclerosis through mechanisms independent of blood pressure lowering. METHODS AND RESULTS: The European Lacidipine Study on Atherosclerosis (ELSA) was a randomized, double-blind trial in 2334 patients with hypertension that compared the effects of a 4-year treatment based on either lacidipine or atenolol on an index of carotid atherosclerosis, the mean of the maximum intima-media thicknesses (IMT) in far walls of common carotids and bifurcations (CBM(max)). This index has been shown by epidemiological studies to be predictive of cardiovascular events. A significant (P<0.0001) effect of lacidipine was found compared with atenolol, with a treatment difference in 4-year CBM(max) progression of -0.0227 mm (intention-to-treat population) and -0.0281 mm (completers). The yearly IMT progression rate was 0.0145 mm/y in atenolol-treated and 0.0087 mm/y in lacidipine-treated patients (completers, 40% reduction; P=0.0073). Patients with plaque progression were significantly less common, and patients with plaque regression were significantly more common in the lacidipine group. Clinic blood pressure reductions were identical with both treatments, but 24-hour ambulatory systolic/diastolic blood pressure changes were greater with atenolol (-10/-9 mm Hg) than with lacidipine (-7/-5 mm Hg). No significant difference between treatments was found in any cardiovascular events, although the relative risk for stroke, major cardiovascular events, and mortality showed a trend favoring lacidipine. CONCLUSION: The greater efficacy of lacidipine on carotid IMT progression and number of plaques per patient, despite a smaller ambulatory blood pressure reduction, indicates an antiatherosclerotic action of lacidipine independent of its antihypertensive action.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carotid_Arteries_MeSH S_drug_effects_MeSH Carotid_Arteries_drug_effects_MeSH S_ultrasonography_MeSH Carotid_Arteries_ultrasonography_MeSH M_Carotid_Artery_Diseases_MeSH S_complications_MeSH Carotid_Artery_Diseases_complications_MeSH S_drug_therapy_MeSH Carotid_Artery_Diseases_drug_therapy_MeSH S_ultrasonography_MeSH Carotid_Artery_Diseases_ultrasonography_MeSH M_Dihydropyridines_MeSH S_adverse_effects_MeSH Dihydropyridines_adverse_effects_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_MeSH M_Treatment_Outcome_MeSH M_Tunica_Intima_MeSH S_drug_effects_MeSH Tunica_Intima_drug_effects_MeSH S_ultrasonography_MeSH Tunica_Intima_ultrasonography_MeSH M_Tunica_Media_MeSH S_drug_effects_MeSH Tunica_Media_drug_effects_MeSH S_ultrasonography_MeSH Tunica_Media_ultrasonography_MeSH M_Ultrasonography_MeSH 
****** 12417542
----K E
----T Effects of valsartan on circulating brain natriuretic peptide and norepinephrine in symptomatic chronic heart failure: the Valsartan Heart Failure Trial (Val-HeFT).
----A BACKGROUND: Brain natriuretic peptide (BNP) and norepinephrine (NE) are strongly related to severity of and are independent predictors of outcome in heart failure. The long-term effects of angiotensin receptor blockers on BNP and NE in heart failure patients are not known. METHODS AND RESULTS: Both BNP and NE were measured in 4284 patients randomized to valsartan or placebo in the Valsartan Heart Failure Trial (Val-HeFT) at baseline and 4, 12, and 24 months after randomization. The effects of valsartan were tested by ANCOVA, controlling for baseline values and concomitant ACE inhibitors and/or beta-blockers. BNP and NE concentrations were similar at baseline in the 2 groups and were decreased by valsartan starting at 4 months and up to 24 months. BNP increased over time in the placebo group. At the end point, least-squares mean (+/-SEM) BNP increased from baseline by 23+/-5 pg/mL in the placebo group (n=1979) but decreased by 21+/-5 pg/mL (n=1940) in the valsartan group (P<0.0001). NE increased by 41+/-6 pg/mL (n=1979) and 12+/-6 pg/mL (n=1941) for placebo and valsartan, respectively (P=0.0003). Concomitant therapy with both ACE inhibitors and beta-blockers significantly reduced the effect of valsartan on BNP but not on NE (P for interaction=0.0223 and 0.2289, respectively). CONCLUSIONS: In Val-HeFT, the largest neurohormone study in patients with symptomatic chronic heart failure, BNP and NE rose over time in the placebo group. Valsartan caused sustained reduction in BNP and attenuated the increase in NE over the course of the study. These neurohormone effects of valsartan are consistent with the clinical benefits reported in Val-HeFT.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Neurotransmitters_MeSH S_blood_MeSH Neurotransmitters_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Time_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 12417543
----K 3
----T Paradoxical effect of sibutramine on autonomic cardiovascular regulation.
----A BACKGROUND: Sibutramine, a serotonin and norepinephrine transporter blocker, is widely used as an adjunctive obesity treatment. Norepinephrine reuptake inhibition with sibutramine conceivably could exacerbate arterial hypertension and promote cardiovascular disease. METHODS AND RESULTS: In 11 healthy subjects (7 men, age 27+/-2 years, body mass index 23.1+/-0.7 kg/m2), we compared the effect of sibutramine or matching placebo (ingested 26, 14, and 2 hours before testing) on cardiovascular responses to autonomic reflex tests and to a graded head-up tilt test. In addition, we tested sibutramine in combination with metoprolol. Testing was conducted in a double-blind and crossover fashion. Supine systolic blood pressure was 113+/-3 mm Hg with placebo, 121+/-3 mm Hg with sibutramine (P<0.001 versus placebo), and 111+/-2 mm Hg with the combination of sibutramine and metoprolol. Similarly, sibutramine increased upright blood pressure. Sibutramine substantially increased upright heart rate. This effect was abolished with metoprolol. The blood pressure response to cold pressor and handgrip testing was attenuated with sibutramine compared with placebo. Furthermore, sibutramine decreased low-frequency oscillations of blood pressure and plasma norepinephrine concentrations in the supine position. CONCLUSIONS: The cardiovascular effect of the antiobesity drug sibutramine results from a complex interaction of peripheral and central nervous system effects. The inhibitory clonidine-like action of sibutramine on the central nervous system attenuates the peripheral stimulatory effect. Our findings strongly suggest that current concepts regarding the action of sibutramine on the sympathetic nervous system should be reconsidered.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Anti-Obesity_Agents_MeSH S_pharmacology_MeSH Anti-Obesity_Agents_pharmacology_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Biological_Clocks_MeSH S_drug_effects_MeSH Biological_Clocks_drug_effects_MeSH S_physiology_MeSH Biological_Clocks_physiology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiovascular_Physiology_MeSH S_drug_effects_MeSH Cardiovascular_Physiology_drug_effects_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH S_innervation_MeSH Cardiovascular_System_innervation_MeSH M_Cold_MeSH M_Cross-Over_Studies_MeSH M_Cyclobutanes_MeSH S_pharmacology_MeSH Cyclobutanes_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hand_Strength_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Physical_Stimulation_MeSH S_methods_MeSH Physical_Stimulation_methods_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Symporters_MeSH S_drug_effects_MeSH Symporters_drug_effects_MeSH S_metabolism_MeSH Symporters_metabolism_MeSH M_Tilt-Table_Test_MeSH M_Valsalva_Maneuver_MeSH S_physiology_MeSH Valsalva_Maneuver_physiology_MeSH 
****** 12417825
----K E
----T Cardiovascular medications taken by patients aged >or=70 years hospitalized for acute coronary syndromes before hospitalization and at hospital discharge.
----A A prospective study was performed in 177 patients, mean age 78+/-6 years, hospitalized with acute coronary syndromes. Obstructive coronary artery disease was documented by coronary angiography in 154 of 177 patients (87%). Coronary revascularization was performed in 96 of 177 patients (54%). Five of 177 patients (3%) died during hospitalization. Compared to use before hospitalization, at hospital discharge the use of aspirin increased from 43% to 84% (p<0.001), the use of clopidogrel increased from 21% to 54% (p<0.001), the use of beta blockers increased from 38% to 76% (p<0.001), the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers increased from 42% to 70% (p<0.001), the use of long-acting nitrates increased from 15% to 31% (p<0.001), and the use of calcium channel blockers decreased from 28% to 23% (p=NS). Dyslipidemia was present in 62% of the 177 patients. The use of statins increased from 34% before hospitalization to 63% at hospital discharge (p<0.001).
----P Journal_Article 
----M M_Acute_Disease_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Revascularization_MeSH M_Patient_Discharge_MeSH M_Probability_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Survival_Rate_MeSH 
****** 12418946
----K I
----T Time trends in high blood pressure control and the use of antihypertensive medications in older adults: the Cardiovascular Health Study.
----A BACKGROUND: Control of high blood pressure (BP) in older adults is an important part of public health efforts at prevention. OBJECTIVE: To assess recent time trends in the awareness, treatment, and control of high BP and in the use of medications to treat high BP. METHODS: In the Cardiovascular Health Study, 5888 adults 65 years and older were recruited from 4 US centers. At baseline, participants underwent an extensive examination that included the measurement of BP, use of medications, and other risk factors. Participants were followed up with annual visits that assessed BP and medication use from baseline in 1989-1990 through the examination in 1998-1999. The primary outcome measures were control of BP to levels lower than than 140/90 mm Hg and the prevalence of use of various classes of antihypertensive medications. RESULTS: The awareness, treatment, and control of high BP improved during the 1990s. The proportions aware and treated were higher among blacks than whites, though control prevalences were similar. For both groups combined, the control of high BP to lower than 140/90 mm Hg increased from 37% at baseline to 49% in 1999. The 51% whose BP was not controlled generally had isolated mild to moderate elevations in systolic BP. Among treated persons, the improvement in control was achieved in part by a mean increase of 0.2 antihypertensive medications per person over the course of 9 years. Improved control was also achieved by increasing the proportion of the entire Cardiovascular Health Study population that was treated for hypertension, from 34.5% in 1990 to 51.1% in 1999. Time trends in antihypertensive drug use were pronounced. Among those without coronary disease, the use of low-dose diuretics and beta-blockers decreased, while the use of newer agents, such as calcium channel blockers, angiotensin-converting enzyme inhibitors, and alpha-blockers increased. CONCLUSIONS: While control of high BP improved in the 1990s, about half the participants with hypertension had uncontrolled BP, primarily mild to moderate elevations in systolic BP. Low-dose diuretics and beta-blockers--the preferred agents since 1993 according to the recommendations of the Joint National Committee on the Detection, Evaluation and Treatment of High Blood Pressure--remained underused. More widespread use of these agents will be an important intervention to prevent the devastating complications of hypertension, including stroke, myocardial infarction, and heart failure.
----P Journal_Article 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Awareness_MeSH M_Cohort_Studies_MeSH M_Drug_Therapy_MeSH S_trends_MeSH Drug_Therapy_trends_MeSH M_Female_MeSH M_Health_Knowledge__Attitudes__Practice_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH 
****** 12423712
----K E
----T Comparison of actions of irbesartan versus atenolol on cardiac repolarization in hypertensive left ventricular hypertrophy: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA).
----A Left ventricular (LV) hypertrophy is associated with a substantial risk for malignant arrhythmias and sudden death. The effects of antihypertensive therapy on QT dispersion, which reflects cardiac repolarization heterogeneity, in relation to changes in LV mass has not been well studied. Repeat echocardiography and QT measurements (standard 12-lead electrocardiograms) were performed in hypertensive patients with LV hypertrophy, who were randomized double-blind to receive the angiotensin II type 1-receptor blocker irbesartan (n = 44) or the beta(1)-receptor blocker atenolol (n = 48) for 48 weeks, and in 37 matched hypertensive control subjects without LV hypertrophy. LV mass index was related to QT dispersion (r = 0.34, p <0.001). The reduction in LV mass was greater using irbesartan than using atenolol (-27 +/- 28 vs -15 +/- 21 g/m(2) at 48 weeks, p = 0.021), with similar reductions in blood pressure. Irbesartan decreased QT dispersion (from 56 +/- 24 ms to 45 +/- 20 ms at 48 weeks; p <0.001) and QTc dispersion (from 57 +/- 24 to 44 +/- 19 ms at 48 weeks; p <0.001). In contrast, atenolol had minor effects. The decreases in QT and QTc dispersions were greater using irbesartan than using atenolol (p = 0.001 and p = 0.011, respectively); the same results were found when changes in LV mass, blood pressure, and heart rate were also included in multivariate analyses. Thus, heterogeneity of ventricular repolarization is related to the degree of LV hypertrophy. Irbesartan, but not atenolol, reduces QT and QTc dispersions independent of changes in LV mass, blood pressure, or heart rate, and thus seems to induce structural and electrical remodeling in a direction that could decrease the risk of fatal events in hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12423713
----K 2
----T Effects of long-term beta-blocker (metoprolol or carvedilol) therapy on QT variability in subjects with chronic heart failure secondary to ischemic cardiomyopathy.
----A Chronic heart failure (CHF) is a risk factor for sudden death. Temporal and spatial changes in repolarization are among the most studied mechanisms for inducing fatal ventricular arrhythmias. Beta blockers effectively reduce the risk of sudden death in CHF. Our aim in this study was to investigate changes induced by metoprolol and carvedilol on the QT variability index (QTVI), a new measure reflecting the temporal heterogeneity of cardiac repolarization. A total of 82 subjects, who were in New York Heart Association functional class II or III, underwent short-term spectral analysis of RR and QT variability before and after a 1-year course of high-dose metoprolol (40 subjects) or carvedilol (42 subjects) at baseline (rest) and after sympathetic stress (head-up tilt). At rest, both drug-treated groups had lower QTVI (p <0.001) than after placebo, but during tilt patients treated with carvedilol had a lower QTVI than those treated with metoprolol (p <0.05). Although both beta-blocker treatments helped to normalize the QTVI measured in normal subjects at rest, they each differentially altered the index after tilt. Carvedilol seemed to improve the QTVI more than metoprolol.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Italy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Single-Blind_Method_MeSH M_Tilt-Table_Test_MeSH M_Treatment_Outcome_MeSH 
****** 12434307
----K 4
----T The safety and efficacy of timolol 0.5% in xanthan gum versus timolol gel forming solution 0.5%.
----A PURPOSE: To evaluate the efficacy and safety of timolol maleate 0.5% gel forming solution (TXE, Merck) versus timolol maleate 0.5% gel forming solution (TXG, Falcon) in primary open-angle glaucoma and ocular hypertension patients. METHODS: Following a washout period patients were randomly begun on either TXE or TXG each given once each morning for six weeks (Period 1). Patients then were crossed over to the opposite medicine for Period 2. Following each 6-week treatment period the intraocular pressure was obtained at 08:00 trough and +2 and +8 hours post-dosing. Anterior segment staining and photography were performed to assess surface irritation. RESULTS: Thirty-two patients were enrolled in this study; 28 completed. The diurnal intraocular pressure as well as the 08:00 trough and +2 hour post dosing pressures were statistically equal between groups, although a trend to a lower mean pressure was observed in the TXE (17.9 +/- 3.2 mm Hg) compared to the TXG (18.6 +/- 3.4 mm Hg) group. However, eight hours after dosing the pressure was 17.5 +/- 3.2 mm Hg in the TXE group and 18.9 +/- 3.3 mm Hg in the TXG group (P = 0.0019). Safety was similar between groups, including corneal and conjunctival staining, conjunctival hyperemia graded by anterior segment photography and at the slit lamp, and unsolicited and solicited side effects. Vision recovery after instillation was similar between groups. CONCLUSIONS: TXE demonstrates a lower intraocular pressure eight hours after dosing than does TXG, but safety appears similar between products.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Anterior_Eye_Segment_MeSH S_metabolism_MeSH Anterior_Eye_Segment_metabolism_MeSH M_Conjunctiva_MeSH S_blood_supply_MeSH Conjunctiva_blood_supply_MeSH M_Gels_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Hyperemia_MeSH S_drug_therapy_MeSH Hyperemia_drug_therapy_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH P_Polysaccharides__Bacterial_MeSH S_adverse_effects_MeSH Polysaccharides__Bacterial_adverse_effects_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Solutions_MeSH M_Staining_and_Labeling_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Visual_Acuity_MeSH S_drug_effects_MeSH Visual_Acuity_drug_effects_MeSH 
****** 12433890
----K I
----T Beta blockers in older persons with heart failure: tolerability and impact on quality of life.
----A OBJECTIVE: To determine tolerability and symptom changes associated with the introduction of bisoprolol treatment in older patients with heart failure. DESIGN: Prospective observational cohort study. SETTING: Geriatric medicine outpatient department of a university hospital. PATIENTS: 51 patients (mean age 78 years, range 70-89 years) with stable symptomatic heart failure caused by left ventricular systolic dysfunction. INTERVENTIONS: Bisoprolol tablets, 1.25-10.0 mg. MAIN OUTCOME MEASURES: Tolerability; changes in symptoms and exercise tolerance. RESULTS: 69% of patients tolerated bisoprolol. Mean tolerated dose was 7.6 mg. There was no change in symptoms or exercise capacity in those who tolerated bisoprolol. Perceived health status and symptoms of anxiety and depression improved during the titration period. CONCLUSIONS: The rate of withdrawal from bisoprolol treatment in older patients with congestive heart failure was twice that previously reported in younger patients. The mean tolerated dose was similar to that found in trials reporting clinical efficacy. There was no evidence of a negative impact on symptoms or exercise capacity in patients who tolerated bisoprolol.
----P Journal_Article 
----M M_Adrenergic_beta-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cohort_Studies_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH S_physiology_MeSH Exercise_Tolerance_physiology_MeSH M_Female_MeSH M_Health_Status_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tablets_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12435222
----K 5
----T Pharmacologic management of acute attacks of migraine and prevention of migraine headache.
----A 
----P Guideline Journal_Article Practice_Guideline Review Review__Academic 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Anticonvulsants_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Ergotamines_MeSH S_therapeutic_use_MeSH Ergotamines_therapeutic_use_MeSH M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Narcotics_MeSH S_therapeutic_use_MeSH Narcotics_therapeutic_use_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12435255
----K E
----T Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial.
----A CONTEXT: Hypertension is a leading cause of end-stage renal disease (ESRD) in the United States, with no known treatment to prevent progressive declines leading to ESRD. OBJECTIVE: To compare the effects of 2 levels of blood pressure (BP) control and 3 antihypertensive drug classes on glomerular filtration rate (GFR) decline in hypertension. DESIGN: Randomized 3 x 2 factorial trial with enrollment from February 1995 to September 1998. SETTING AND PARTICIPANTS: A total of 1094 African Americans aged 18 to 70 years with hypertensive renal disease (GFR, 20-65 mL/min per 1.73 m(2)) were recruited from 21 clinical centers throughout the United States and followed up for 3 to 6.4 years. INTERVENTIONS: Participants were randomly assigned to 1 of 2 mean arterial pressure goals, 102 to 107 mm Hg (usual; n = 554) or 92 mm Hg or less (lower; n = 540), and to initial treatment with either a beta-blocker (metoprolol 50-200 mg/d; n = 441), an angiotensin-converting enzyme inhibitor (ramipril 2.5-10 mg/d; n = 436) or a dihydropyridine calcium channel blocker, (amlodipine 5-10 mg/d; n = 217). Open-label agents were added to achieve the assigned BP goals. MAIN OUTCOME MEASURES: Rate of change in GFR (GFR slope); clinical composite outcome of reduction in GFR by 50% or more (or > or =25 mL/min per 1.73 m2) from baseline, ESRD, or death. Three primary treatment comparisons were specified: lower vs usual BP goal; ramipril vs metoprolol; and amlodipine vs metoprolol. RESULTS: Achieved BP averaged (SD) 128/78 (12/8) mm Hg in the lower BP group and 141/85 (12/7) mm Hg in the usual BP group. The mean (SE) GFR slope from baseline through 4 years did not differ significantly between the lower BP group (-2.21 [0.17] mL/min per 1.73 m2 per year) and the usual BP group (-1.95 [0.17] mL/min per 1.73 m2 per year; P =.24), and the lower BP goal did not significantly reduce the rate of the clinical composite outcome (risk reduction for lower BP group = 2%; 95% confidence interval [CI], -22% to 21%; P =.85). None of the drug group comparisons showed consistent significant differences in the GFR slope. However, compared with the metoprolol and amlodipine groups, the ramipril group manifested risk reductions in the clinical composite outcome of 22% (95% CI, 1%-38%; P =.04) and 38% (95% CI, 14%-56%; P =.004), respectively. There was no significant difference in the clinical composite outcome between the amlodipine and metoprolol groups. CONCLUSIONS: No additional benefit of slowing progression of hypertensive nephrosclerosis was observed with the lower BP goal. Angiotensin-converting enzyme inhibitors appear to be more effective than beta-blockers or dihydropyridine calcium channel blockers in slowing GFR decline.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_African_Americans_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Disease_Progression_MeSH M_Female_MeSH P_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_epidemiology_MeSH Kidney_Failure__Chronic_epidemiology_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Proteinuria_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12440556
----K I
----T Beta-blockers in chronic heart failure: considerations for selecting an agent.
----A Patients with chronic heart failure have increased sympathetic nervous system activity that contributes to deterioration of cardiovascular function over time. Long-term beta-blocker therapy prevents such deterioration through inhibition of this neurohormonal pathway. The impressive survival data collected from several large studies have made beta-blockers a component of standard therapy for New York Heart Association class II to III heart failure. Although there are differences in the pharmacological properties of the beta-blockers shown to improve morbidity and mortality in heart failure, there is little evidence to suggest that such properties constitute any major advantages in clinical outcome. Carvedilol and extended-release metoprolol succinate are 2 beta-blockers currently approved in the United States for the treatment of patients with heart failure. Both agents have shown similar risk reductions in overall and cause-specific mortality; however, no outcome data from a comparative trial are available to support the use of one agent over the other. Regardless of the agent chosen, appropriate dosing and titration of beta-blockers are essential for successful therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Chronic_Disease_MeSH M_Controlled_Clinical_Trials_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12440651
----K 5
----T Effect of beta blockers after coronary artery bypass in postinfarct patients: what can we learn from available literature?
----A Studies have shown that beta adrenergic antagonist therapy benefits patients with coronary disease through reduced mortality rate after acute myocardial infarction and reduced incidence of postoperative atrial fibrillation after coronary artery bypass grafting. The long-term benefit of this therapy in survivors of myocardial infarction who are subsequently revascularized, however, has not been defined or studied rigorously. We reviewed the published data to clarify the role of beta blockade in patients who had surgical revascularization after myocardial infarction. We found that patients who received beta blockers after myocardial infarction had a reduced mortality rate and fewer cardiac events in most clinical situations, a benefit which likely extends to patients who have had subsequent surgical revascularization.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_surgery_MeSH Myocardial_Infarction_surgery_MeSH M_Postoperative_Care_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH M_Survival_Rate_MeSH 
****** 12449448
----K E
----T Renin angiotensin aldosterone and adrenergic modulation in chronic heart failure: contemporary concepts.
----A Whereas the earlier conceptual targets of heart failure therapy, such as the cardio-renal and hemodynamic models, all fulfilled the basic needs of symptomatic relief and hemodynamic improvement, only the neurohormonal model has provided an effective target to address symptom relief in concert with survival benefits. Recent data allude to a disease-modifying effect of angiotensin-converting enzyme inhibitors (ACE-Is) in retarding the new development of heart failure in high-risk populations. Angiotensin receptor antagonists (ARBs) have not been demonstrated to be superior to ACE-Is and their value in achieving incremental benefits in addition to ACE-Is is limited to scenarios in which beta-adrenergic receptor blocker therapy is not applicable. Beta-adrenergic receptor blockade in addition to ACE inhibition offers incremental benefits that are achieved early and are beneficial in most stages of severity except in the presence of overt decompensation. Unlike ACE-Is, beta-adrenergic receptor blockers cannot be construed as a class but are heterogeneous in their therapeutic response.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Synergism_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH P_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH 
****** 12479763
----K I
----T Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
----A CONTEXT: Antihypertensive therapy is well established to reduce hypertension-related morbidity and mortality, but the optimal first-step therapy is unknown. OBJECTIVE: To determine whether treatment with a calcium channel blocker or an angiotensin-converting enzyme inhibitor lowers the incidence of coronary heart disease (CHD) or other cardiovascular disease (CVD) events vs treatment with a diuretic. DESIGN: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), a randomized, double-blind, active-controlled clinical trial conducted from February 1994 through March 2002. SETTING AND PARTICIPANTS: A total of 33 357 participants aged 55 years or older with hypertension and at least 1 other CHD risk factor from 623 North American centers. INTERVENTIONS: Participants were randomly assigned to receive chlorthalidone, 12.5 to 25 mg/d (n = 15 255); amlodipine, 2.5 to 10 mg/d (n = 9048); or lisinopril, 10 to 40 mg/d (n = 9054) for planned follow-up of approximately 4 to 8 years. MAIN OUTCOME MEASURES: The primary outcome was combined fatal CHD or nonfatal myocardial infarction, analyzed by intent-to-treat. Secondary outcomes were all-cause mortality, stroke, combined CHD (primary outcome, coronary revascularization, or angina with hospitalization), and combined CVD (combined CHD, stroke, treated angina without hospitalization, heart failure [HF], and peripheral arterial disease). RESULTS: Mean follow-up was 4.9 years. The primary outcome occurred in 2956 participants, with no difference between treatments. Compared with chlorthalidone (6-year rate, 11.5%), the relative risks (RRs) were 0.98 (95% CI, 0.90-1.07) for amlodipine (6-year rate, 11.3%) and 0.99 (95% CI, 0.91-1.08) for lisinopril (6-year rate, 11.4%). Likewise, all-cause mortality did not differ between groups. Five-year systolic blood pressures were significantly higher in the amlodipine (0.8 mm Hg, P =.03) and lisinopril (2 mm Hg, P<.001) groups compared with chlorthalidone, and 5-year diastolic blood pressure was significantly lower with amlodipine (0.8 mm Hg, P<.001). For amlodipine vs chlorthalidone, secondary outcomes were similar except for a higher 6-year rate of HF with amlodipine (10.2% vs 7.7%; RR, 1.38; 95% CI, 1.25-1.52). For lisinopril vs chlorthalidone, lisinopril had higher 6-year rates of combined CVD (33.3% vs 30.9%; RR, 1.10; 95% CI, 1.05-1.16); stroke (6.3% vs 5.6%; RR, 1.15; 95% CI, 1.02-1.30); and HF (8.7% vs 7.7%; RR, 1.19; 95% CI, 1.07-1.31). CONCLUSION: Thiazide-type diuretics are superior in preventing 1 or more major forms of CVD and are less expensive. They should be preferred for first-step antihypertensive therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_economics_MeSH Amlodipine_economics_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_economics_MeSH Calcium_Channel_Blockers_economics_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Chlorthalidone_MeSH S_economics_MeSH Chlorthalidone_economics_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_economics_MeSH Diuretics_economics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_economics_MeSH Lisinopril_economics_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 7992988
----K E
----T Effects of antihypertensive therapy on serum lipids.
----A PURPOSE: To compare and contrast the effects of antihypertensive agents on serum lipids and blood pressure in different patient populations. DATA SOURCES: A MEDLINE search and bibliographies from recent comprehensive reviews were used to identify trials that provided sufficient data to calculate the change in one or more serum lipid values measured before and after antihypertensive therapy. STUDY SELECTION: 474 controlled and uncontrolled clinical trials investigated the effects of 85 antihypertensive agents on lipids and blood pressure in more than 65,000 patients. DATA EXTRACTION: Data on triglyceride and total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol levels; blood pressure; patient characteristics; and study design. DATA SYNTHESIS: Differences in the effects of agents, adjusted for differences in patient populations and study design, were examined using multiple linear regression analysis that was weighted by study quality and inverse variance. Diuretics caused relative increases in cholesterol levels (regression coefficient = 0.13 mmol/L; 95% CI, 0.09 to 0.18 mmol/L) that were greater with higher doses (additional effect of high dose, 0.12 mmol/L; CI, 0.04 to 0.20 mmol/L) and were worse in blacks than in nonblacks (additional effect in blacks, 0.13 mmol/L; CI, 0.01 to 0.26 mmol/L). Beta-blockers caused increases in triglyceride levels (0.35 mmol/L; CI, 0.31 to 0.39 mmol/L) that were substantially smaller for agents with intrinsic sympathomimetic activity (amelioration of beta-blocker increase, -0.21 mmol/L; CI, -0.27 to -0.16 mmol/L). When combined with cardioselectivity, beta-blockers with intrinsic sympathomimetic activity favorably affected lipids and reduced both total (-0.14 mmol/L; CI, -0.24 to -0.04 mmol/L) and LDL cholesterol levels (-0.17 mmol/L; CI, -0.28 to -0.07 mmol/L). alpha-Blockers beneficially affected total cholesterol (-0.23 mmol/L; CI, -0.28 to -0.18 mmol/L), LDL cholesterol (-0.20 mmol/L; CI, -0.25 to 0.15 mmol/L), triglycerides (-0.07 mmol/L; CI, -0.11 to -0.03 mmol/L), and, in younger persons, HDL cholesterol (0.02 mmol/L; 0.01 to 0.04 mmol/L). Converting enzyme inhibitors reduced triglycerides (-0.07 mmol/L; CI, -0.12 to -0.02 mmol/L), and, in patients with diabetes, total cholesterol (-0.22 mmol/L; CI, -0.34 to -0.10 mmol/L). Vasodilators reduced total (-0.22 mmol/l; CI, -0.30 to -0.10 mmol/L) and LDL cholesterol (-0.22 mmol/L; CI, -0.29 to -0.11 mmol/L) and increased HDL cholesterol (0.06 mmol/L; CI, 0.02 to 0.09 mmol/L). CONCLUSION: With the exception of calcium antagonists, nearly all antihypertensive agents affect serum lipids. These effects differ among patient populations.
----P Journal_Article Meta-Analysis 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Controlled_Clinical_Trials_MeSH M_Female_MeSH M_Human_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Risk_Factors_MeSH 
****** 7798494
----K E
----T Predictors of systolic and diastolic improvement in patients with dilated cardiomyopathy treated with metoprolol.
----A OBJECTIVES. The aim of this study was to determine which patients will have systolic and diastolic improvement after beta-blockade with metoprolol. BACKGROUND. Beta-adrenergic blocking agents improve systolic and diastolic function in patients with heart failure. However, it is unclear which patients will respond best to therapy. METHODS. We retrospectively examined baseline characteristics of 24 patients who underwent double-blind then open-label treatment with metoprolol to determine which characteristic predicted improvement in systolic and diastolic function. Degree of improvement in systolic function (22 patients) was defined by the change in left ventricular ejection fraction after 3 months of therapy. Degree of improvement in diastolic function (15 patients) was defined as the change in left ventricular end-diastolic pressure and change in the slope of the isovolumetric relaxation rate-end-systolic pressure relation. RESULTS. Both systolic blood pressure at baseline (r = 0.54, p = 0.009) and the maximal positive value of the first derivative of left ventricular pressure with respect to time (peak +dP/dt) at baseline (r = 0.39, p = 0.07) correlated with improvement in ejection fraction after metoprolol treatment. Stepwise logistic regression demonstrated that only peak systolic pressure was an independent predictor of systolic improvement. Baseline heart rate, ventricular volumes, ejection fraction and adrenergic activation, as reflected by coronary sinus norepinephrine, did not predict response. Patients with the most diastolic impairment at baseline had the most favorable diastolic improvement. Those with the lowest myocardial respiratory quotient (most fatty acid utilization) at baseline also had the most marked reduction in left ventricular end-diastolic pressure. CONCLUSIONS. These data suggest that those patients with the highest peak systolic pressure, highest left ventricular end-diastolic pressure and most prolonged isovolumetric relaxation at baseline will respond best to therapy with metoprolol. However, other patients without these characteristics may also benefit.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_radionuclide_imaging_MeSH Cardiomyopathy__Congestive_radionuclide_imaging_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Heart_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Retrospective_Studies_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH 
****** 7798508
----K E
----T Medical treatment to reduce total ischemic burden: total ischemic burden bisoprolol study (TIBBS), a multicenter trial comparing bisoprolol and nifedipine. The TIBBS Investigators.
----A OBJECTIVES. We compared the effects of bisoprolol on transient myocardial ischemia with those of nifedipine in patients with chronic stable angina. BACKGROUND. Both beta-adrenergic blocking agents and calcium antagonists reduce transient ischemic episodes, but comparisons of these agents have been made in only a few larger studies. METHODS. The Total Ischemic Burden Bisoprolol Study (TIBBS) was a randomized double-blind controlled study with two parallel groups; 330 patients from 30 centers in seven European countries with stable angina pectoris, a positive exercise test and more than two transient ischemic episodes during 48 h of Holter monitoring (central evaluation) were included. Of these patients 161 were randomized to receive bisoprolol and 169 to receive nifedipine slow release. There were two treatment phases of 4 weeks each, with 48-h Holter monitoring after each phase. During phase 1, patients received either 10 mg of bisoprolol daily or 2 x 20 mg of nifedipine slow release. During phase 2, they received either 20 mg of bisoprolol daily or 2 x 40 mg of nifedipine slow release. RESULTS. In phase 1 of the trial, 4 weeks of bisoprolol therapy (10 mg daily) reduced the mean [+/- SD] number of transient ischemic episodes from 8.1 +/- 0.6 to 3.2 +/- 0.4/48 h. Nifedipine (2 x 20 mg) reduced transient ischemic episodes from 8.3 +/- 0.5 to 5.9 +/- 0.4/48 h. Total duration of ischemia was reduced from 99.3 +/- 10.1 to 31.9 +/- 5.5 min/48 h with bisoprolol and from 101 +/- 9.1 to 72.6 +/- 8.1 min/48 h with nifedipine. Reductions were statistically significant for both drugs; the difference between bisoprolol and nifedipine was also significant (p < 0.0001). Bisoprolol reduced the heart rate at onset of episodes by 13.7 +/- 1.4 beats/min from a baseline value of 99.5 +/- 1.2 beats/min (p < 0.001). Heart rate was unchanged with nifedipine. Bisoprolol had significantly higher responder rates than nifedipine. Doubling of the dose in phase 2 of the trial had small additive effects. Only bisoprolol showed a marked circadian effect by reducing the morning peak of transient ischemic episodes (by 68% at peak time, 8:00 to 8:59 AM). CONCLUSIONS. Both bisoprolol and nifedipine reduced the number and duration of transient ischemic episodes in patients with chronic stable angina. Bisoprolol was significantly more effective than nifedipine in both doses tested and reduced the morning peak of ischemic activity.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Europe_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH M_Remission_Induction_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 7801853
----K I
----T Platelet aggregability in vivo is attenuated by verapamil but not by metoprolol in patients with stable angina pectoris.
----A The effects of 1 month of treatment with either verapamil or metoprolol on several aspects of platelet function were studied at rest and during physical exercise or mental stress in patients with stable angina pectoris participating in the Angina Prognosis Study in Stockholm. Platelet aggregability was measured by filtragometry ex vivo, which reflects platelet aggregability in vivo and by Born aggregometry in vitro. Platelet secretion in vivo was assessed by measurements of beta-thromboglobulin in plasma. Verapamil reduced plasma norepinephrine levels (from 2.6 +/- 1.0 to 2.2 +/- 1.0 nmol/L; p < 0.01) and attenuated platelet aggregability at rest (filtragometry readings were prolonged from 219 to 295 seconds; p < 0.05, n = 46). Aggregability in platelet-rich plasma was not influenced. Metoprolol did not significantly affect filtragometry readings (n = 58) or aggregability in vitro (there was a tendency toward enhanced adenosine diphosphate sensitivity; p = 0.08). beta-thromboglobulin levels were low (approximately 25 ng/ml) and not influenced by either treatment. Physical exercise (bicycle ergometry) increased platelet aggregability in vivo both before and after drug treatment. Verapamil also attenuated platelet aggregability after exercise, whereas metoprolol had no such effect. Platelet function was not seriously altered by mental stress (Stroop's color word test) despite significant effects on hemodynamics and plasma catecholamines either before or after treatment with either drug. Thus, verapamil attenuates platelet aggregability in patients with stable angina pectoris, whereas metoprolol has no such effect.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Double-Blind_Method_MeSH M_Exertion_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH M_Stress__Psychological_MeSH S_physiopathology_MeSH Stress__Psychological_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 7806173
----K E
----T Noninvasive measurement of femoral blood flow and portal pressure response to propranolol in patients with cirrhosis.
----A This study investigated the correlation between changes in hepatic and systemic hemodynamics and femoral blood flow (FBF), measured by dual-beam pulsed wave Doppler, in 58 portal hypertensive patients receiving propranolol (0.15 mg/Kg intravenously; n = 44) or placebo (n = 14) under double-blind conditions. Placebo administration had no effects. Propranolol caused significant reductions (P < .0001) in hepatic venous pressure gradient (HVPG; from 19.1 +/- 4.1 to 16.2 +/- 4.2 mm Hg), azygos blood flow (from 563 +/- 204 to 387 +/- 176 mL/min), cardiac index (CI; from 4.4 +/- 1.0 to 3.3 +/- 0.8 L/m2/min), and FBF (from 237 +/- 79 to 176 +/- 58 mL/m2/min). In 17 patients HVPG decreased below 12 mm Hg and/or more than 20% of the baseline value (good response; mean change, -26 +/- 8%); in the remaining 27 patients (poor response) the mean change in HVPG was less: -9 +/- 6%. Patients with a good response had bled less often from varices, had significantly higher FBF (272 +/- 73 vs. 215 +/- 76 mL/m2/min) and lower baseline HVPG (16.8 +/- 3.9 vs. 20.6 +/- 3.6 mm Hg) than those with poor response in HVPG. The good response was also associated with greater decreases in FBF (-33 +/- 12 vs. -19 +/- 13% in poor responders), CI (-30 +/- 9 vs. -19 +/- 12%), and heart rate (-19 +/- 5 vs. -16 +/- 6%). A decrease in FBF of > 20% predicted a good response in 16 of 28 patients (positive predictive value, 57%).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Femoral_Vein_MeSH S_physiopathology_MeSH Femoral_Vein_physiopathology_MeSH S_ultrasonography_MeSH Femoral_Vein_ultrasonography_MeSH M_Hepatic_Veins_MeSH S_physiopathology_MeSH Hepatic_Veins_physiopathology_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH S_ultrasonography_MeSH Hypertension__Portal_ultrasonography_MeSH M_Liver_Cirrhosis_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH S_ultrasonography_MeSH Liver_Cirrhosis_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_Vein_MeSH S_physiopathology_MeSH Portal_Vein_physiopathology_MeSH S_ultrasonography_MeSH Portal_Vein_ultrasonography_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Regional_Blood_Flow_MeSH M_Support__Non-U_S__Gov't_MeSH M_Venous_Pressure_MeSH S_drug_effects_MeSH Venous_Pressure_drug_effects_MeSH 
****** 7828294
----K E
----T Role of cardiac beta 2-receptors in cardiac responses to exercise in cardiac transplant patients.
----A BACKGROUND: In healthy human hearts, beta 2-receptor-mediated chronotropic and inotropic responses contribute to the cardiac responses to beta-agonists. A (patho)physiological relevance for beta 2-receptor-mediated responses has so far not been demonstrated, in part because beta 1-receptor-mediated responses to cardiac neuronally released norepinephrine can mask beta 2-receptor-mediated responses. METHODS AND RESULTS: In the present study, we evaluated the blood pressure and heart rate responses to bicycle exercise in cardiac transplant patients (n = 7) compared with patients with essential hypertension (n = 8) on placebo and two doses of the beta 1-selective beta-blocker atenolol (25 and 50 mg/d) and the nonselective beta-blocker nadolol (20 and 40 mg/d), each dose for 1 week using a double-blind, randomized, crossover design. Exercise was performed 3 hours after dosing, using a stepwise increase in load until exhaustion. Exercise performance was less in the transplant patients and significantly further (25%) decreased by nadolol. Exercise caused equivalent increases in plasma norepinephrine in the two groups, but more marked increases in plasma epinephrine in the transplant patients despite less exercise. In the essential hypertension patients, systolic blood pressure increased by 80 mm Hg on placebo and 60 mm Hg on either blocker. The increase in heart rate (by about 75 beats per minute) was inhibited by 10% and 20% by the lower and higher doses, respectively, similar for the two blockers. In contrast, in the transplant patients, systolic blood pressure increased by 60 mm Hg on placebo, but this increase was totally blocked by either blocker. The heart rate increase (by 50 beats per minute on placebo) was blunted (dose related) by either blocker but 50% more by nadolol versus atenolol. CONCLUSIONS: The present study shows that cardiac beta 2-receptors contribute to a clear extent to the heart rate responses to endogenous circulating catecholamines in the absence of cardiac neuronally released norepinephrine. Nonselective beta-blockade probably is less well tolerated in cardiac transplant patients compared with beta 1-selective blockade.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH P_Exercise_MeSH M_Female_MeSH M_Heart_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH P_Heart_Transplantation_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Adrenergic__beta-2_MeSH S_physiology_MeSH Receptors__Adrenergic__beta-2_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7832129
----K E
----T How do smokers differ from nonsmokers in their response to thrombolysis? (the TIMI-4 trial)
----A Smokers with acute myocardial infarction appear to have a better outcome after thrombolysis than do nonsmokers. To identify factors that could contribute to this curious finding, we analyzed data from the Thrombolysis in Myocardial Infarction (TIMI-4) trial, in which 382 patients with acute myocardial infarction were randomized to tissue plasminogen activator, anistreplase, or both. Coronary angiography was performed 90 minutes and 18 to 36 hours after randomization, a myocardial perfusion scan was performed at 18 to 36 hours and before discharge, and a radionuclide ventriculogram was obtained before discharge. Angiographic and clinical outcome variables were determined in current smokers, ex-smokers, and nonsmokers, and regression analysis was used to correct for differences in baseline characteristics. The in-hospital mortality of current smokers was lower than that of ex-smokers and nonsmokers: 2.3% versus 5.2% versus 7.0%, respectively (p = 0.04 by paired comparison, current vs nonsmokers). Ninety minutes after randomization, the incidence of TIMI grade 3 flow was significantly higher in smokers than in ex-smokers and nonsmokers (55% vs 43% and 45%, p = 0.02); this difference was no longer observed at the second angiogram, nor did smokers differ from nonsmokers with respect to residual stenosis, thrombus grade, infarct size, ejection fraction, or recurrent ischemia. Because a strong inverse relation exists between TIMI grade 3 flow at 90 minutes and mortality, our findings suggest that the lower mortality of current smokers after thrombolytic therapy may be related to a higher incidence of early, complete reperfusion.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Double-Blind_Method_MeSH M_Female_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_radionuclide_imaging_MeSH Myocardial_Infarction_radionuclide_imaging_MeSH M_Plasminogen_Activators_MeSH S_therapeutic_use_MeSH Plasminogen_Activators_therapeutic_use_MeSH M_Regression_Analysis_MeSH P_Smoking_MeSH S_mortality_MeSH Smoking_mortality_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH 
****** 7832135
----K E
----T Effect of doxazosin or atenolol on exercise performance in physically active, hypertensive men.
----A The effects of doxazosin or atenolol on exercise capacity in 15 male distance runners (mean age +/- SD 43 +/- 10 years) were compared in a double-blind, crossover study. Subjects performed a maximal treadmill test and a timed 2-mile run before and after each drug treatment. Cardiac output was determined by acetylene rebreathing at rest and at 30%, 50%, and 75% of maximal oxygen consumption. Oxygen consumption was determined at the above-mentioned workloads and at maximal effort. Both drugs were titrated to produce similar reductions in blood pressure and the final doses of atenolol and doxazosin were 43 +/- 22 and 6 +/- 6 mg, respectively. Atenolol reduced cardiac output (p < 0.05) and heart rate (p < 0.001) at rest and at all exercise intensities compared with the prior placebo phase, whereas doxazosin increased cardiac output at rest and at 50% effort (p < 0.05). Consequently, cardiac output was higher (p < 0.01) with doxazosin than with atenolol at rest and at 30% and 50% effort. Heart rate was higher with doxazosin (p < 0.01) during all exercise workloads. Despite these changes in cardiovascular function, there were no significant differences between the effect of the 2 study drugs on maximal oxygen consumption or 2-mile run times. We conclude that atenolol decreases rest and exercise heart rate and cardiac output compared with doxazosin, but that at modest doses neither drug adversely affects exercise performance in male hypertensive runners.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Exercise_Test_MeSH M_Exertion_MeSH S_drug_effects_MeSH Exertion_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Physical_Endurance_MeSH S_drug_effects_MeSH Physical_Endurance_drug_effects_MeSH M_Running_MeSH S_physiology_MeSH Running_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7850941
----K E
----T Differential effects of chronic oral antihypertensive therapies on systemic arterial circulation and ventricular energetics in African-American patients.
----A BACKGROUND: A comprehensive evaluation of arterial load characteristics and left ventricular energetics in systemic hypertension has been limited by the need for invasive techniques to access instantaneous aortic pressure and flow. As a consequence of this methodological limitation, no data exist on the effects of long-term antihypertensive therapy on global arterial impedance properties and indexes of myocardial oxygen consumption (MVO2). Using recently validated noninvasive techniques, we compared in hypertensive patients the effects of chronic oral treatment with ramipril, nifedipine, and atenolol on arterial impedance and mechanical power dissipation as well as indexes of MVO2. METHODS AND RESULTS: Sixteen African-American subjects with systemic hypertension were studied with a randomized, double-blind, crossover protocol. Instantaneous central aortic pressure and flow, from which arterial load characteristics can be derived, were estimated from calibrated subclavian pulse tracings (SPTs) and continuous-wave aortic Doppler velocity in conjunction with two-dimensional (2D) echocardiographic measurements of the aortic annulus, respectively. To derive ventricular wall stress and indexes of MVO2, left ventricular short- (M-mode) and long-axis (2D echo) images were acquired simultaneously with SPTs. Data were collected at the end of a 2-week washout period (predrug control) and after 6 weeks of treatment with each agent. Although all three agents reduced diastolic blood pressure to the same extent, different effects on mean and systolic pressures and vascular impedance properties were noted. Nifedipine reduced total peripheral resistance (TPR; 1744 +/- 398 versus 1290 +/- 215 dyne-s/cm5) and increased arterial compliance (ACL; 1.234 +/- 0.253 versus 1.776 +/- 0.415 mL/mm Hg). This improvement in arterial compliance was not entirely accounted for by the reduction in distending pressure. Ramipril also decreased TPR (1740 +/- 292 versus 1437 +/- 290 dyne-s/cm5) and increased ACL (1.214 +/- 0.190 versus 1.569 +/- 0.424 mL/mm Hg), but with this agent, the change in arterial compliance was explained solely on the basis of a reduction in distending pressure. Atenolol, in contrast, did not affect either TPR or ACL. In agreement with the compliance results, nifedipine and ramipril significantly lowered the first two harmonics of the impedance spectrum, but atenolol did not. None of these agents resulted in a significant change in characteristic impedance or in the relative amplitude of the reflected pressure wave. Total vascular mechanical power and percent of oscillatory power remained unaltered with all antihypertensive treatments. Only ramipril and nifedipine reduced the integral of both meridional and circumferential systolic wall stresses, indicating that MVO2 per beat was reduced with these agents. Stress-time index, a measure of MVO2 per unit time, decreased significantly with ramipril but not with nifedipine because of an increase in heart rate noted in 10 of 16 patients (mean increase, 10 beats per minute). Thus, a reduction in MVO2 coupled with unchanged total vascular mechanical power suggests improved efficiency of ventriculoarterial coupling with ramipril and with nifedipine in the subset of patients in whom heart rate remained unchanged. In contrast, there was no evidence of a reduction in wall stress, stress integral, or stress-time index with atenolol. CONCLUSIONS: The noninvasive methodology used in this study constitutes a new tool for serial and simultaneous evaluation of arterial hemodynamics and left ventricular energetics in systemic hypertension. In this study, we demonstrate the differential effects of chronic antihypertensive therapies on systemic arterial circulation and indexes of MVO2 in African-American subjects. Consideration of drug-induced differential responses of arterial load and indexes of MVO2 with each drug may provide a more physiological approach to the treatment of systemic hypertension in indivi
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH P_African_Continental_Ancestry_Group_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Ultrasonography__Doppler_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7856528
----K E
----T Hemodynamic and energetic comparison of bucindolol and metoprolol for the treatment of congestive heart failure.
----A Although beta blockers have demonstrated a salutary effect on ventricular function in patients with heart failure, it is unclear whether a nonselective third-generation beta blocker produces different hemodynamic and energetic effects than a second-generation beta 1 selective agent. In 30 male patients with heart failure, we retrospectively analyzed hemodynamic data from 2 protocols examining the effects of a nonselective beta antagonist bucindolol (n = 15), and a highly selective beta 1 antagonist metoprolol (n = 15). Both studies were conducted in a similar fashion with patients undergoing cardiac catheterization before and after receiving 3 months of beta blockade. Both groups were matched at baseline in terms of ventricular function. beta blockade resulted in similar reductions in heart rate and similar improvements in ejection fraction, ventricular volumes, stroke and minute work, peak +dP/dt, and isovolumic relaxation in both groups. Only patients taking bucindolol had a significant within-group decrease in resting left ventricular end-diastolic pressure. The metoprolol group had a greater decrease in coronary sinus blood flow and myocardial oxygen consumption. Bucindolol increased cardiac index more than metoprolol, but did not increase stroke volume index more than metoprolol. The bucindolol group had an increase in systolic elastance, whereas the metoprolol group had a parallel left shift in this relation. Thus, metoprolol reduces coronary blood flow and myocardial oxygen consumption more than bucindolol, whereas bucindolol produces slightly more favorable improvements in resting cardiac index and end-diastolic pressure. Otherwise, these 2 agents produced similar hemodynamic changes.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7860905
----K E
----T Effect of amlodipine, atenolol and their combination on myocardial ischemia during treadmill exercise and ambulatory monitoring. Canadian Amlodipine/Atenolol in Silent Ischemia Study (CASIS) Investigators.
----A OBJECTIVES. This study compared the effects of amlodipine, atenolol and their combination on ischemia during treadmill testing and 48-h ambulatory monitoring. BACKGROUND. It is not known whether anti-ischemic drugs exert similar effects on ischemia during ambulatory monitoring and exercise treadmill testing. METHODS. Patients with stable coronary artery disease and ischemia during treadmill testing and ambulatory monitoring were randomized to receive amlodipine (n = 51) or atenolol (n = 49). Each group underwent a counterbalanced, crossover evaluation of single drug and placebo, followed by evaluation of the combination. RESULTS. Amlodipine and the combination prolonged exercise time to 0.1-mV ST segment depression by 29% and 34%, respectively (p < 0.001) versus 3% for atenolol (p = NS). During ambulatory monitoring, the frequency of ischemic episodes decreased by 28% with amlodipine (p = 0.083 [NS]), by 57% with atenolol (p < 0.001) and by 72% with the combination (p < 0.05 vs. both single drugs; p < 0.001 vs. placebo). Suppression of ischemia during exercise testing and ambulatory monitoring was similar in patients with and without exercise-induced angina. Exercise time to angina improved by 29% with amlodipine (p < 0.01), by 16% with atenolol (p < 0.05) and by 39% with the combination (p < 0.005 vs. placebo, atenolol and amlodipine). In patients with angina, total exercise time improved by 16% with amlodipine (p < 0.001), by 4% with atenolol (p = NS) and by 19% with the combination (p < 0.05 vs. placebo and either single drug). In those patients without angina, no therapy significantly improved total exercise time. CONCLUSIONS. Ischemia during treadmill testing was more effectively suppressed by amlodipine, whereas ischemia during ambulatory monitoring was more effectively suppressed by atenolol. The combination was more effective than either single drug in both settings.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Amlodipine_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Drug_Therapy__Combination_MeSH P_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 7532352
----K E
----T Effect of propranolol on circadian variation of ventricular arrhythmias in elderly patients with heart disease and complex ventricular arrhythmias.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cardiac_Complexes__Premature_MeSH S_drug_therapy_MeSH Cardiac_Complexes__Premature_drug_therapy_MeSH S_physiopathology_MeSH Cardiac_Complexes__Premature_physiopathology_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 7864430
----K E
----T Intraoperative hemodynamic, renin, and catecholamine responses after prophylactic and intraoperative administration of intravenous enalaprilat.
----A This study was designed to evaluate effects of enalaprilat, an angiotensin-converting enzyme inhibitor, on hemodynamic and hormonal responses during surgery at endotracheal intubation, incision, and limb-tourniquet inflation. Thirty patients undergoing limb procedures with general anesthesia (N2O/narcotic technique) and a pneumatic tourniquet were randomized to receive either preoperative enalaprilat (1.25 mg intravenously [i.v.] 20 min prior to induction) or intraoperative enalaprilat (0.625 mg i.v. at the onset of tourniquet-associated hypertension), with appropriate placebo controls. Arterial blood pressure and heart rate increased significantly in response to intubation in the placebo group. Although there were no significant differences in catecholamine levels, plasma renin activity was significantly increased at postincision in the preoperative-enalaprilat group versus the placebo group. This suggests that activation of the renin-angiotensin system may play a key role in mediation of intraoperative hemodynamic responses to endotracheal intubation. With respect to tourniquet hypertension, preoperative or intraoperative treatment with enalaprilat reduced neither the pressor response to tourniquet inflation nor the amount of enflurane subsequently required to control arterial blood pressure. These findings suggest that this response is mediated by pain pathways, and may be treated more effectively with anesthesia/analgesia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Enalaprilat_MeSH S_administration_&_dosage_MeSH Enalaprilat_administration_&_dosage_MeSH S_pharmacology_MeSH Enalaprilat_pharmacology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Intraoperative_Period_MeSH M_Middle_Aged_MeSH M_Preoperative_Care_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH P_Surgical_Procedures__Operative_MeSH 
****** 7871179
----K E
----T Cost-effectiveness analysis in heart disease, Part III: Ischemia, congestive heart failure, and arrhythmias.
----A Cost-effectiveness analyses were reviewed in the following diagnostic and treatment categories: acute myocardial infarction (MI) and diagnostic strategies for coronary artery disease (CAD), coronary artery bypass graft (CABG) surgery, percutaneous transluminal coronary angioplasty (PTCA), congestive heart failure (CHF), and arrhythmias. In the case of acute MI, coronary care units, as presently used, are rather expensive but could be made much more efficient with more effective triage and resource utilization; reperfusion via thrombolysis is cost-effective, as are beta-blockers and angiotensin-converting enzyme (ACE) inhibitors post-MI in appropriate patients. Cost-effectiveness of CAD screening tests depends strongly on the prevalence of disease in the population studied. Cost-effectiveness of CABG surgery depends on targeting; eg, it is highly effective for such conditions as left-main and three-vessel disease but not for lesser disease. PTCA appears to be cost-effective in situations where there is clinical consensus for its use, eg, severe ischemia and one-vessel disease, but requires further analysis based on randomized data; coronary stents also appear to be cost-effective. In preliminary analysis, ACE inhibition for CHF dominates, ie, saves both money and lives. Cardiac transplant appears to be cost-effective but requires further study. For arrhythmias, implantable cardioverter defibrillators are cost-effective, especially the transvenous device, in life-threatening situations; radiofrequency ablation is also cost-effective in patients with Wolff-Parkinson-White syndrome apart from asymptomatic individuals; and pacemakers have not been analyzed except in the case of biofascicular block, where results were variable depending on the situation and preceding tests.
----P Journal_Article Review Review__Academic 
----M M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_economics_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_economics_MeSH M_Anti-Arrhythmia_Agents_MeSH S_economics_MeSH Anti-Arrhythmia_Agents_economics_MeSH M_Arrhythmia_MeSH S_economics_MeSH Arrhythmia_economics_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Catheter_Ablation_MeSH S_economics_MeSH Catheter_Ablation_economics_MeSH M_Coronary_Artery_Bypass_MeSH S_economics_MeSH Coronary_Artery_Bypass_economics_MeSH M_Coronary_Care_Units_MeSH S_economics_MeSH Coronary_Care_Units_economics_MeSH M_Cost-Benefit_Analysis_MeSH M_Defibrillators__Implantable_MeSH S_economics_MeSH Defibrillators__Implantable_economics_MeSH M_Heart_Failure__Congestive_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_economics_MeSH Myocardial_Ischemia_economics_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Pacemaker__Artificial_MeSH S_economics_MeSH Pacemaker__Artificial_economics_MeSH M_Thrombolytic_Therapy_MeSH S_economics_MeSH Thrombolytic_Therapy_economics_MeSH 
****** 7887361
----K E
----T NSAIDs, antihypertensive agents and loss of blood pressure control.
----A It is common for patients seen by primary care physicians to be taking both nonsteroidal anti-inflammatory drugs (NSAIDs) and antihypertensive agents. If blood pressure control diminishes in these patients, the physician must evaluate the potential interaction between the two classes of medication. Although the increase in blood pressure secondary to NSAID use may be only 5 to 10 mm Hg, this increase may be enough to justify a change in medication. For this reason, it is important to evaluate the interaction between the two types of drugs and determine its clinical significance in specific patients.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_pharmacology_MeSH Anti-Inflammatory_Agents__Non-Steroidal_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_antagonists_&_inhibitors_MeSH Antihypertensive_Agents_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 7887841
----K 3
----T The efficacy of apraclonidine as an adjunct to timolol therapy. Apraclonidine Adjunctive Therapy Study Group [published errata  appear in Arch Ophthalmol 1995 Sep;113(9):1112 and 1995 Nov;113(11):1465]
----A OBJECTIVE: To compare the intraocular pressure (IOP) lowering efficacy of 0.5% and 1.0% apraclonidine hydrochloride when used adjunctively with 0.5% timolol maleate in 129 patients. DESIGN: A multicenter, randomized, double-masked clinical trial. Adult patients of either sex diagnosed as having either open-angle glaucoma or ocular hypertension were enrolled in the study. Patients using only 0.5% timolol maleate twice daily for at least 4 weeks and who had 8 AM IOPs of at least 22 mm Hg and no greater than 30 mm Hg 12 hours after dosing were eligible for the study. After 8 AM baseline IOPs were obtained while patients were taking timolol only, they were then randomized to receive either 0.5% or 1.0% apraclonidine twice daily in addition to their timolol. Intraocular pressures were measured at 8 AM (before morning dosing) and at 11 AM (3 hours after dosing) on days 14 and 90 and at 8 AM only on day 45. RESULTS: Both concentrations of apraclonidine produced significant IOP reductions from baseline at all visits (P < .001). At 8 AM, after the nighttime dose, the additional mean IOP reduction from the timolol baseline ranged from 2.5 to 3.3 mm Hg (10.3% to 13.6% reduction, respectively). At 11 AM, 3 hours after the morning dose, the additional IOP reduction from the timolol baseline ranged from 4.7 to 5.2 mm Hg (20.0% to 21.7%, respectively). No difference in IOP reduction was observed between the 0.5% and 1.0% apraclonidine concentrations and no loss of IOP efficacy was observed for either concentration for the duration of the study. Sensitivity to 0.5% and 1.0% apraclonidine was observed in nine (13.8%) and 13 (20.3%) patients, respectively. Overall, therapy was discontinued owing to ocular or nonocular side effects with 0.5% and 1.0% apraclonidine in 14 (21.5%) and 16 (25%) patients, respectively. CONCLUSIONS: We believe that 0.5% apraclonidine is equally effective as 1.0% apraclonidine when used twice daily as the first adjunctive drug to timolol. The drug effect is maintained for at least 90 days.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH M_Clonidine_MeSH S_administration_&_dosage_MeSH Clonidine_administration_&_dosage_MeSH S_adverse_effects_MeSH Clonidine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Clonidine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Synergism_MeSH M_Drug_Tolerance_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 7897129
----K E
----T Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta-adrenergic blockade.
----A OBJECTIVES. We examined the time course of ventricular functional improvement in patients with dilated cardiomyopathy who received beta-blockade and the long-term effects of beta-blockade on ventricular mass and geometry in these patients. BACKGROUND. Previous studies have shown that beta-adrenergic blocking agents when administered long term improve ventricular function in patients with heart failure. However, the time course of improvement in ventricular function and the long-term effects of beta-blockade on ventricular mass and geometry are not known. METHODS. Twenty-six men with dilated cardiomyopathy underwent serial echocardiography on days 0 and 1 and months 1 and 3 of either metoprolol (n = 16) or standard therapy (n = 10). At 3 months all patients on standard therapy were crossed over to metoprolol, and late echocardiograms were obtained after 18 +/- 5 (mean +/- SD) months of metoprolol therapy. All echocardiograms were read in blinded manner. RESULTS. Patients treated with metoprolol had an initial decline (day 1 vs. day 0) in ventricular function (increase in end-systolic volume and decrease in ejection fraction). Ventricular function improved between months 1 and 3 (p = 0.013, metoprolol vs. standard therapy). Left ventricular mass regressed at 18 months (333 +/- 85 to 275 +/- 53 g, p = 0.011) but not at 3 months. Left ventricular shape became less spherical and assumed a more normal elliptical shape by 18 months (major/minor axis ratio 1.5 +/- 0.2 to 1.7 +/- 0.2, p = 0.0001). CONCLUSIONS. Patients with heart failure treated with metoprolol do not demonstrate an improvement in systolic performance until after 1 month of therapy and may have a mild reduction in function initially. Long-term therapy with metoprolol results in a reversal of maladaptive remodeling with reduction in left ventricular volumes, regression of left ventricular mass and improved ventricular geometry by 18 months.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Analysis_of_Variance_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Observer_Variation_MeSH M_Systole_MeSH S_physiology_MeSH Systole_physiology_MeSH M_Time_Factors_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7900617
----K E
----T Time-series analysis of long-term ambulatory myocardial ischemia: effects of beta-adrenergic and calcium channel blockade.
----A We have previously demonstrated the utility of time-series analysis applied to 72-hour ambulatory electrocardiographic data in patients with coronary artery disease. The present investigation applied time-series analysis to long-term (120-hour) ambulatory electrocardiographic data to determine the minimal period of monitoring needed (1) to detect periodicity of ischemia-related variables in ambulatory patients, (2) to describe auto-correlation and cross-correlation functions for heart rate and ischemia, and (3) to describe the effects of beta-adrenergic and calcium channel blockade on circadian characteristics and coupling of heart rate and ischemia. A double-blind crossover design was used to obtain 120-hour recordings during placebo, atenolol (200 mg/day), and diltiazem (360 mg/day) administration. During all three treatment periods, distinct circadian variation of heart rate was documented by autocorrelation and Fourier analysis. Ischemia did not exhibit clear periodicity as indexed by autocorrelation in any period; however, it was coupled to heart rate in all treatment periods as reflected in cross-correlation analysis. Although diltiazem did not quantitatively alter the circadian characteristics of heart rate or ischemia, atenolol produced a shift in the coupling between remaining ischemia and heart rate in time. Significant autocorrelation was detected for all treatment periods after 72 hours of monitoring, suggesting that 72 hours is the minimum amount of time needed for analysis of ambulatory electrocardiographic data in patients with coronary artery disease.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH P_Electrocardiography__Ambulatory_MeSH M_Fourier_Analysis_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Signal_Processing__Computer-Assisted_MeSH M_Time_Factors_MeSH 
****** 7900628
----K E
----T Angiotensin-converting enzyme inhibitors and beta-blockers in long-term treatment of dilated cardiomyopathy.
----A This double-blind, randomized, long-term study investigated the effects of the angiotensin-converting enzyme inhibitor enalapril and the beta-blocker metoprolol on clinical, hemodynamic, angiographic, and neurohormonal parameters in patients with dilated cardiomyopathy and moderate cardiac functional impairment (left ventricular ejection fraction [LVEF] 35% +/- 6%). After 12 months of treatment, a 12% reduction in 24-hour heart rate was observed in both groups (p < 0.05), whereas heart rate during exercise was reduced only in the metoprolol group. Echocardiographic fractional shortening increased (enalapril: 17% +/- 6% to 21% +/- 7%; metoprolol: 21% +/- 9% to 29% +/- 7%; both p < 0.05), as did the angiographic LVEF (enalapril: 35% +/- 7% to 43% +/- 12%, p = 0.1; metoprolol: 34% +/- 7% to 44% +/- 9%, p < 0.05), whereas ventricular volume decreased. Initially, both groups were comparable in terms of all parameters investigated. After 12 months fractional shortening was greater, and the heart rate at 50 W was lower in the beta-blocker group. At the doses used, the effect of the beta-blocker on dilated cardiomyopathy with moderate functional impairment was at least as great as that of the angiotensin-converting enzyme inhibitor.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_diagnosis_MeSH Cardiomyopathy__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Cardiomyopathy__Congestive_epidemiology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH 
****** 7695954
----K 1
----T [The midterm inefficacy of 2 different dosages of chlorthalidone (50 and 25 mg/day) in the regression of left ventricular mass in arterial hypertension]
----A BACKGROUND: To evaluate the antihypertensive efficacy at rest and under exercise, and the modifications induced on the left ventricular mass in patients treated with two different doses of a diuretic. METHODS: Fifty hypertensive males, mean age 51 years, received during nine months 50 mg/day of chlortalidone and thirteen 25 mg/day for the next nine months. Baseline tension control and echocardiogram and each three months after starting therapy during the two phases of the study were performed. Thickness of the interventricular septum and posterior left ventricular wall in mm, left ventricular mass index in g/m2 were determined. RESULTS: The baseline septum was 15 +/- 3.3 mm, 14.6 +/- 3.1 mm at 9 months and 14.5 +/- 2.9 mm at 18 months, the posterior wall was 14.1 +/- 3.1 mm at baseline, 13.7 +/- 2.9 mm at 9 months and 13.6 +/- 2.9 mm at 18 months. The left ventricular mass index was 153 +/- 45 g/m2 at baseline, 146 +/- 36 g/m2 at 9 months and 144 +/- 39 g/m2 at 18 months. The antihypertensive efficacy at rest and under exertion was similar for the two doses of chlortalidone. CONCLUSIONS: After nine months of therapy the two doses of chlortalidone (50 and 25 mg/day) failed in reducing left ventricular mass. However, the design of the study and the small number of subjects enrolled introduce several important limitations to both the interpretation of our results and conclusions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chi-Square_Distribution_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_English_Abstract_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Remission_Induction_MeSH M_Time_Factors_MeSH 
****** 7702198
----K I
----T Celiprolol vs propranolol in unstable angina pectoris: a double-blind, randomized, parallel-group study.
----A Celiprolol, a novel beta blocker, may be more effective than propranolol in unstable angina pectoris because of both its beta-1-receptor selectivity and its vasodilator property. In the present report 53 patients with angiographic coronary artery disease but uncompromised left ventricular function and with electrocardiographically documented recurrent angina pectoris in spite of bed rest, aspirin, and repeated sublingual administration of nitroglycerin were studied. They were randomized for treatment with equipotent doses of either the nonselective beta blocker propranolol (80 mg/day) or the selective beta blocker with beta-2-agonistic property, celiprolol (200 mg/day) during one week. Angina frequency was higher in the propranolol group (P < 0.01), whereas myocardial oxygen demand as estimated by the double product (DP = SBP x HR, systolic blood pressure x heart rate) was equally reduced by the two beta blockers. Forearm blood flow was essentially higher in the celiprolol group (P < 0.001). A stepwise logistic regression analysis showed that the beneficial effects of the beta blockers were largely dependent on their effect on peripheral flow, in addition to reduction of the double product. The authors conclude that (1) Both celiprolol and propranolol largely reduce angina pectoris frequency in unstable angina pectoris. (2) Celiprolol contributes to nearly complete relief in three times as many patients as propranolol; after adjustment for double product or for systolic blood pressure plus heart rate it performs even eight times better. (3) The similar effects of the two compounds on the double product and the essentially different effects on peripheral flow support the conclusion that celiprolol exerts its beneficial effect to a large extent through its vasodilator property.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH S_physiopathology_MeSH Angina__Unstable_physiopathology_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH 
****** 7717013
----K 1
----T [Increased vagal activity after administration of the calcium antagonist diltiazem in patients with coronary heart disease]
----A The effects of the calcium channel blockers diltiazem on the parasympathetic nervous system were studied by using spectral analysis of heart rate variability, and were compared with the effects of the beta-receptor blocker metoprolol. The area under the curve of the high-frequency range (f = 0.18-0.35 Hz) during controlled respiratory rate (f = 0.25 Hz) was used as a quantitative index of parasympathetic activity. Twenty-four male patients with proven coronary artery disease and normal left ventricular function (LVEF > 60%) were studied 2 weeks after chronic treatment with diltiazem (3 x 60 mg daily) or metoprolol (3 x 50 mg daily) before and after administration of the drug. Twelve patients received diltiazem and 12 patients metoprolol. After administration of diltiazem the peripheral systolic blood pressure was reduced, but the parasympathetic activity was significantly higher than compared with the initial measurement. The same effect was seen for metoprolol, but a significant lower heart rate was present after administration. The relative area under the high-frequency range significantly increased at rest, by 110% after diltiazem and 70% after metoprolol. Diltiazem and metoprolol enhance the vagal influence at the heart, thereby leading to an enhancement of barosensitivity and of the respiratory sinus arrhythmia. This action may contribute to the beneficial effects of both drugs in patients with coronary artery disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Arrhythmia__Sinus_MeSH S_chemically_induced_MeSH Arrhythmia__Sinus_chemically_induced_MeSH S_diagnosis_MeSH Arrhythmia__Sinus_diagnosis_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_English_Abstract_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Homeostasis_MeSH S_drug_effects_MeSH Homeostasis_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Parasympathetic_Nervous_System_MeSH S_drug_effects_MeSH Parasympathetic_Nervous_System_drug_effects_MeSH M_Signal_Processing__Computer-Assisted_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Vagus_Nerve_MeSH S_drug_effects_MeSH Vagus_Nerve_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7717294
----K E
----T Effect of propranolol on circadian variation of myocardial ischemia in elderly patients with heart disease and complex ventricular arrhythmias.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Electrocardiography__Ambulatory_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Regression_Analysis_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7721386
----K E
----T Effect of antihypertensive treatment on small arteries of patients with previously untreated essential hypertension.
----A In a double-blind randomized trial, the effects of treatment with an angiotensin-converting enzyme (ACE) inhibitor (perindopril) and a beta-blocker (atenolol) on small artery structure were compared in previously untreated essential hypertensive patients. Subjects (diastolic blood pressure > or = 100 and < or = 120 mm Hg) were randomly assigned to treatment for 12 months with either perindopril (n = 13, 4 to 8 mg/d) or atenolol (n = 12, 50 to 100 mg/d); the dosage was adjusted upward and in some cases combined (n = 5, perindopril; n = 2, atenolol) with thiazide diuretic to achieve target blood pressure (diastolic blood pressure below 90 mm Hg). Before and at the end of treatment, gluteal biopsies were taken under local anesthetic; from these biopsies, two small arteries were dissected and mounted on a myograph for morphometry. The reduction in blood pressure with atenolol (drop in mean blood pressure 28.4 +/- 1.8 mm Hg) was greater than with perindopril (20.6 +/- 1.8 mm Hg, P < .05). Perindopril treatment caused an increase in small artery diameter (231 +/- 14 to 274 +/- 13 microns, P < .05) and a reduction in the ratio of media thickness to lumen diameter (7.94 +/- 0.65% to 5.96 +/- 0.42%, P < .05), whereas atenolol had no effect (246 +/- 14 to 231 +/- 13 microns and 7.14 +/- 0.47% to 6.79 +/- 0.45%, respectively). The change in small artery morphology caused by perindopril was not accompanied by any change in media cross-sectional area, suggesting that the change was due to "remodeling."(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7721419
----K E
----T Comparison of effects of angiotensin I-converting enzyme inhibition and beta-blockade for 2 years on function of small arteries from hypertensive patients.
----A The effect of treatment with two different antihypertensive agents on the function of small arteries from 17 patients with essential hypertension randomly assigned to receive either the angiotensin I-converting enzyme inhibitor cilazapril or the beta-blocker atenolol was investigated. Subcutaneous small arteries obtained from gluteal fat biopsies were studied on a wire myograph before treatment and at 1 and 2 years of treatment. Blood pressure was mildly elevated in both groups of patients (mean, 150/100 mm Hg) and was well controlled throughout the 2 years of treatment (mean, 130/85 mm Hg). We previously reported, in arteries from patients treated with cilazapril, an improvement at 1 year of treatment of the vasoconstrictor effect of endothelin-1, which had been significantly attenuated in the untreated hypertensive patients compared with normotensive subjects. After 2 years of treatment, this normalization of endothelin-1 response was still present in small arteries of patients treated with the angiotensin I-converting enzyme inhibitor, whereas in patients treated with atenolol, responses were still unchanged after 2 years of treatment. Endothelial function was tested by examining the response of norepinephrine-precontracted arteries to acetylcholine. Untreated hypertensive patients exhibited a slightly but significantly blunted vasorelaxation in response to 10 mumol/L acetylcholine compared with normotensive subjects. After 1 and 2 years of effective antihypertensive treatment, cilazapril-treated patients exhibited responses to acetylcholine that were not different from those of normotensive subjects, whereas atenolol-treated patients still had impaired responses.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_diagnostic_use_MeSH Acetylcholine_diagnostic_use_MeSH M_Adipose_Tissue_MeSH S_blood_supply_MeSH Adipose_Tissue_blood_supply_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Buttocks_MeSH M_Cilazapril_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Endothelins_MeSH S_therapeutic_use_MeSH Endothelins_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 7721498
----K I
----T Which drug to choose for stable angina pectoris: a comparative study between bisoprolol and nitrates.
----A The choice between beta-blockade or nitrates as first line treatment for stable angina pectoris is based upon the different mechanisms of action and patient characteristics. We performed a clinical trial comparing the efficacy of the longacting beta-blocker bisoprolol once daily and the short acting nitrate, isosorbide dinitrate, three times daily in the reduction of anginal complaints in daily life and under stress. Thirty patients were enrolled in a double-blind randomised cross-over study. Both bisoprolol and isosorbide dinitrate were effective in reducing anginal attacks and nitroglycerin consumption significantly, but bisoprolol was significantly more effective than isosorbide dinitrate. Bisoprolol improved the workload during bicycle exercise testing significantly, but the improvement with isosorbide dinitrate was not significant. Despite the reduction in maximal rate pressure product, bisoprolol was significantly (P < 0.05) more effective at improving total workload and reducing the time to onset of angina than isosorbide dinitrate. The rate pressure product did not change significantly with isosorbide dinitrate. In this study, bisoprolol 10 mg once daily was more effective and caused less side effects than isosorbide dinitrate 20 mg three times a day. It seems questionable if monotherapy of isosorbide dinitrate 20 mg t.i.d is an adequate drug regime for stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 7722114
----K E
----T Carvedilol improves left ventricular function and symptoms in chronic heart failure: a double-blind randomized study.
----A OBJECTIVES. This study assessed the safety and efficacy of carvedilol in patients with heart failure caused by idiopathic or ischemic cardiomyopathy. BACKGROUND. Carvedilol is a mildly beta 1-selective beta-adrenergic blocking agent with vasodilator properties. Beta-blockade may be beneficial in patients with heart failure, but the effects of carvedilol are not known. METHODS. Sixty patients with heart failure (New York Heart Association functional classes II to IV) and left ventricular ejection fraction < or = 0.35 were enrolled in the study. All patients tolerated challenge with carvedilol, 3.125 mg twice a day, and were randomized to receive carvedilol (n = 36) versus placebo (n = 24). Study medication was titrated over 1 month from 6.25 to 25 mg twice a day (< 75 kg) or 50 mg twice a day (> 75 kg) and continued for 3 months. One placebo-treated and two carvedilol-treated patients did not complete the study. RESULTS. Carvedilol therapy resulted in a significant reduction in heart rate and mean pulmonary artery and pulmonary capillary wedge pressures and a significant increase in stroke volume and left ventricular stroke work. Left ventricular ejection fraction increased 52% in the carvedilol group (from 0.21 to 0.32, p < 0.0001 vs. placebo group). Carvedilol-treated patients also reported a significant lessening of heart failure symptoms (p < 0.05 vs. placebo group). Submaximal exercise duration tended to increase with carvedilol therapy (from 688 +/- 31 s to 871 +/- 32 s), but this change was not significantly different from that with placebo therapy by between-group analysis. Peak oxygen consumption during maximal exercise did not change. CONCLUSIONS. Long-term carvedilol therapy improves rest cardiac function and lessens symptoms in patients with heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7722129
----K E
----T Treatment with beta-adrenergic blocking agents after myocardial infarction: from randomized trials to clinical practice.
----A OBJECTIVES. Our aim was to determine the percent of patients with myocardial infarction who are treated with beta-adrenergic blocking agents in dosages proved to be effective in preventing death after a heart attack. BACKGROUND. In the prospective randomized trials showing that beta-blocker treatment improves survival rates after myocardial infarction, relatively high dosages of these agents were used. However, it is not known whether these dosages are used in current clinical practice. METHODS. In a retrospective analysis of clinical data from 606 consecutive survivors of myocardial infarction at four university hospitals in three countries, we assessed the number of infarct survivors receiving prospectively defined "effective dosages" of beta-blockers. We defined these dosages as those that demonstrated improved survival rates of infarct survivors who received active drug in large, prospective, double-blind, placebo-controlled trials. RESULTS. Only 58% of infarct survivors with no contraindications to beta-blockers received these drugs at the time of hospital discharge, and only 11% received dosages equivalent to > 50% of the effective dosages. Independent predictors of failure to prescribe beta-blockers to infarct survivors without contraindications to these drugs were the use of diuretic agents, transient heart failure, impaired left ventricular function and increased patient age. Among patients receiving beta-blockers, only the use of propranolol predicted prescription of a low beta-blocker dosage. CONCLUSIONS. Failure to prescribe beta-blockers after myocardial infarction is common but in most cases is not due to clear contraindications. Many patients not receiving beta-blockers belong to subgroups that would derive the greatest benefit from such treatment. Finally, even when beta-blockers are prescribed, the dosages used are considerably lower than those proved to be effective in preventing death after myocardial infarction.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH M_Aged_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Survivors_MeSH 
****** 7723351
----K I
----T Increase in plasma levels of adenosine and adenine nucleotides after intravenous infusion of buflomedil in humans.
----A To clarify the mode of action of the vasoactive agent buflomedil, we evaluated plasma levels of adenosine and adenine nucleotides after intravenous (i.v.) infusion in humans of 50, 100, and 200 mg of the drug in 20 min. Buflomedil induced an increase of the same order of magnitude in plasma levels of adenosine and adenine nucleotides. Maximal adenosine increase (84%) was observed at the end of the infusion period, whereas peak plasma levels of ATP and ADP (69 and 55%, respectively) and of AMP (61%) were detected 10 and 5 min after discontinuation of infusion, respectively. Although the exact mode of action of buflomedil at the molecular level remains unclear, some indirect findings suggest that the increase in adenosine may be due to enhanced release rather than to inhibition of cell uptake. Because such activity of buflomedil consists of enhancement of physiologic mechanisms of vasodilation and tissue protection occurring in the course of ischemic events, new pharmacologic perspectives for the drug may arise.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adenine_Nucleotides_MeSH S_blood_MeSH Adenine_Nucleotides_blood_MeSH M_Adenosine_MeSH S_blood_MeSH Adenosine_blood_MeSH M_Adenosine_Diphosphate_MeSH S_blood_MeSH Adenosine_Diphosphate_blood_MeSH M_Adenosine_Monophosphate_MeSH S_blood_MeSH Adenosine_Monophosphate_blood_MeSH M_Adenosine_Triphosphate_MeSH S_blood_MeSH Adenosine_Triphosphate_blood_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Arterial_Occlusive_Diseases_MeSH S_drug_therapy_MeSH Arterial_Occlusive_Diseases_drug_therapy_MeSH M_Chromatography__High_Pressure_Liquid_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pyrrolidines_MeSH S_administration_&_dosage_MeSH Pyrrolidines_administration_&_dosage_MeSH S_pharmacology_MeSH Pyrrolidines_pharmacology_MeSH S_therapeutic_use_MeSH Pyrrolidines_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 7723358
----K E
----T Does calcium channel blockade and beta-adrenergic blockade affect platelet function and fibrinolysis to a varying degree?
----A The effects of isradipine and atenolol on platelet function and fibrinolytic activity were studied in 10 male patients with mild untreated hypertension. After a 2-week placebo run-in period, the volunteers were randomized to either isradipine 2.5 mg twice daily or atenolol 100 mg daily for a 6-month period. Those initially receiving isradipine then received atenolol and vice versa. After each therapy regimen, blood was drawn at rest and 1 h after exercise during a maximum exercise test. Platelet activity in vivo was estimated as release of B-TG and PF-4. Fibrinolytic activity was estimated as the fast-acting inhibitor against tissue plasminogen activator usually termed PAI-1. During atenolol and isradipine therapy, blood pressure (BP) was equally reduced (p < 0.05). Heart rate (HR) decreased during atenolol treatment but was not changed by isradipine. Platelet activity in vivo estimated as B-TG and PF-4 decreased irrespective of therapy (p < 0.02). During atenolol, as during placebo therapy, exercise resulted in a significant increase in platelet activity, as shown by an increase in B-TG (p < 0.02) and in PF-4 (p < 0.01). Such increase was not observed during isradipine treatment. Both treatments tended to improve fibrinolysis, as shown by a decrease in PAI, 1 h after exercise. Reducing BP with isradipine or atenolol results in a similar decrease in platelet activity and PAI-level, tested at rest and 1 h after rest, respectively. During exercise, platelet activity increased during atenolol treatment; such change did not occur during isradipine treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Platelets_MeSH S_drug_effects_MeSH Blood_Platelets_drug_effects_MeSH S_physiology_MeSH Blood_Platelets_physiology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_MeSH M_Female_MeSH M_Fibrinolysis_MeSH S_drug_effects_MeSH Fibrinolysis_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isradipine_MeSH S_administration_&_dosage_MeSH Isradipine_administration_&_dosage_MeSH S_pharmacology_MeSH Isradipine_pharmacology_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Plasminogen_Activator_Inhibitor_1_MeSH S_metabolism_MeSH Plasminogen_Activator_Inhibitor_1_metabolism_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH M_Radioimmunoassay_MeSH M_beta-Thromboglobulin_MeSH S_metabolism_MeSH beta-Thromboglobulin_metabolism_MeSH 
****** 7731256
----K E
----T Adjunctive therapy in the management of patients with acute myocardial infarction.
----A Adjunctive therapy for acute myocardial infarction should include aspirin, beta-adrenergic blocking agents, and, in most patients, consideration of the use of angiotensin-converting enzyme inhibitors, especially if left ventricular function is reduced. Heparin has an important adjunctive role in enhancing early vessel patency in patients who receive tissue-type plasminogen activator and in decreasing the frequency of reocclusion of an infarct-related artery during any thrombolytic therapy. Heparin must also be administered to all patients who undergo primary angioplasty. Intravenously administered nitroglycerin and orally administered nitrates are probably most effective in patients with symptomatic ischemia. Calcium channel blockers and prophylactic antiarrhythmic agents are not indicated for most patients with acute myocardial infarction. Currently, insufficient evidence is available to recommend the widespread use of intravenously administered magnesium sulfate in the setting of acute myocardial infarction. In patients with ischemic pain, judicious intravenous administration of morphine can provide relief. Use of warfarin sodium should be reserved for patients at risk for left ventricular mural thrombus. Although the use of lipid-lowering agents after myocardial infarction has been controversial, recent studies have demonstrated the importance of such therapy for secondary prevention of death and morbidity.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Magnesium_Sulfate_MeSH S_therapeutic_use_MeSH Magnesium_Sulfate_therapeutic_use_MeSH M_Morphine_MeSH S_therapeutic_use_MeSH Morphine_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Warfarin_MeSH S_therapeutic_use_MeSH Warfarin_therapeutic_use_MeSH 
****** 7731301
----K E
----T [Effect of 3 hypertensive++ agents on ventricular geometry and function]
----A BACKGROUND: To assess the prevalence of left ventricular hypertrophy in hypertensive patients referred to an outpatient cardiology unit, and to assess its evolution under antihypertensive treatment. METHODS: One hundred and seven mild to moderate hypertensive patients were randomized to receive either xipamide, verapamil or atenolol. Cross-sectional echocardiography was performed in order to assess left ventricular mass and function. RESULTS: Mean age was 56 years, with a 4:1 female/male ratio. Mean follow-up was 120 days. Left ventricular hypertrophy was very common (65%) and decreased to 54% under antihypertensive treatment. Left ventricular mass decreased from 134.3 g/m2 to 118.1 g/m2 (p < 0.001). Concentric hypertrophy was the most common geometric pattern (42%), decreasing to 30% with treatment. Xipamide decreased ventricular mass by decreasing left ventricular diameters, while verapamil and atenolol decreased left ventricular thickness, mainly in septal wall. Systolic function was not modified during the treatment period. Diastolic function was not modified by xipamide and verapamil, and improved with atenolol. CONCLUSIONS: Left ventricular hypertrophy is very frequent when determined by echocardiography and all three drugs produced regression of left ventricular hypertrophy in a different way with respect to left ventricle geometry, an effect which could have potential therapeutic implications.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_epidemiology_MeSH Hypertrophy__Left_Ventricular_epidemiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Verapamil_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH M_Xipamide_MeSH S_pharmacology_MeSH Xipamide_pharmacology_MeSH S_therapeutic_use_MeSH Xipamide_therapeutic_use_MeSH 
****** 7737712
----K E
----T Different effects of fosinopril and atenolol on wave reflections in hypertensive patients.
----A We conducted this study to compare the effects of fosinopril versus atenolol on peripheral blood pressure, central arterial wave reflection, and left ventricular mass in a group of patients with essential hypertension. We conducted a double-blind, randomized trial of fosinopril and atenolol in 79 hypertensive patients (52 men, 27 women; mean age, 45.8 +/- 8.5 years; range, 30 to 68 years). Carotid pressure waveforms were recorded noninvasively by applanation tonometry with a Millar micromanometer-tipped probe. The extent of wave reflection was estimated by the augmentation index defined as the ratio of the amplitude of pressure wave above its systolic shoulder to the pulse pressure. The augmentation index, left ventricular mass index by two-dimensional echocardiography, and 24-hour ambulatory blood pressures were determined before and after 8 weeks of daily treatment with fosinopril (10 to 20 mg) or atenolol (50 to 100 mg) with or without diuretics and compared with those values in 79 normotensive control subjects. After 8 weeks of treatment, both drugs lowered 24-hour ambulatory peripheral systolic and diastolic pressures into the normal range to a similar extent (fosinopril, -18/-13 mm Hg; atenolol, -23/-17 mm Hg, both P = NS). On the other hand, whereas the elevated augmentation index in hypertensive patients compared with normotensive subjects (16 +/- 11% versus 10 +/- 8%) was completely normalized by fosinopril (-9.3 +/- 9.8%, P < or = .002), it was lowered by atenolol (-4.8 +/- 8.9%, P < .002) but to a significantly smaller extent (fosinopril versus atenolol effect, P = .04).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fosinopril_MeSH S_pharmacology_MeSH Fosinopril_pharmacology_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 7738291
----K 4
----T [Hypotensive action of 0.5% carteolol versus 0.1% timolol in patients with intraocular hypertension]
----A PURPOSE: The aim of the study was to compare 2 beta-blocker eye drops at a low concentration: 0.5% carteolol and 0.1% timolol. METHODS: The study was designed as a random-order, double-blinded comparison of 2 parallel treatment groups. Fifty patients with early primary open angle glaucoma or high intraocular pressure were included. The treatment lasted 4 weeks, on the basis of 1 drop twice daily. Diurnal I.O.P. curve was assessed with 4 measurements from 8.30 a.m. to 4.30 p.m. before and after treatment. The 8.30 a.m. measure of the final assessment of I.O.P. curve was established prior to morning medication. The mean values of the 4 measures were compared. RESULTS: Both treatments reduced IOP by a comparable amount: 4.25 +/- 1.2 mmHg (mean +/- SD) for carteolol and 4.69 +/- 1.9 mmHg for timolol. The decrease of IOP was found at every time of assessment, without any significant difference between treatments. Both eye drops were very well tolerated. CONCLUSION: The results of this study show that the new beta-blocker eye drop solution 0.5% carteolol is effective for initial management of high intraocular pressure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Carteolol_MeSH S_therapeutic_use_MeSH Carteolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 7745771
----K E
----T Variations in patient management and outcomes for acute myocardial infarction in the United States and other countries. Results from the GUSTO trial. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.
----A OBJECTIVE--To examine differences in outcomes and patient management between patients in the United States and outside the United States undergoing thrombolysis for acute myocardial infarction. DESIGN, SETTING, AND PATIENTS--Patients in the United States (n = 23,105) and 14 other countries (n = 17,916) were randomized to receive streptokinase plus either subcutaneous or intravenous (IV) heparin, accelerated recombinant tissue-type plasminogen activator (rt-PA) plus IV heparin, or combined streptokinase and rt-PA plus IV heparin. OUTCOME MEASURES--Differences in 30-day mortality and patient management were compared among treatments and between US and non-US patients. Treatment-by-country interactions were assessed by logistic regression analyses. Expected mortality of US and non-US patients was estimated using a predictive model and was compared with observed mortality. RESULTS--Mortality reduction with accelerated rt-PA vs streptokinase was greater in the United States (1.2% absolute decrease vs 0.7% elsewhere), but the test for treatment-by-country interaction against streptokinase was not significant (P = .30). Benefits of accelerated rt-PA over combination therapy were observed in the United States, but not in other countries (P = .02). Despite differences in base-line characteristics and patient management, 30-day mortality was not significantly different: 6.8% in the United States vs 7.2% elsewhere (P = .09). After adjustment for baseline differences, observed vs predicted outcomes were slightly better in the United States (6.8% vs 7.0%) than elsewhere (7.2% vs 7.0%), indicating that enrollment in the United States was a marginally significant predictor of better survival (P = .047). CONCLUSIONS--No significant evidence for a differentially greater benefit of accelerated rt-PA over streptokinase was found in US vs non-US patients. However, increased procedure and treatment use in the United States was associated with only a small decrease in short-term mortality. Long-term follow-up is required to clarify the relationship between survival and the more intensive US management approach.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Australia_MeSH M_Belgium_MeSH M_Canada_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_France_MeSH M_Germany_MeSH M_Great_Britain_MeSH M_Heparin_MeSH S_administration_&_dosage_MeSH Heparin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Ireland_MeSH M_Israel_MeSH M_Logistic_Models_MeSH M_Luxembourg_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Netherlands_MeSH M_New_Zealand_MeSH M_Poland_MeSH M_Recombinant_Proteins_MeSH S_therapeutic_use_MeSH Recombinant_Proteins_therapeutic_use_MeSH M_Spain_MeSH M_Streptokinase_MeSH S_administration_&_dosage_MeSH Streptokinase_administration_&_dosage_MeSH S_therapeutic_use_MeSH Streptokinase_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Switzerland_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_administration_&_dosage_MeSH Tissue_Plasminogen_Activator_administration_&_dosage_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH 
****** 7751430
----K E
----T First-line therapy option with low-dose bisoprolol fumarate and low-dose hydrochlorothiazide in patients with stage I and stage II systemic hypertension.
----A This 30-center, randomized, double-blind, placebo-controlled, parallel-group study was designed to (1) establish that 6.25 mg of hydrochlorothiazide (HCTZ) given once daily with 5 mg of bisoprolol fumarate can contribute to antihypertensive effectiveness in patients with stage I and stage II (mild to moderate) systemic hypertension; and (2) assess whether this formulation was more effective or possessed a safety advantage over standard monotherapy with bisoprolol or 25 mg of HCTZ. Results showed that HCTZ 6.25 mg contributed significantly to the antihypertensive effectiveness of bisoprolol 5 mg. Bisoprolol 5 mg/HCTZ 6.25 mg (B5/H6.25) produced significantly greater mean reductions from baseline in sitting systolic and diastolic blood pressure (-15.8 mm Hg/-12.6 mm Hg) than bisoprolol 5 mg alone (-10.0 mm Hg/-10.5 mm Hg) and HCTZ 25 mg alone (-10.2 mm Hg/-8.5 mm Hg). A 73% response rate was achieved with the low-dose formulation compared with 61% for the bisoprolol 5 mg (B5) group and 47% for the HCTZ 25 mg (H25) group. B5/H6.25 was found to be significantly more effective than B5 or H25 in all subgroups of patients, regardless of gender, race, age, or smoking history. Antihypertensive effects were maintained during the 24-hour dosing interval. The incremental effectiveness of B5/H6.25 was not accompanied by an increase in the frequency or severity of adverse experiences; the incidence of adverse experiences in the B5/H6.25 group was comparable to that in the placebo group. B5/H6.25 was shown to provide safety advantages over H25, as shown by less hypokalemia (< 1% with B5/H6.25 versus 6.5% with H25).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7752174
----K E
----T Effect of celiprolol and metoprolol on lipids, fibrinogen and airways function in hyperlipidaemic hypertensives: a randomised double-blind long-term parallel group trial.
----A The effects of celiprolol 200 mg or 400 mg once daily on blood pressure (BP), serum lipids, plasma fibrinogen and airways function was compared with the effects of metoprolol 100 mg or 200 mg once daily in 171 patients with mild to moderate hypertension and coexistent hyperlipidaemia in a double-blind, multicentre study lasting 1 year. Significant decreases in systolic and diastolic blood pressure and heart rate were observed compared with baseline (DBP: celiprolol -13.3 mm Hg, P < 0.0001; metoprolol -14.3 mm Hg, P < 0.0001; SBP: celiprolol -18.2 mm Hg, P < 0.0001; metoprolol -20.5 mm Hg, P < 0.0001; heart rate celiprolol -4 beats/min, P < 0.003; metoprolol -12 beats/min, P < 0.0001). There was no difference between the effects of the two treatments on BP but celiprolol had less effect on heart rate than metoprolol, (celiprolol-metoprolol 7.3 beats/min, P = 0.0002). When compared with baseline values celiprolol significantly reduced serum low density lipoprotein cholesterol (LDL-C) (-5.8%, P = 0.0401) and produced a slight increase in high density lipoprotein cholesterol (HDL-C) which approached statistical significance (4.1%, P = 0.0659). Metoprolol significantly increased serum triglycerides (32%, P = 0.0001) and the total/HDL-C ratio (7.4%, P = 0.0192). Compared with metoprolol, celiprolol significantly reduced LDL-C (-7.3%, P = 0.0062), total cholesterol (-4.5%, P = 0.0085), apoliproprotein B (-10.1%, P = 0.0001), the apolipoprotein B/A1 ratio (-10.9%, P = 0.0001), the total cholesterol/HDL-C ratio (-10.8%, P = 0.0001) and triglycerides (-24.8%, P = 0.0001), and significantly increased HDL-C (6.0%, P = 0.0043).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Celiprolol_MeSH S_administration_&_dosage_MeSH Celiprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Celiprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_drug_effects_MeSH Fibrinogen_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipoproteins_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH M_Lipoproteins__HDL_MeSH S_drug_effects_MeSH Lipoproteins__HDL_drug_effects_MeSH M_Lipoproteins__LDL_MeSH S_drug_effects_MeSH Lipoproteins__LDL_drug_effects_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Peak_Expiratory_Flow_Rate_MeSH S_drug_effects_MeSH Peak_Expiratory_Flow_Rate_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 7752178
----K E
----T Different long-term metabolic effects of enalapril and atenolol in patients with mild hypertension. EGTA Group.
----A The primary objective in this multicentre, double-blind randomised, parallel study was to compare the metabolic effects of 12 months of treatment with an ACE inhibitor (enalapril) with those of a selective beta-blocker (atenolol) in patients with mild hypertension. The patients (35-69 years of age) were included if they were without antihypertensive drugs and after six months of nonpharmacological treatment had supine DBPs between 90 and 104 mmHg; 220 patients were randomised to enalapril (20 or 40 mg/day) and 218 to atenolol (50 or 100 mg/day). After 12 months of treatment, atenolol significantly increased the glucose concentrations at 60, 90 and 120 minutes after an oral intake of 75 g glucose (P < 0.01), while enalapril did not. Atenolol significantly increased fasting blood glucose and insulin concentration 120 minutes after glucose intake, while enalapril did not. Plasma total cholesterol and triglycerides increased significantly in patients having atenolol but not in those having enalapril. HDL cholesterol decreased significantly in the atenolol group but not in the enalapril group. The proportions of patients with clinical adverse experiences were similar in both treatment groups. These results indicate that enalapril does not influence either glucose tolerance or lipoprotein metabolism while atenolol does. These findings are consistent over the 12 month treatment period and confirm earlier short-term study results.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Glucose_MeSH S_metabolism_MeSH Glucose_metabolism_MeSH M_Glucose_Tolerance_Test_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_metabolism_MeSH Hemoglobin_A__Glycosylated_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipoproteins_MeSH S_metabolism_MeSH Lipoproteins_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Time_Factors_MeSH 
****** 7755948
----K E
----T Department of veterans Affairs single-drug therapy of hypertension study. Revised figures and new data. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A The antihypertensive efficacy of six drugs and placebo was compared in 1292 men with untreated diastolic blood pressure of 95 to 109 mm Hg. The primary end point "success" was defined as the patient having achieved a diastolic blood pressure of < 90 mm Hg at the end of the drug titration period and having maintained a diastolic blood pressure of < 95 mm Hg for 1 year without drug intolerance. The original published success rate data (N Engl J Med 1993;328:914-921) were discovered to be in error due to a computer programming code omission (N Engl J Med 1994;330:1689). This paper presents corrected graphic figures. The corrected success rates were generally higher than originally published. Overall, diltiazem (72%) was significantly higher than hydrochlorothiazide (55%), prazosin (54%), captopril (50%), and placebo (31%); clonidine (62%) and atenolol (60%) were intermediate. There were some changes in the hierarchy of drug response, but important differences in success rates according to age by race subgroups remained. Whites responded well to all drug classes, except for lower efficacy of hydrochlorothiazide in younger whites. Blacks responded better to diltiazem than other agents. In addition, we have analyzed the data using a definition of success based on < 90 mm Hg for 1 year. Use of the <90 mm Hg criterion reduced the rate of success, but had only a minor effect on the drug success rate hierarchy. We conclude that single-drug antihypertensive therapy is effective in a majority of stage 1 to 2 diastolic hypertensive patients, although there are important age-by-race differences in success rates among various drug classes.
----P Journal_Article 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Data_Interpretation__Statistical_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_United_States_MeSH M_Veterans_MeSH 
****** 7759701
----K I
----T Selection of medical treatment in stable angina pectoris: results of the International Multicenter Angina Exercise (IMAGE) Study.
----A OBJECTIVES. The present study was designed to investigate which characteristics of anginal symptoms or exercise test results could predict the favorable anti-ischemic effect of the beta-adrenergic blocking agent metoprolol and the calcium antagonist nifedipine in patients with stable angina pectoris. BACKGROUND. The characteristics of anginal symptoms and the results of exercise testing are considered of great importance for selecting medical treatment in patients with chronic stable angina pectoris. However, little information is available on how this first evaluation may be used to select the best pharmacologic approach in individual patients. METHODS. In this prospective multicenter study, 280 patients with stable angina pectoris were enrolled in 25 European centers. After baseline evaluation, consisting of an exercise test and a questionnaire investigating patients' anginal symptoms, the patients were randomly allocated to double-blind treatment for 6 weeks with either metoprolol (Controlled Release, 200 mg once daily) or nifedipine (Retard, 20 mg twice daily) according to a parallel group design. At the end of this period, exercise tests were repeated 1 to 4 h after drug intake. RESULTS. Both metoprolol and nifedipine prolonged exercise tolerance over baseline levels; the improvement was greater in the patients receiving metoprolol (p < 0.05). Multivariate analysis revealed that low exercise tolerance was the only variable associated with a more favorable effect within each treatment group. Metoprolol was more effective than nifedipine in patients with a lower exercise tolerance or with a higher rate-pressure product at rest and at ischemic threshold. None of the characteristics of anginal symptoms or exercise test results predicted a greater efficacy of nifedipine over metoprolol. CONCLUSIONS. The results of a baseline exercise test, but not the characteristics of anginal symptoms, may offer useful information for selecting medical treatment in stable angina pectoris.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Questionnaires_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10150325
----K E
----T Effect of atenolol and ramipril on regression of left ventricular hypertrophy: comparative echocardiographic assessment.
----A Left ventricular hypertrophy (LVH) dramatically worsens hypertensive illness. Because the genesis of LVH appears to be multifactorial, antihypertensive treatment should aim to reduce not only pressor values but also the hypertrophic ventricular mass. This result can be obtained only when drugs able to act on both pathogenetic factors are used. To evaluate the effectiveness of antihypertensive therapy on regression of LVH, 21 patients with stage 2 essential hypertension were treated for a year with either atenolol (120 mg/d orally), a cardioselective beta-blocker without intrinsic sympathomimetic activity, or ramipril (5 mg/d orally), an angiotensin-converting enzyme inhibitor with high tissue activity. Both treatments produced significant control of hypertension and regression of LVH. No statistically significant difference between treatments was noted, except for heart rate, which was substantially unchanged by ramipril but significantly decreased by atenolol. Both drugs were well tolerated. Atenolol and ramipril have a major role in the long-term treatment of hypertension and in the regression of hypertension-associated LVH.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH P_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7774515
----K E
----T Ramipril. An updated review of its therapeutic use in essential hypertension and heart failure.
----A Ramipril is a second generation angiotensin converting enzyme (ACE) inhibitor. Like enalapril, it is a prodrug and is hydrolysed in vivo to release the active metabolite, ramiprilat, which has a long elimination half-life, permitting once-daily administration. The antihypertensive efficacy of ramipril has been confirmed in large-scale noncomparative studies conducted in general practice as well as in more rigorously controlled clinical trials. In the former, approximately 85% of patients with mild to moderate essential hypertension have responded successfully to treatment with ramipril 2.5 or 5 mg/day, while comparative trials indicate that the antihypertensive efficacy of the drug is equivalent to that of other established ACE inhibitors and the beta-adrenoceptor antagonist atenolol. As expected, the response rate to ramipril monotherapy is lower in patients with severe hypertension (around 40%), although the blood pressure lowering effect can be enhanced with the addition of a diuretic such as hydrochlorothiazide or piretanide. The antihypertensive efficacy of ramipril is maintained in patients with diabetes mellitus and preliminary data indicate that the drug has the beneficial effect of decreasing urinary albumin excretion in diabetic patients with nephropathy. Ramipril is superior to atenolol in causing regression of left ventricular hypertrophy, although the clinical significance of this effect per se remains to be established. The large-scale Acute Infarction Ramipril Efficacy (AIRE) study demonstrated that ramipril 5 or 10 mg/day significantly decreased the risk of all-cause mortality by 27% in patients with clinical evidence of heart failure after acute myocardial infarction, even if transient. The beneficial effect of ramipril was apparent by 30 days of treatment and appeared to be greatest in patients with more severe ventricular damage after infarction. Ramipril is well tolerated in general practice, with 5% or fewer patients discontinuing therapy because of drug intolerance. The data available suggest that ramipril shares a similar tolerability profile to that of other established ACE inhibitors. Thus, clinical data confirm ramipril as a useful alternative ACE inhibitor for the treatment of patients with mild to moderate hypertension, and indicate a beneficial effect of the drug in patients with clinical evidence of heart failure after acute myocardial infarction. It is also reasonable to assume that ramipril will be of value in the treatment of patients with more established heart failure or asymptomatic left ventricular dysfunction.
----P Journal_Article Review Review__Tutorial 
----M M_Aging_MeSH S_metabolism_MeSH Aging_metabolism_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Kallikrein-Kinin_System_MeSH S_drug_effects_MeSH Kallikrein-Kinin_System_drug_effects_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Ramipril_MeSH S_pharmacokinetics_MeSH Ramipril_pharmacokinetics_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 7774991
----K I
----T Comparison of efficacy of nisoldipine, metoprolol, and isosorbide dinitrate in patients with stable exertional angina: a randomized, cross-over, placebo-controlled study.
----A We evaluated the acute antianginal effect of oral nisoldipine (10 mg), metoprolol (40 mg), and long-acting isosorbide dinitrate (20 mg) in 15 patients with stable exertional angina. The patients performed symptom-limited treadmill exercise at 2 h after the administration of placebo (Placebo stages 1 and 2) and each of the active drugs. After Placebo stage 1, the patients were randomized for cross-over evaluation of the acute effect of a single oral dose of placebo (Placebo stage 2), nisoldipine, metoprolol, or long-acting isosorbide dinitrate. All 15 patients developed angina during all of exercise tests and their exercise tests were terminated at the onset of angina. The time until development of 0.1 mV ST segment depression was increased by all three drugs compared to placebo, and it was significantly longer with metoprolol than with isosorbide dinitrate. Similarly, the time to ceasing exercise because of angina was also prolonged by all three drugs. The exercise time was longer with nisoldipine and metoprolol compared to isosorbide dinitrate, but there was no significant difference between nisoldipine and metoprolol. In conclusion, metoprolol and nisoldipine more effectively prolonged exercise compared to long-acting isosorbide dinitrate in patients with stable exertional angina.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Exertion_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_pharmacology_MeSH Isosorbide_Dinitrate_pharmacology_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nisoldipine_MeSH S_pharmacology_MeSH Nisoldipine_pharmacology_MeSH S_therapeutic_use_MeSH Nisoldipine_therapeutic_use_MeSH M_Rest_MeSH M_Treatment_Outcome_MeSH 
****** 7539822
----K E
----T Treatment of ventricular arrhythmias in older adults.
----A OBJECTIVE: To review the prognosis and management of ventricular arrhythmias (VA) in persons with and without heart disease with emphasis on older adults. DATA SOURCES: A computer-assisted search of the English language literature (MEDLINE database) followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies on the prognosis and management of VA in persons with and without heart disease were screened for review. Studies in older people and recent studies were emphasized. DATA EXTRACTION: Pertinent data were extracted from the reviewed articles. Emphasis was on studies involving the older persons. Relevant articles were reviewed in depth. DATA SYNTHESIS: Available data about the prognosis and management of VA in persons with and without heart disease, with emphasis on studies involving older people, were summarized. CONCLUSIONS: VA in older persons without heart disease should not be treated with antiarrhythmic drugs. Class I antiarrhythmic drugs should not be used to treat VA in older persons with heart disease. Beta blockers should be used to treat complex VA in older persons with ischemic or nonischemic heart disease if there are no contraindications to beta blocker therapy. The use of amiodarone in treating complex VA should be reserved for life-threatening ventricular tachyarrhythmias in older persons who cannot tolerate or who do not respond to beta blockers. VA associated with congestive heart failure should be treated with angiotensin converting enzyme inhibitors. If older patients have life-threatening recurrent ventricular tachycardia or ventricular fibrillation resistant to antiarrhythmic drugs, invasive intervention should be performed. The automatic implantable cardioverter-defibrillator is recommended in older patients who have medically refractory sustained ventricular tachycardia or ventricular fibrillation.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Cardiac_Complexes__Premature_MeSH S_therapy_MeSH Cardiac_Complexes__Premature_therapy_MeSH M_Defibrillators__Implantable_MeSH M_Female_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Tachycardia__Ventricular_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Dysfunction_MeSH S_therapy_MeSH Ventricular_Dysfunction_therapy_MeSH 
****** 7779149
----K E
----T Study on the possible interaction between tenoxicam and atenolol in hypertensive patients.
----A Sixteen hypertensive male out-patients (33-54 y), whose blood pressure (BP) had been normalized (diastolic BP < 90 mmHg) by treatment with a daily dose of 50 mg atenolol (CAS 29122-68-7), participated in this double-blind, placebo-controlled, parallel group study, which investigated the possible influence of the non-steroidal anti-inflammatory drug tenoxicam (CAS 59804-37-4) on the control of BP by atenolol. After a run-in of 10 days, to assess the stability of BP control by atenolol, and to determine baseline parameters, 8 patients in group A received 20 mg tenoxicam (2 x 20 mg on days 1 and 2), and 8 patients in group B received placebo, daily over 15 days (days 0-14), concomitantly with their atenolol regimen. BP was measured under standardized conditions on several days. Heart rate (EHR) after 5 min of exercise by bicycle ergometry (constant 75W), and parameters of renal function were assessed before (baseline) and during concomitant dosing of atenolol and tenoxicam. On day 14 the mean changes (delta A, delta B) from baseline of pre-dose BP (mmHg) and EHR (beats/min) in groups A and B, and the one-sided 95% confidence regions (R) for delta A, respectively, were (delta A, delta B, R): 4.4, 1.6, < 9.5 for sitting systolic BP, 2.8, -0.3, < 4.5 for sitting diastolic BP, -0.3, -0.6, < 5.5 for standing systolic BP, -0.6, -1.9, < 3.0 for standing diastolic BP, 0.4, -7.5, < 0.4 for EHR at pre-dose, 3.1, 0.6, < 7.8 for EHR at 3.5 h post-dose.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH S_pharmacokinetics_MeSH Anti-Inflammatory_Agents__Non-Steroidal_pharmacokinetics_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chromatography__High_Pressure_Liquid_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Piroxicam_MeSH S_adverse_effects_MeSH Piroxicam_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Piroxicam_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Piroxicam_pharmacokinetics_MeSH S_therapeutic_use_MeSH Piroxicam_therapeutic_use_MeSH 
****** 7782140
----K E
----T Effect of verapamil on the prognosis of patients with early postinfarction electrical or mechanical complications. The Danish Verapamil Infarction Trial II (DAVIT II).
----A The Danish Verapamil Infarction Trial II (DAVIT II) demonstrated from the second postinfarction week, that long term treatment with verapamil significantly improved reinfarction free survival after an acute myocardial infarction (AMI). The present post hoc analysis of DAVIT II was undertaken with the purpose of evaluating the effect of treatment with verapamil in patients with early electrical complications, i.e. ventricular or atrial fibrillation, ventricular tachycardia, or second or third degree atrioventricular block, with or without mechanical complication, i.e. heart failure, during the first post-AMI week. In the placebo group, the 18-month mortality rate was lowest (9.5%) in patients without electrical or mechanical complications, highest (24.6%) in patients with electrical events only, and in-between (17.5%) in patients with mechanical problems regardless of presence of electrical complications. Verapamil significantly reduced the 18-month mortality rate in patients with early electrical without mechanical complications (60% reduction, P = 0.02), and in patients without mechanical complications (35% reduction, P = 0.02). Verapamil did not change the mortality rate in patients with mechanical complications.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH S_mortality_MeSH Arrhythmia_mortality_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 7783099
----K E
----T Assessment of effects of two anti-hypertensive regimens on overall cardiovascular risk.
----A Anti-hypertensive drugs differ in their effects on other cardiovascular risk factors. To date there have been few attempts to quantitate the impact of such differences. Twenty five unmedicated patients with primary hypertension were randomised to initial therapy with either the calcium antagonist, felodipine, or a diuretic and doses titrated to achieve similar levels of blood pressure (BP). Second drugs were added if needed (metoprolol and prazosin, respectively). The aim was to determine over 1 year whether similar anti-hypertensive effects were associated with differences in a multivariate index of overall cardiovascular risk. The target supine diastolic blood pressure (DBP) (85 mm Hg) required the second agent in four of 13 evaluable patients in the felodipine group and six of 10 in the diuretic group. There was a significant rise in serum cholesterol and a fall in serum potassium in the diuretic group, but not in the felodipine group. Cardiovascular risk scores were ranked in percentiles in relation to the age-matched general population. This score fell to a greater degree in felodipine patients particularly over the first 6 months, but remaining lower at 12 months. Left ventricular hypertrophy assessed by echocardiography, another measure of cardiovascular risk, was generally unchanged by either regimen. At equivalent blood pressure levels, the calcium antagonist-based regimen had a greater benefit on cardiovascular risk, particularly in the first 6 months of therapy. This method may be widely applicable in the assessment of anti-hypertensive therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Prazosin_MeSH S_administration_&_dosage_MeSH Prazosin_administration_&_dosage_MeSH S_pharmacology_MeSH Prazosin_pharmacology_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7786531
----K I
----T Comparison of propafenone to atenolol for the prophylaxis of postcardiotomy supraventricular tachyarrhythmias: a prospective trial.
----A To compare the efficacy of propafenone to atenolol in the prevention of supraventricular tachyarrhythmias (SVT) following cardiac surgery, 207 consecutive patients were randomly allocated to receive either propafenone 300 mg twice daily (105 patients) or atenolol 50 mg once daily (102 patients) orally for 7 days after operation. Double blinding was achieved using placebos. The end point was the development of a SVT which was symptomatic, recurrent, or lasting over 2 minutes, or the occurrence of adverse effects possibly attributable to the drugs. The groups were well matched for age, sex, bypass- and cross-clamp times, and other data. Thirteen patients in the propafenone group and 11 in the atenolol group developed SVT during the first week after operation. (P = 0.89, non significant, chi-squared with Yates' correction). In our study propafenone and atenolol were of approximately equal efficacy in preventing post cardiotomy SVT. Propafenone may have an advantage in being less negatively inotropic than atenolol; it could therefore be used in patients with poor left ventricular function or marginal haemodynamics when a beta blocker is contraindicated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_Valve_Diseases_MeSH S_surgery_MeSH Heart_Valve_Diseases_surgery_MeSH M_Heart_Valve_Prosthesis_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Propafenone_MeSH S_administration_&_dosage_MeSH Propafenone_administration_&_dosage_MeSH S_adverse_effects_MeSH Propafenone_adverse_effects_MeSH M_Tachycardia__Supraventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Supraventricular_prevention_&_control_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7794571
----K E
----T Progressive improvement in the structure of resistance arteries of hypertensive patients after 2 years of treatment with an angiotensin I-converting enzyme inhibitor. Comparison with effects of a beta-blocker.
----A To investigate the effects of antihypertensive drugs on resistance artery structure, 17 essential hypertensive patients were randomly assigned to be treated with an angiotensin I-converting enzyme inhibitor, cilazapril, or a beta-blocker, atenolol, for 2 years. Blood pressure was well controlled throughout the 2 years. Before starting treatment, at the end of the first year and at the end of the second year, patients were subjected to gluteal subcutaneous fat biopsies, from which resistance-size arteries were dissected to be studied. The media width to lumen diameter ratio of arteries from patients in the cilazapril group was 7.5 +/- 0.3% before starting treatment, and decreased significantly (P < .05) to 6.3 +/- 0.2% at the end of the first year, and to 5.8 +/- 0.2% at the end of the second year, at which time it was not different from that of arteries from normotensive subjects (5.2 +/- 0.2%). In patients treated with atenolol, resistance arteries exhibited a media-to-lumen ratio of 8.0 +/- 0.6% before treatment, 8.1 +/- 0.5% after 1 year of treatment, and 7.9 +/- 0.3% at the end of the second year of treatment, all significantly higher (P < .01) than that of arteries from normotensive subjects. Thus, treatment for 2 years with the angiotensin I-converting enzyme inhibitor cilazapril resulted in progressive normalization of the structure (media-to-lumen ratio) of gluteal subcutaneous fat resistance arteries of essential hypertensive patients, whereas there was no change in patients treated with the beta-blocker atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Arteries_MeSH S_pathology_MeSH Arteries_pathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 7599749
----K E
----T Neurohormonal activation in patients with acute myocardial infarction or chronic congestive heart failure. With special reference to treatment with angiotensin converting enzyme inhibitors.
----A Neurohormonal activation may provide a pathophysiological link between acute myocardial infarction and chronic congestive heart failure, and modulation of neurohormonal activity may be an important therapeutic target in these conditions. Plasma neurohormones were studied in 55 patients with acute myocardial infarction. Angiotensin II, noradrenaline and ANP were elevated in the early phase but tended to normalize during the first week in patients without signs of heart failure. In patients with heart failure angiotensin II and noradrenaline remained elevated for 1 month and ANP for 4-6 months. During head-up tilt, angiotensin II and noradrenaline increased most in patients with heart failure. In patients with a first myocardial infarction there was a positive correlation between sustained neurohormonal activity and infarct size. Almost complete suppression of plasma ACE activity was achieved within 30 min in 48 patients treated with intravenous enalaprilat, initiated within 24 h from the onset of infarction. The drug was tolerated in dosages of 1.0-1.2 mg given over 1-2h. Patients with systolic blood pressure between 100 and 110 mmHg incurred a greater risk of hypotension than those with higher blood pressure at baseline. Tolerance was not worse among patients treated with intravenous diuretics, metoprolol or nitroglycerin. A total of 98 patients were randomized to treatment with enalapril or placebo, initiated within 24 h from onset of infarction and continued for 4-6 months. During treatment there were no significant differences in plasma levels of angiotensin II, aldosterone, ANP or catecholamines between groups. Echocardiographic recordings were performed in 28 patients. Among patients on placebo there was a positive correlation between plasma levels of noradrenaline at days 5-7 and the increase in left ventricular volumes during the study period, and an inverse correlation between plasma aldosterone at days 5-7 and the increase in left ventricular ejection fraction during the study. No such correlation was found among patients on enalapril. ANP levels at 1 month correlated inversely with the left ventricular ejection fraction at the same time. Plasma neurohormones were measured in 223 patients with mild or moderately severe chronic heart failure, randomized to treatment with ramipril or placebo for 3 months. There was wide variation in hormone levels. Noradrenaline and aldosterone correlated inversely with exercise duration at baseline. Noradrenaline correlated positively with the degree of symptoms. Aldosterone and ANP were reduced with ramipril compared with placebo. Noradrenaline was reduced among patients with baseline levels in the highest tertile. Plasma hormones were also measured at peak exercise in 54 patients. Hormonal levels at rest correlated strongly with those at peak exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Enalaprilat_MeSH S_therapeutic_use_MeSH Enalaprilat_therapeutic_use_MeSH M_Exercise_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Neurosecretory_Systems_MeSH S_physiopathology_MeSH Neurosecretory_Systems_physiopathology_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7599759
----K E
----T ACE inhibition preserves renal function better than beta-blockade in the treatment of essential hypertension.
----A Antihypertensive treatment can slow down the decline in glomerular filtration rate (GFR) with time. In patients with diabetic nephropathy, angiotensin converting enzyme (ACE) inhibition has been shown to be more effective in this regard than conventional antihypertensive therapy. Whether this applies to the much larger population of patients with essential hypertension is not yet known. In the present study, the effects of two different antihypertensive therapies on the loss of GFR with time, determined with Cr51-EDTA clearance after 6, 12 and 24 months of treatment, were assessed in a prospective, randomised, double-blind trial in 257 patients with essential hypertension. All had normal renal function and none had diabetes mellitus or glucosuria. Proteinuria (dipstick positive or trace) was detected in 7 patients initially. The two therapeutic modalities were the ACE inhibitor cilazapril and the beta-adrenoceptor blocking agent atenolol. Both therapies were equally effective in lowering systolic blood pressure (e.g. from 168 mmHg to 152 mmHg with cilazapril and from 170 mmHg to 155 mmHg with atenolol after 6 months, p < 0.001 for both). However, atenolol was slightly but significantly more effective in lowering the diastolic blood pressure at 6, 12 and 24 months. The decline in GFR with time was significantly smaller with cilazapril than with atenolol. After 6 months the reduction in GFR was 1.0 vs. 4.0 ml/min x 1.73 m2, p = 0.008 (cilazapril vs. atenolol) and after 12 months the corresponding changes were 2.0 vs. 4.5 ml/min x 1.73 m2, p = 0.04 and after 24 months 3.0 vs. 4.0 ml/min x 1.73 m2, respectively (n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH 
****** 7600653
----K I
----T Effects of carvedilol, a vasodilator-beta-blocker, in patients with congestive heart failure due to ischemic heart disease. Australia-New Zealand Heart Failure Research Collaborative Group.
----A BACKGROUND: beta-Blocker therapy has been shown to increase ejection fraction in patients with heart failure of idiopathic etiology. However, in patients with heart failure of ischemic etiology, the effects of this treatment on left ventricular function remain uncertain, as do the effects on exercise performance and symptoms. METHODS AND RESULTS: This study investigated the effects of carvedilol, a beta-blocker with alpha 1-blocking properties, on left ventricular size and function, maximal and submaximal exercise performance, and symptoms in 415 patients with stable heart failure of ischemic etiology (ejection fraction < 45%). After a 2- to 3-week run-in phase on open-label low-dose carvedilol, patients were randomized to continued treatment with carvedilol (up to 25 mg BID) or to matching placebo. After 6 months, left ventricular ejection fraction measured by radionuclide ventriculography had increased by 5.2% (2P < .0001) in the carvedilol group compared with the placebo group, and left ventricular end-systolic and end-diastolic dimensions measured by two-dimensionally guided M-mode echocardiography had decreased by 2.6 mm (2P = .0005) and 1.3 mm (2P = .05), respectively. There were no significant changes in either treadmill exercise duration or 6-minute walk distance between carvedilol and placebo groups (both 2P > .1); in the carvedilol group, exercise performance was therefore maintained with a 23% lower rate-pressure product. Symptoms assessed by the New York Heart Association (NYHA) scale and the Specific Activity Scale (SAS) were unchanged in two thirds of patients in both groups, but there was a small excess of patients whose symptoms worsened and a deficit of patients whose symptoms improved among those assigned carvedilol (NYHA, 2P = .05; SAS, 2P = .02). CONCLUSIONS: In patients with heart failure of ischemic etiology, 6-month treatment with carvedilol improved left ventricular function and maintained exercise performance at a lower rate-pressure product, but symptoms assessed by functional class were slightly worsened. A larger-scale trial is now required to determine whether this treatment will reduce serious morbidity and mortality from heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Radionuclide_Ventriculography_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7601014
----K E
----T Spirapril. A preliminary review of its pharmacology and therapeutic efficacy in the treatment of hypertension.
----A Spirapril is a non-sulfhydryl angiotensin converting enzyme (ACE) inhibitor prodrug which is converted to the active metabolite spiraprilat following oral administration, and which has been evaluated primarily for the treatment of hypertension. In dose-finding studies of patients with mild to severe hypertension, spirapril > or = 6 mg once daily produced reductions in blood pressure of approximately 10 to 18 mm Hg (systolic) and 7 to 13 mm Hg (diastolic) [24-hour postdose trough readings at the end of the treatment period]. Blood pressure normalisation (trough diastolic blood pressure < or = 90 mm Hg) had occurred in 29 to 50% of patients at the end of these investigations. The dose-response curve for spirapril appears to be flat for doses of 6 to 24 mg once daily. Comparisons with other ACE inhibitors are limited in number, and further studies are required before the relative antihypertensive efficacy of spirapril can be fully evaluated. However, in single, well controlled clinical trials, spirapril produced similar reductions in blood pressure to those seen with enalapril or captopril. When given as monotherapy or in combination with hydrochlorothiazide, spirapril may offer potential advantages over the calcium antagonist nitrendipine. Spirapril is generally well tolerated and produces an adverse event profile similar to that of other ACE inhibitors. Data from small studies suggest that spirapril can be used without dosage adjustment in patients with renal impairment, as a consequence of its dual renal and hepatic clearance mechanisms. This is in contrast to most ACE inhibitors, which are eliminated by a predominantly renal mechanism that results in accumulation of the active metabolite when renal function is impaired. However, the utility of spirapril in this patient group has yet to be fully determined because of conflicting data regarding its effects on renal function. Thus, spirapril is an effective antihypertensive agent which is well tolerated. Further comparative trials are needed to fully determine its efficacy with respect to other ACE inhibitors, and a better understanding of its effects on renal function will clarify its role in hypertensive patients with renal failure.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Clinical_Trials_MeSH M_Enalapril_MeSH S_analogs_&_derivatives_MeSH Enalapril_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Enalapril_pharmacokinetics_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 7601427
----K I
----T The treatment of portal hypertension: a meta-analytic review.
----A 
----P Journal_Article Meta-Analysis 
----M M_Clinical_Trials_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH S_therapy_MeSH Hemorrhage_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Recurrence_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Varicose_Veins_MeSH S_etiology_MeSH Varicose_Veins_etiology_MeSH 
****** 7607766
----K E
----T Left ventricular and aortic root structure and function changes with beta blocker antihypertensive therapy. A one-year double blind study of celiprolol and metoprolol.
----A Using echocardiographic and Doppler methodology, we evaluated the effects of celiprolol 200-400 mg/day and metoprolol 100-200 mg/day, given for one year, on haemodynamics, left ventricular structure and function, and aortic root distensibility in 40 hypertensive patients. Total peripheral resistance was unchanged with metoprolol (-1.7%) but decreased with celiprolol (-11.2%), a significant difference between the two treatments (P = 0.01). Left ventricular mass index was reduced by 5.7% in those patients receiving metoprolol and by 11.8% in those receiving celiprolol (P < 0.001). Cardiac index fell significantly with metoprolol and marginally with celiprolol (-13.9% vs. 5.9%, P = 0.003). Left ventricular diastolic function-as shown by the transmitral early to late peak filling velocity ratio-was not altered with metoprolol, but a significant increase (17%, P = 0.2) was seen with celiprolol. Both metoprolol and celiprolol increased aortic root distensibility, with celiprolol having a significantly greater effect (80% vs. 30%, P < 0.01). We conclude that, in comparison to metoprolol, long term antihypertensive therapy with celiprolol improves left ventricular diastolic and aortic root function, whilst reducing total peripheral resistance and left ventricular hypertrophy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aorta_MeSH S_drug_effects_MeSH Aorta_drug_effects_MeSH M_Celiprolol_MeSH S_administration_&_dosage_MeSH Celiprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Celiprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler__Pulsed_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 7614494
----K E
----T Beta-1-selectivity is not essential to achieve therapeutic efficacy with beta-blockade therapy for idiopathic dilated cardiomyopathy.
----A This study investigated the therapeutic efficacy of two different beta-blockers, metoprolol (beta 1-selective) and nipradilol (nonselective) for the treatment of idiopathic dilated cardiomyopathy (DCM). The New York Heart Association functional class improved in the metoprolol group (n = 9) and the nipradilol group (n = 9), but not in the control group who received conventional therapy (n = 8). The left ventricular ejection fraction increased in both the beta-blocker groups (p < 0.01, p < 0.05). Lymphocyte beta-adrenoceptors were upregulated in the nipradilol group (p < 0.01). Cardiac events were less common in both the beta-blocker groups than in the control group (both p < 0.05). Thus, nipradilol improved symptoms and cardiac function with a favorable effect on sympathoneuronal activity as well as metoprolol in patients with DCM. Therefore, beta 1-selectivity is not essential to achieve therapeutic efficacy with beta-blockade therapy for DCM.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_metabolism_MeSH Cardiomyopathy__Congestive_metabolism_MeSH S_radionuclide_imaging_MeSH Cardiomyopathy__Congestive_radionuclide_imaging_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Coronary_Angiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Lymphocytes_MeSH S_drug_effects_MeSH Lymphocytes_drug_effects_MeSH S_metabolism_MeSH Lymphocytes_metabolism_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Radionuclide_Ventriculography_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7614501
----K E
----T Remodeling of resistance arteries in human hypertension: effects of cilazapril, an angiotensin-I-converting enzyme inhibitor.
----A Studies on the effect of antihypertensive agents on resistance arteries in hypertensive patients have in the past yielded inconclusive results regarding the ability of these drugs to induce a regression toward normal of either the structure or the function of these critically important vessels. We have recently compared the effects of the angiotensin-I-converting enzyme inhibitor cilazapril and of the beta blocker atenolol on the structure and the function of subcutaneous resistance arteries of essential hypertensive patients. The patients were randomly assigned to receive either cilazapril or atenolol for a period of 2 years. The blood pressure was normalized for the duration of the trial by both drugs. The media-to-lumen ratio of resistance arteries, which was significantly increased in all hypertensive patients before starting treatment, was normalized by the 2-year treatment with cilazapril, whereas treatment with atenolol did not result in any change in this vascular parameter. Treatment with cilazapril also returned to normal the contractile responses to several vasoconstrictors, particularly endothelin 1. Endothelium-dependent relaxation responses of blood vessels to acetylcholine were abnormal in hypertensive patients and improved in the cilazapril-treated patients, but remained unchanged in the atenolol-treated ones. We conclude that treatment with the angiotensin-I-converting enzyme inhibitor cilazapril corrects in part the vascular remodeling and the functional abnormalities of resistance arteries of hypertensive patients, whereas treatment with the beta blocker atenolol does not. These results may indicate that treatment with cilazapril and perhaps with other angiotensin-I-converting enzyme inhibitors as well may improve the clinical outcome in hypertension by inducing a regression of abnormal resistance vessel structure and function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Animals_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cilazapril_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 7614504
----K E
----T Effects of angiotensin-converting enzyme inhibition versus conventional antihypertensive therapy on the glomerular filtration rate.
----A Antihypertensive treatment has been shown to slow down the decline in glomerular filtration rate (GFR) with time. This has been most extensively studied in patients with diabetic nephropathy and, to some extent, with other forms of renal disease. Angiotensin-converting enzyme (ACE) inhibition has been shown to be more effective in this regard than conventional antihypertensive therapy. This important aspect of antihypertensive treatment has not been studied previously in patients with essential hypertension. Preliminary results regarding the effects of two different antihypertensive therapies on the loss of GFR with time, determined with 51Cr-EDTA clearance after 6, 12, and 24 months of treatment, are presented here. The GFR was assessed in a prospective, randomized, double-blind trial in 257 patients with essential hypertension. All had a normal renal function, and none had diabetes mellitus or glucosuria. The two therapeutic modalities were the ACE inhibitor cilazapril and the beta-adrenoceptor blocking agent atenolol. Both therapies were equally effective in lowering the systolic blood pressure. However, atenolol was slightly but significantly more effective in lowering the diastolic blood pressure after 6, 12, and 24 months. The decline in GFR with time was significantly smaller with cilazapril than with atenolol. After 6 months, the reduction in GFR was 1.0 (cilazapril) vs. 4.0 (atenolol) ml/min x 1.73 m2 (p < 0.01). After 12 months the corresponding changes were 2.0 vs. 4.5 ml/min x 1.73 m2 (p < 0.05) and after 24 months 3.0 vs. 4.0 ml/min x 1.73 m2 (n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cilazapril_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH S_physiology_MeSH Glomerular_Filtration_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Prospective_Studies_MeSH 
****** 7621844
----K I
----T Muscle cramps and elevated serum creatine phosphokinase levels induced by beta-adrenoceptor blockers.
----A We have assessed the propensity of beta-adrenoceptor blockers to cause muscle cramps and to raise the serum creatine phosphokinase (CPK) level in 78 patients with essential hypertension. After a control period, a beta-adrenoceptor blocker without intrinsic sympathomimetic activity (ISA; propranolol, metoprolol or arotinolol) was administered for three months. Thereafter, the patients were randomised to receive a beta-adrenoceptor blocker with ISA (pindolol or carteolol) for three months or a beta-adrenoceptor blocker without ISA for a further three months. This pattern was continued until all beta-adrenoceptor blockers had been given. At the end of each period, CPK and CPK-MB levels were measured. Of the 78 subjects, muscle cramps occurred in 27 during treatment with pindolol and 32 during treatment with carteolol. No complaints were made by subjects treated with propranolol and arotinolol, but muscle cramps were reported in 2 treated with metoprolol. While muscle cramps were caused both by pindolol and carteolol in 16 subjects, they were caused by either of these drugs in the remainder of the subjects. Muscle cramp occurred mainly in the calves when the patients were in bed at night. Serum CPK and CPK-MB levels increased significantly during treatment with pindolol (control period vs pindolol, CPK = 96 vs 133 IU.ml-1, CPK-MB = 14 vs 18 IU.ml-1) or carteolol (CPK = 117 IU.ml-1, CPK-MB = 18 IU.ml-1) while the levels during treatment with propranolol, arotinolol and metoprolol did not change from those in the control period.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle_Cramp_MeSH S_chemically_induced_MeSH Muscle_Cramp_chemically_induced_MeSH M_Muscles_MeSH S_enzymology_MeSH Muscles_enzymology_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7631621
----K E
----T Low-dose drug combination therapy: an alternative first-line approach to hypertension treatment.
----A To investigate the concept that the initial treatment of hypertension with low doses of two antihypertensives that have different modes of action and additive effects may achieve control of blood pressure and minimize the dose-dependent adverse effects seen with conventional monotherapy, a randomized, double-blind parallel group dose-escalation study was conducted. After a 4 to 5 week placebo washout period, 218 men and women with diastolic blood pressure between 95 and 114 mm Hg were randomly allocated to take: amlodipine (2.5 to 10 mg), enalapril (5 to 20 mg), and the low-dose combination of bisoprolol (2.5 to 10 mg) with 6.25 mg of hydrochlorothiazide (HCTZ). All drugs were administered once daily, titrated to optimal response, and taken for a total of 12 weeks. Blood pressure was measured 24 hours after dose. The response rates (either a diastolic blood pressure < or = 90 mm Hg or a decrease of diastolic pressure > or = 10 mm Hg) were 71% for bisoprolol-6.25 mg HCTZ, 69% for amlodipine, and 45% for enalapril. The mean decreases in systolic/diastolic blood pressure from baseline were 13.4/10.7, 12.8/10.2, and 7.3/6.6 mm Hg for bisoprolol-6.25 mg HCTZ, amlodipine, and enalapril, respectively. The mean change with enalapril was less than the other drugs (p < 0.01), although the once-daily dosing of enalapril and the maximum dose of 20 mg might not have been optimal for this agent.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_United_States_MeSH 
****** 7639651
----K 4
----T A double-masked, randomized 1-year study comparing dorzolamide (Trusopt), timolol, and betaxolol. International Dorzolamide Study Group.
----A OBJECTIVE: To investigate the safety profile and efficacy of 2.0% dorzolamide hydrochloride, when administered three times daily for up to 1 year, compared with that of 0.5% timolol maleate and 0.5% betaxolol hydrochloride, each administered twice daily. In addition, the effect of adding dorzolamide to the regimen of patients with inadequate ocular hypotensive efficacy while they were receiving one of the two beta-adrenoceptor antagonists and the effect of adding timolol to the regimen of patients receiving dorzolamide were also evaluated. DESIGN: A double-masked, randomized, parallel comparison. SETTING: Multinational study at 34 international sites. PATIENTS: Five hundred twenty-three patients with open-angle glaucoma or ocular hypertension, 17 to 85 years of age. Patients currently using ocular hypotensive medications were required to undergo a washout. INTERVENTION: Two percent dorzolamide three times a day, 0.5% timolol (Timoptic, Merck, Whitehouse Station, NJ) twice daily, and 0.5% betaxolol solution (Betoptic, Alcon, Fort Worth, Tex) twice daily. RESULTS: At 1 year, the mean percent reduction in intraocular pressure at peak of 2% dorzolamide, 0.5% timolol, and 0.5% betaxolol was approximately 23%, 25%, and 21%, respectively. At afternoon trough, the mean percent reduction in intraocular pressure was 17%, 20%, and 15% for dorzolamide, timolol, and betaxolol, respectively. CONCLUSIONS: The ocular hypotensive efficacy of 2.0% dorzolamide, given three times a day, is comparable with that of 0.5% betaxolol, given twice daily, for up to 1 year. In addition, long-term use of dorzolamide was not associated with clinically meaningful electrolyte disturbances or systemic side effects commonly observed with the use of oral carbonic anhydrase inhibitors.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Betaxolol_adverse_effects_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_administration_&_dosage_MeSH Carbonic_Anhydrase_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Tolerance_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 7642847
----K E
----T Asymptomatic Cardiac Ischemia Pilot (ACIP) study: impact of anti-ischemia therapy on 12-week rest electrocardiogram and exercise test outcomes. The ACIP Investigators.
----A OBJECTIVES. This report from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study examines differences in the magnitude of reduction of myocardial ischemia as determined by exercise treadmill testing in patients randomized to three different treatment strategies: angina-guided medical therapy, ischemia-guided medical therapy and coronary revascularization. BACKGROUND. No prospective randomized clinical trials in patients with exercise electrocardiographic (ECG) abnormalities and asymptomatic cardiac ischemia on ambulatory ECG monitoring have compared the impact of different treatment strategies, including coronary revascularization, in terms of reducing myocardial ischemia. METHODS. The ACIP exercise protocol was used. Exercise variables measured included final exercise stage; presence of exercise-induced angina or ischemia; time to angina; time to 1-mm ST segment depression; number of exercise ECG leads with abnormalities; maximal depth of ST segment depression in any lead; sum of ST segment depression; ST/HR index; and rate-pressure product at time to angina, at time to 1-mm ST segment depression and at peak exertion. RESULTS. Peak exercise time was increased by 0.5, 0.7 and 1.6 min in patients assigned to the angina-guided, ischemia-guided and coronary revascularization strategies, respectively, from the qualifying visit to the 12-week visit (p < 0.001). At the qualifying visit, the sum of exercise-induced ST segment depression was 9.4 +/- 5.0 (mean +/- SD), 9.6 +/- 4.7 and 9.9 +/- 5.5 mm (p = NS) in the three treatment strategies, respectively. At the 12-week visit, the sum of exercise-induced ST segment depression was 7.4 +/- 5.7, 6.8 +/- 5.3 and 5.6 +/- 5.6 mm (p = 0.02) in the three treatment strategies, respectively. Each treatment strategy resulted in a significant reduction in all exercise-induced variables of myocardial ischemia measured at 12 weeks. CONCLUSIONS. Coronary revascularization significantly reduced the extent and frequency of exercise-induced myocardial ischemia compared with either medical strategy. The prognostic impact of these observations should be evaluated in a large-scale multicenter clinical trial.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Analysis_of_Variance_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_statistics_&_numerical_data_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_statistics_&_numerical_data_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH S_statistics_&_numerical_data_MeSH Coronary_Artery_Bypass_statistics_&_numerical_data_MeSH M_Drug_Therapy__Combination_MeSH P_Electrocardiography__Ambulatory_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography__Ambulatory_statistics_&_numerical_data_MeSH P_Exercise_Test_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Pilot_Projects_MeSH M_Prospective_Studies_MeSH M_Remission_Induction_MeSH M_Rest_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 7642848
----K E
----T Asymptomatic Cardiac Ischemia Pilot (ACIP) study: outcome at 1 year for patients with asymptomatic cardiac ischemia randomized to medical therapy or revascularization. The ACIP Investigators.
----A OBJECTIVES. This report discusses the outcome at 1 year in patients in the Asymptomatic Cardiac Ischemia Pilot (ACIP) study. BACKGROUND. Comparative efficacy of medical therapy versus revascularization in treatment of asymptomatic ischemia is unknown. The ACIP study assessed the ability of three treatment strategies to suppress ambulatory electrocardiographic (ECG) ischemia to determine whether a large-scale trial studying the impact of these strategies on clinical outcomes was feasible. METHODS. Five hundred fifty-eight patients with coronary anatomy amenable to revascularization, at least one episode of asymptomatic ischemia on the 48-h ambulatory ECG and ischemia on treadmill exercise testing were randomized to one of three treatment strategies: 1) medication to suppress angina (angina-guided strategy, n = 183); 2) medication to suppress both angina and ambulatory ECG ischemia (ischemia-guided strategy, n = 183); or 3) revascularization strategy (angioplasty or bypass surgery, n = 192). Medication was titrated atenolol-nifedipine or diltiazem-isosorbide dinitrate. RESULTS. The revascularization group received less medication and had less ischemia on serial ambulatory ECG recordings and exercise testing than those assigned to the medical strategies. The ischemia-guided group received more medication but had suppression of ischemia similar to the angina-guided group. At 1 year, the mortality rate was 4.4% in the angina-guided group (8 of 183), 1.6% in the ischemia-guided group (3 of 183) and 0% in the revascularization group (overall, p = 0.004; angina-guided vs. revascularization, p = 0.003; other pairwise comparisons, p = NS). Frequency of myocardial infarction, unstable angina, stroke and congestive heart failure was not significantly different among the three strategies. The revascularization group had significantly fewer hospital admissions and nonprotocol revascularizations at 1 year. The incidence of death, myocardial infarction, nonprotocol revascularization or hospital admissions at 1 year was 32% with the angina-guided medical strategy, 31% with the ischemia-guided medical strategy and 18% with the revascularization strategy (p = 0.003). CONCLUSIONS. After 1 year, revascularization was superior to both angina-guided and ischemia-guided medical strategies in suppressing asymptomatic ischemia and was associated with better outcome. These findings require confirmation by a larger scale trial.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_statistics_&_numerical_data_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_statistics_&_numerical_data_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH S_statistics_&_numerical_data_MeSH Coronary_Artery_Bypass_statistics_&_numerical_data_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography__Ambulatory_statistics_&_numerical_data_MeSH M_Exercise_Test_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH S_therapy_MeSH Myocardial_Ischemia_therapy_MeSH M_Pilot_Projects_MeSH M_Prospective_Studies_MeSH M_Remission_Induction_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 7642857
----K E
----T Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.
----A OBJECTIVES. This study sought to examine the incidence, temporal profile and clinical implications of shock in a large trial of thrombolytic therapy for acute myocardial infarction. BACKGROUND. Despite advances in the treatment of acute ischemic syndromes, cardiogenic shock remains associated with significant morbidity and mortality. METHODS. Patients who presented within 6 h of symptom onset were randomized to four treatment strategies: 1) streptokinase plus subcutaneous heparin; 2) streptokinase plus intravenous heparin; 3) accelerated recombinant tissue-type plasminogen activator (rt-PA) plus intravenous heparin; or 4) streptokinase and rt-PA plus intravenous heparin. The primary end point was 30-day all-cause mortality. RESULTS. Shock occurred in 2,972 patients (7.2%): 315 (11%) had shock on arrival, and 2,657 (89%) developed shock after hospital admission. Reinfarction occurred in 11% of patients who developed shock compared with 3% of patients without shock. The mortality rate was significantly higher in patients who presented with (57%) or developed (55%) shock than in those without shock (3%) (p < 0.001). Shock developed significantly less frequently in patients receiving rt-PA. There were fewer deaths in patients who presented with shock and were treated with streptokinase plus intravenous heparin or who developed shock and were treated with streptokinase plus subcutaneous heparin. Patients who developed shock had a significantly lower 30-day mortality rate if angioplasty was performed. CONCLUSIONS. Because cardiogenic shock occurred most often after admission and with recurrent ischemia and reinfarction, recognizing signs of incipient shock may improve outcome. Fewer patients treated with rt-PA developed shock, yet those developing shock had the same high mortality rate as those presenting with shock, regardless of treatment. Only angioplasty was associated with a significantly lower mortality rate.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_statistics_&_numerical_data_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_statistics_&_numerical_data_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Reperfusion_MeSH S_methods_MeSH Myocardial_Reperfusion_methods_MeSH S_statistics_&_numerical_data_MeSH Myocardial_Reperfusion_statistics_&_numerical_data_MeSH M_Recombinant_Proteins_MeSH S_administration_&_dosage_MeSH Recombinant_Proteins_administration_&_dosage_MeSH M_Recurrence_MeSH M_Shock__Cardiogenic_MeSH S_complications_MeSH Shock__Cardiogenic_complications_MeSH S_drug_therapy_MeSH Shock__Cardiogenic_drug_therapy_MeSH S_epidemiology_MeSH Shock__Cardiogenic_epidemiology_MeSH S_etiology_MeSH Shock__Cardiogenic_etiology_MeSH M_Streptokinase_MeSH S_administration_&_dosage_MeSH Streptokinase_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thrombolytic_Therapy_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH S_statistics_&_numerical_data_MeSH Thrombolytic_Therapy_statistics_&_numerical_data_MeSH M_Time_Factors_MeSH M_Tissue_Plasminogen_Activator_MeSH S_administration_&_dosage_MeSH Tissue_Plasminogen_Activator_administration_&_dosage_MeSH M_Treatment_Outcome_MeSH 
****** 7642858
----K E
----T ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction.
----A OBJECTIVES. This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND. Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS. Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS. ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS. ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.
----P Clinical_Trial Journal_Article 
----M M_Anistreplase_MeSH S_administration_&_dosage_MeSH Anistreplase_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH S_instrumentation_MeSH Electrocardiography__Ambulatory_instrumentation_MeSH S_methods_MeSH Electrocardiography__Ambulatory_methods_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography__Ambulatory_statistics_&_numerical_data_MeSH M_Heart_Catheterization_MeSH M_Human_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Observer_Variation_MeSH M_Prospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH M_Thrombolytic_Therapy_MeSH S_methods_MeSH Thrombolytic_Therapy_methods_MeSH S_statistics_&_numerical_data_MeSH Thrombolytic_Therapy_statistics_&_numerical_data_MeSH M_Time_Factors_MeSH M_Tissue_Plasminogen_Activator_MeSH S_administration_&_dosage_MeSH Tissue_Plasminogen_Activator_administration_&_dosage_MeSH P_Vascular_Patency_MeSH 
****** 7648243
----K E
----T A double-blind comparison of bisoprolol and atenolol in patients with essential hypertension.
----A We compared the beta 1-selective adrenoceptor antagonists bisoprolol and atenolol in a double-blind, randomized crossover study. After 4 weeks placebo phase, 59 patients with essential hypertension received either 10 mg bisoprolol or 50 mg atenolol once daily for 8 weeks, increased if necessary (target BP < or = 150/90 mmHg) to 20 and 100 mg, respectively, after 4 weeks. After a second placebo phase, crossover occurred to the alternative drug. We measured resting systolic and diastolic blood pressures and heart rate at 24 h post-dose baseline and after 4 and 8 weeks treatment. Both drugs significantly lowered systolic and diastolic blood pressures and heart rate at 8 weeks compared to baseline (all p < 0.05). Bisoprolol reduced heart rate significantly more than atenolol (p < 0.01), but systolic and diastolic blood pressure changes were not different between the two drugs. There was no difference in patient acceptability of the drugs as assessed by visual analogue scale. Despite theoretical and circumstantial evidence to suggest superiority of bisoprolol over atenolol, no significant difference between the two was found except for greater heart rate reduction with bisoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 7649315
----K E
----T Labetalol vs. methyldopa in the treatment of pregnancy-induced hypertension.
----A OBJECTIVE: To assess the efficacy and safety of labetalol compared with methyldopa in the management of mild and moderate cases of pregnancy-induced hypertension (PIH). METHODS: One hundred four primigravidas with PIH were randomly allocated to receive either labetalol (group A) or methyldopa (group B). The dose of the drugs was doubled every 48 h to maintain a mean arterial blood pressure < or = 103.6 mmHg. Clinico-biochemical effects and frequency of side effects were studied. The statistical level of significance was taken at P < 0.05. RESULTS: Ten patients in group B (18.5%) developed significant proteinuria (> 30 mg/dl) whereas none developed proteinuria in group A. Labetalol was quicker and more efficient at controlling blood pressure, having a beneficial effect on renal functions and causing fewer side effects compared with methyldopa. The rate of induction of labor and rate of cesarean section for uncontrolled PIH was less in group A (48% and 1%, respectively) compared with group B (63.0% and 5.6%, respectively). Moreover a higher Bishop score at induction of labor was noticed in group A. CONCLUSIONS: Labetalol is better tolerated than methyldopa, gives more efficient control of blood pressure and may have a ripening effect on the uterine cervix.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cesarean_Section_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant__Newborn_MeSH M_Kuwait_MeSH M_Labetalol_MeSH S_adverse_effects_MeSH Labetalol_adverse_effects_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Labor__Induced_MeSH M_Methyldopa_MeSH S_adverse_effects_MeSH Methyldopa_adverse_effects_MeSH S_therapeutic_use_MeSH Methyldopa_therapeutic_use_MeSH M_Pre-Eclampsia_MeSH S_diagnosis_MeSH Pre-Eclampsia_diagnosis_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_diagnosis_MeSH Pregnancy_Complications__Cardiovascular_diagnosis_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH 
****** 7649498
----K I
----T Cyclandelate versus propranolol in the prophylaxis of migraine--a double-blind placebo-controlled study.
----A The aim of the present study was to ascertain the comparative efficacy of cyclandelate, a migraine prophylactic with calcium overload blocking properties, versus propranolol, a non-selective beta-adrenergic blocker, and placebo. Based on different statistical analysis procedures (including time series analysis) a responder and nonresponder evaluation for cyclandelate and propranolol was performed. In addition, an attempt was made to identify the dose relationship of the various drugs on headache parameters. In a double-blind placebo-controlled study 84 patients were treated in a placebo run-in phase (4 weeks). The patients were then randomized by the statistical criterion of placebo responder and nonresponder to either the cyclandelate or the propranolol group. The total treatment period included a low-dosage phase (8 weeks) and high-dosage phase (8 weeks). All patients kept a headache diary before, during and after treatment. The data were assessed by time series analysis (ARIMA), as well as by analysis of variance and nonparametric statistics. Based on ARIMA statistics, 39.3% of the patients showed a significant improvement of migraine during treatment with cyclandelate compared with 29.4% placed on propranolol. Higher doses of cyclandelate and propranolol were more effective. Using the qualitative response-criterion of a 50% reduction in migraine symptoms, cyclandelate showed a response in 67.9% and propranolol in 41.2% of all cases. It can therefore be concluded that cyclandelate as well as propranolol are two comparable substances in the prophylactic treatment of migraine, with cyclandelate showing fewer side effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Cyclandelate_MeSH S_administration_&_dosage_MeSH Cyclandelate_administration_&_dosage_MeSH S_adverse_effects_MeSH Cyclandelate_adverse_effects_MeSH S_therapeutic_use_MeSH Cyclandelate_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 7649593
----K E
----T Short- and long-term effects of antihypertensive drugs on arterial reflections, compliance, and impedance.
----A This article reviews our work on the effects of different classes of antihypertensive agents on the hemodynamic alterations in essential human hypertension. Short-term studies were done during cardiac catheterization in young normotensive subjects (mean age, 33 years; range, 19 to 40) and several different age-matched (range, 25 to 53 years) groups of patients with essential hypertension. Aortic impedance, resistance, wave reflections, and compliance were calculated from high-fidelity recordings of ascending aortic pressure and flow signals during baseline and after nitroprusside, propranolol followed by phentolamine, phentolamine, captopril, and nifedipine, respectively, at doses sufficient to normalize blood pressure in each hypertensive group. Propranolol exacerbated all the hemodynamic parameters; these effects were only partially overcome by phentolamine. Among the other agents only phentolamine did not completely normalize compliance, and only captopril did not completely normalize wave reflections. The long-term study was a randomized, double-blind comparison of fosinopril and atenolol in 79 normotensive subjects and 79 essential hypertensive patients. Baseline 24-hour ambulatory blood pressures and carotid artery tonometry to index wave reflections were performed in all subjects and in hypertensive patients after 8 weeks of therapy. Both fosinopril and atenolol normalized blood pressure and lowered the elevated augmentation index, but fosinopril had a significantly larger effect than atenolol. Both short- and long-term beta-blockade did not have as beneficial an effect as the other agents. Thus, the differing hemodynamic effects of the various classes of antihypertensive agents might be a consideration in the choice of therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Comparative_Study_MeSH M_Compliance_MeSH M_Double-Blind_Method_MeSH M_Electric_Impedance_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7654109
----K E
----T Response to a second single antihypertensive agent used as monotherapy for hypertension after failure of the initial drug. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A BACKGROUND: An important issue in clinical practice is how to treat patients whose blood pressure does not respond to the first antihypertensive drug selected. OBJECTIVE: To analyze the antihypertensive response of patients who had failed to achieve their diastolic blood pressure goal (< 90 mm Hg at the end of 8 to 12 weeks of titration) with one of six randomly allocated drugs or placebo to the random allocation of an alternate drug. METHODS: We initially randomized 1292 men with diastolic blood pressure of 95 to 109 mm Hg to treatment with hydrochlorothiazide, atenolol, captopril, clonidine hydrochloride, diltiazem hydrochloride (sustained release), prazosin hydrochloride, or placebo. Of 410 men in whom initial treatment failed, 352 qualified for randomization to the alternate drug. RESULTS: Of the 352 patients, 173 (49.1%) achieved their goal diastolic blood pressure, in 133 (37.8%) the alternate drug failed, and 46 (13.1%) left the study for various reasons. Overall response rates were as follows: diltiazem, 63%; clonidine, 59%; prazosin, 47%; hydrochlorothiazide, 46%; atenolol, 41%; and captopril, 37%. The best response rate for patients in whom hydrochlorothiazide failed was achieved with diltiazem (70%); after atenolol failure, clonidine (86%); after captopril failure, prazosin (54%); after clonidine failure, diltiazem (100%); after diltiazem failure, captopril (67%); and after prazosin failure, clonidine (53%). The combined response rate for patients initially randomized to an active treatment was 76.0%, which is similar to that achieved by the combination of two drugs in previous studies. CONCLUSIONS: We conclude that sequential single-drug therapy is a rational approach for treatment of hypertension in patients in whom initial drug therapy has failed.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Treatment_Failure_MeSH M_Treatment_Outcome_MeSH 
****** 7656846
----K E
----T [Coronary sinus blood flow after intracoronary or intravenous administration of bisoprolol in coronary disease]
----A OBJECTIVE: To measure changes in haemodynamics and myocardial blood flow after acute intravenous (i.v.) and intracoronary (i.c.) injection of bisoprolol in patients with coronary heart disease. PATIENTS AND METHODS: A prospective, randomized controlled study of 14 patients (12 men, 2 women; mean age 65 [50-73] years) with angio-graphically proven coronary artery stenosis (reduced in lumen of at least 70%) in one or more major vessels. Seven patients received, before balloon angioplasty, either 0.01 mg/kg body weight directly into the coronaries (group 1, infusion through the guiding catheter) or 2.5 mg (group 2, via the sheath). Heart rate and blood pressure were measured before and after bisoprolol injection. Coronary blood flow was measured by the thermodilution method via two indwelling catheters in the coronary sinus. RESULTS: After bisoprolol there was a reduction in heart rate (group 1: from 83/min to 75/min; group 2: from 77/min to 72/min) and blood pressure (group 1: from 137/80 mm Hg to 125/70 mm Hg; group 2: from 135/86 mm Hg to 126/80 mm Hg). Coronary blood flow was lower after i.c. bisoprolol injection than before (group 1: 383 ml/min vs 352 ml/min, but higher after i.v. injection (group 2: 353 ml/min vs 384 ml/min). These differences were statistically not significant. CONCLUSION: While after-load was clearly reduced and myocardial blood flow remained unchanged, bisoprolol improved myocardial oxygen balance. No different effects could be detected after intracoronary vs intravenous application of bisoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Coronary_Vessels_MeSH M_Data_Interpretation__Statistical_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Injections__Intra-Arterial_MeSH M_Injections__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 7657286
----K 3
----T Long-term effect of nadolol or nadolol plus isosorbide-5-mononitrate on renal function and ascites formation in patients with cirrhosis. GTIP Gruppo Triveneto per l'Ipertensione Portale.
----A The association beta-blockers plus nitrates has been reported to impair renal function and renal sodium handling, leading to increased risk of development of ascites, or worsening of a preexisting ascites, or increase in the requirements of diuretic agents. In 81 patients with cirrhosis and esophageal varices, participating in a multicenter controlled clinical trial of prophylaxis of variceal bleeding comparing nadolol (NAD) plus isosorbide-5-mononitrate (I5M) with NAD alone, renal function, presence of ascites, and diuretic requirements were assessed at inclusion and after 6 months of follow-up. No significant variation in s-urea or s-creatinine was observed in either group, Three patients in the nadolol group and two in the NAD plus I5M developed ascites at 6 months (P = .70), and a need to increase diuretic regimen was observed in four and three patients, respectively (P = .76). Decrease in heart rate and in mean arterial pressure was similar in the two groups. There was a significant correlation between increases in s-creatinine and decrease in mean arterial pressure in the whole series (P = .015). Only in patients treated with the association was there a significant larger proportion of patients ascitic who became anascitic, than of patients anascitic who became ascitic (P = .03). In patients treated with the association, there was a significantly larger decrease in hepatic venous pressure gradient (P = .05). It is concluded that patients treated with the association NAD plus I5M are not at increased risk of developing renal dysfunction or worsening of ascites compared with patients treated with NAD alone.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Ascites_MeSH S_etiology_MeSH Ascites_etiology_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Venous_Pressure_MeSH S_drug_effects_MeSH Venous_Pressure_drug_effects_MeSH 
****** 7662225
----K E
----T Effect of antihypertensive treatment on the increased beta 2-adrenoceptor density in patients with essential hypertension.
----A The effect of different antihypertensive drugs on the increased surface beta 2-adrenoceptor density in essential hypertension was evaluated to elucidate whether the possible effect of the treatment on these receptors was secondary to blood pressure decreases or a specific effect of the drugs. Thirty-nine untreated essential hypertensive patients and 28 normotensive control subjects were studied in basal conditions. Hypertensive patients were randomly assigned to three treatment groups: bisoprolol (10 mg/day, n = 15), enalapril (20 mg/day, n = 12), and verapamil SR (240 mg/day, n = 12), and were studied before and after 1 month of treatment. Plasma catecholamines were determined by a radioenzymatic assay. Surface beta 2-adrenoceptors were measured in intact lymphocytes by radioligand binding assay using the hydrophilic ligand [3H]-CGP12177. beta 2-adrenoceptor density was increased in hypertensive patients (P < .01). After treatment, mean blood pressure decreased similarly in the three groups, while plasma catecholamines showed no significant changes in any group. beta 2-adrenoceptor number decreased only in bisoprolol-treated patients (P < .05). Mean blood pressure decreases correlated with beta 2-adrenoceptor decrements only in bisoprolol-treated patients (r = 0.65, P < .05). beta 2-adrenoceptor density correlated with plasma epinephrine levels in the control group (r = -0.50, P < .01), but not in hypertensive patients before treatment. This correlation was also observed in hypertensive patients treated with bisoprolol (r = -0.52, P < .05), but not in those treated with verapamil or enalapril. Our results suggest that bisoprolol treatment reduces the increased surface beta 2-adrenoceptor density and restores its regulation by epinephrine in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Mass_Index_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lymphocytes_MeSH S_drug_effects_MeSH Lymphocytes_drug_effects_MeSH S_metabolism_MeSH Lymphocytes_metabolism_MeSH M_Male_MeSH M_Radioligand_Assay_MeSH M_Receptors__Adrenergic__beta-2_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta-2_drug_effects_MeSH S_metabolism_MeSH Receptors__Adrenergic__beta-2_metabolism_MeSH 
****** 7662242
----K E
----T Efficacy and tolerability of losartan potassium and atenolol in patients with mild to moderate essential hypertension.
----A The objective of this study was to compare the antihypertensive efficacy and tolerability of losartan potassium (losartan) and atenolol in patients with mild-to-moderate essential hypertension. This was a multinational, prospective, randomized, 12-week double-blind parallel study with a follow-up of 4 to 10 days posttreatment to assess any adverse effects of abrupt therapy withdrawal. Two hundred two patients were randomized (2:1) to treatment with losartan or atenolol, 50 mg once daily. Patients were titrated after 6 weeks to 100 mg once daily if their blood pressure was uncontrolled (sitting diastolic blood pressure > or = 90 mm Hg). Trough sitting diastolic blood pressure reductions at weeks 6 and 12 were similar in both the losartan (-9.2 mm Hg and -8.3 mm Hg) and atenolol (-10.8 mm Hg and -10.1 mm Hg) groups and a similar percentage of patients responded to each drug. Both agents were generally well tolerated, although eight patients (two patients taking losartan, and six taking atenolol) were withdrawn because of clinical adverse events (P < or = .05). Reduction in pulse rate from baseline averaged 10 beats/min in the atenolol group with no pulse rate reduction observed in the losartan group (P < .01). No evidence of rebound hypertension was observed in either group. In conclusion, losartan was as efficacious as atenolol in blood pressure reduction, and was at least as well tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_administration_&_dosage_MeSH Biphenyl_Compounds_administration_&_dosage_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Imidazoles_MeSH S_administration_&_dosage_MeSH Imidazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Imidazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Pulse_MeSH S_drug_effects_MeSH Pulse_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Time_Factors_MeSH 
****** 7664433
----K E
----T Double-blind, placebo-controlled study of the long-term efficacy of carvedilol in patients with severe chronic heart failure.
----A BACKGROUND: Clinical trials have shown that beta-adrenergic blocking drugs are effective and well tolerated in patients with mild to moderate heart failure, but the utility and safety of these drugs in patients with advanced disease have not been evaluated. METHODS AND RESULTS: We enrolled 56 patients with severe chronic heart failure into a double-blind, placebo-controlled study of the vasodilating beta-blocker carvedilol. All patients had advanced heart failure, as evidenced by a mean left ventricular ejection fraction of 0.16 +/- 0.01 and a mean maximal oxygen consumption of 13.6 +/- 0.6 mL.kg-1.min-1 despite digitalis, diuretics, and an angiotensin-converting enzyme inhibitor (if tolerated). After a 3-week, open-label, up-titration period, 49 of the 56 patients were assigned (in a double-blind fashion using a 2:1 randomization) to receive either carvedilol (25 mg BID, n = 33) or matching placebo (n = 16) for 14 weeks, while background therapy remained constant. Hemodynamic and functional variables were measured at the start and end of the study. Compared with the placebo group, patients in the carvedilol group showed improved cardiac performance, as reflected by an increase in left ventricular ejection fraction (P = .005) and stroke volume index (P = .010) and a decrease in pulmonary wedge pressure, mean right atrial pressure, and systemic vascular resistance (P = .003, .002, and .017, respectively). In addition, compared with placebo, patients treated with carvedilol benefited clinically, as shown by an improvement in symptom scores (P = .002), functional class (P = .013), and submaximal exercise tolerance (P = .006). The combined risk of death, worsening heart failure, and life-threatening ventricular tachyarrhythmia was lower in the carvedilol group than in the placebo group (P = .028), but carvedilol-treated patients had more dizziness and advanced heart block. CONCLUSIONS: Carvedilol produces clinical and hemodynamic improvement in patients who have severe heart failure despite treatment with angiotensin-converting enzyme inhibitors.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 7664508
----K E
----T Exercise metabolism during 1 hour of treadmill walking while taking high and low doses of propranolol, metoprolol, or placebo.
----A Aerobic exercise and beta-blocking drugs are regularly prescribed as treatment for hypertension and as a prophylactic for patients at risk from coronary heart disease and for those recovering from an infarct. Some beta blockers, particularly non-beta 1-selective drugs, may make exercise more difficult, possibly by interfering with substrate metabolism during exercise. This study examined the effects of low and high doses of a beta 1-selective blocker, metoprolol, and a non-selective beta blocker, propranolol, on exercise metabolism. The study involved 20 healthy subjects (10 men, 10 women) who walked on a treadmill at 50% of their maximal oxygen uptake for 1 h on five occasions, separated by 7 days. On each of the five occasions they received one of the following treatments, given in random order: placebo, metoprolol 50 mg, metoprolol 100 mg, propranolol 40 mg, or propranolol 80 mg, all taken twice daily. Fat oxidation, expressed as a percentage of total energy expenditure, was significantly lower than with placebo for all of the active treatments except metoprolol 50 mg (placebo: 42.7 +/- 11.6%; metoprolol 50 mg: 38.7 +/- 14.1%, p = NS; metoprolol 100 mg: 36.3 +/- 13.7%, p = 0.05; propranolol 40 mg: 31.2 +/- 9.3%, p = 0.01; propranolol 80 mg: 29.5 +/- 10.9%, p = 0.01); and significantly lower with propranolol than with metoprolol (propranolol 40 mg: p = 0.0036; propranolol 80 mg: p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Cross-Over_Studies_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Energy_Metabolism_MeSH S_drug_effects_MeSH Energy_Metabolism_drug_effects_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7669306
----K E
----T Does monitoring end-tidal isoflurane concentration improve titration during general anesthesia?
----A STUDY OBJECTIVE: To assess the value of end-tidal anesthetic gas monitoring with respect to intraoperative hemodynamic stability and recovery times. DESIGN: Randomized blinded study. SETTING: Operating rooms at a university teaching hospital. PATIENTS: 120 ASA I and II patients receiving general anesthesia maintained with isoflurane and nitrous oxide (N2O). INTERVENTIONS: Following a standardized induction technique, patients were assigned to either an end-tidal isoflurane monitored (n = 60) or unmonitored (n = 60) group. During each operation, the anesthesiologist attempted to maintain an adequate "depth of anesthesia" by varying the administered concentration of isoflurane with or without information from an end-tidal isoflurane monitor. Intraoperative hemodynamic stability was assessed by determining the variation from a preincisional "baseline" mean arterial pressure (MAP) value established during a 10 minute interval immediately prior to the surgical incision. Recovery times were recorded from discontinuation of isoflurane and N2O until awakening, orientation, and postanesthesia care unit discharge. MEASUREMENTS AND MAIN RESULTS: Intraoperative hemodynamic stability was assessed in each patient and reported as the average error from the baseline MAP, absolute average error from the baseline MAP, coefficients of variation of heart rate (HR), systolic and diastolic MAP, and end-tidal isoflurane concentrations. Both study groups had similar intraoperative MAP and HR values, average error and coefficients of variation for the hemodynamic variables, as well as similar numbers of episodes of hypertension, hypotension, tachycardia, and bradycardia. Finally, the two groups were comparable with respect to early recovery times and postoperative side effects. CONCLUSIONS: This study suggests that end-tidal isoflurane monitoring does not improve the titration of isoflurane during general anesthesia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH P_Isoflurane_MeSH M_Middle_Aged_MeSH P_Monitoring__Intraoperative_MeSH M_Tidal_Volume_MeSH M_Titrimetry_MeSH 
****** 7669481
----K E
----T Effects of different antihypertensive drugs on plasma fibrinogen in hypertensive patients.
----A 1. In order to evaluate whether treatment with different antihypertensive drugs would affect plasma fibrinogen levels, 118 mild to moderate essential hypertensive subjects, all males, aged 18 to 65 years, were randomly treated with amlodipine 10 mg, atenolol 100 mg, hydrochlorothiazide 25 mg or lisinopril 20 mg, all given once daily for 8 weeks. 2. Before and after 8 weeks' treatment, blood pressure (BP), heart rate (HR), fibrinogen, total cholesterol (TC), HDL-C, LDL-C, triglycerides (TG), plasma glucose, plasma uric acid, serum creatinine and serum potassium were evaluated. 3. All four medications significantly reduced BP values, although the BP lowering effect of lisinopril, amlodipine and atenolol was significantly greater compared with that of hydrochlorothiazide. 4. Plasma fibrinogen levels were unaffected by atenolol, hydrochlorothiazide and amlodipine, whereas they were significantly decreased by lisinopril (-11.2%, P = 0.002). This fibrinogen lowering effect was more evident in smokers (-17.7%) than in non smokers (-7.4%). 5. Atenolol and amlodipine did not significantly affect plasma lipids, hydrochlorothiazide increased TC, LDL-C and TG and reduced HDL-C; lisinopril increased HDL-C and decreased TC and LDL-C. 6. Hydrochlorothiazide increased plasma glucose and uric acid concentrations, which were unaffected by the other drugs. The diuretic also reduced serum potassium. 7. The results of this study indicate that lisinopril reduces levels of plasma fibrinogen and confirm that different antihypertensive drugs may elicit different metabolic effects, which may variously influence the overall risk profile of the hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Fibrinogen_MeSH S_metabolism_MeSH Fibrinogen_metabolism_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Lisinopril_MeSH S_administration_&_dosage_MeSH Lisinopril_administration_&_dosage_MeSH S_pharmacology_MeSH Lisinopril_pharmacology_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH M_Uric_Acid_MeSH S_blood_MeSH Uric_Acid_blood_MeSH 
****** 7545768
----K E
----T Current approaches in patients with ventricular tachyarrhythmias.
----A The article has summarized the studies and ongoing trials looking at the significance and treatment of ventricular tachyarrhythmias. In most instances, the presence of these arrhythmias is associated with an increased risk of future arrhythmic events. Electrophysiologic studies are helpful in risk stratification in patients with coronary artery disease but can be misleading in the setting of dilated cardiomyopathy and often produce nonspecific results in patients with HCM. The need for an invasive electrophysiologic study is crucial in the diagnosis of certain ventricular arrhythmias that are amenable to cure with radiofrequency catheter ablation, such as idiopathic ventricular tachycardia and BBR-VT. The correct approach for patients with SVT not amenable to catheter ablation remains to be determined. In deciding whether to use a device or drug therapy, however, one should take into consideration the degree of left ventricular dysfunction and the overall health status of the patient. For example, device implantation clearly reduces sudden death in patients with severe left ventricular dysfunction but may not change total mortality because these same patients may die of congestive heart failure. Device therapy might be more cost-effective for patients with less severe depression of left ventricular function.
----P Journal_Article Review Review__Tutorial 
----M M_Cardiac_Complexes__Premature_MeSH S_diagnosis_MeSH Cardiac_Complexes__Premature_diagnosis_MeSH S_mortality_MeSH Cardiac_Complexes__Premature_mortality_MeSH S_therapy_MeSH Cardiac_Complexes__Premature_therapy_MeSH M_Electrocardiography__Ambulatory_MeSH M_Human_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 7555159
----K E
----T Changes in wall motion in patients treated for unstable angina. A suggestion of the stunned and hibernating myocardium in humans. UNASEM Collaborative Study Group. Unstable Angina Study Using Eminase.
----A BACKGROUND: A double-blind, placebo-controlled study using anistreplase was performed in 159 patients with unstable angina. All patients had a history of unstable angina combined with typical ECG changes and without evidence of a previous, recent, or ongoing myocardial infarction. The purpose of the present study was to analyze the relationship between the patency of the culprit artery and the behavior of the ischemia-related regional left ventricular (LV) wall motion. METHODS AND RESULTS: On entry to the study, all patients received conventional drug therapy: i.v. nitroglycerin therapy, an oral beta-blocking agent, and a calcium antagonist. Baseline angiography was carried out within 3 h after randomization, a mean of 4.2 +/- 3.0 h (range, 1 to 17 h) after the last attack of chest pain. Treatment with trial medication was withheld in 33 cases. Sixty-five patients with coronary artery disease received anistreplase (30 U/5 min)/heparin and 61 patients heparin-only therapy. Angiography was repeated 20.6 +/- 4.6 h (mean +/- SD; range, 12 to 39 h) after the baseline angiographic study. To assess changes in regional myocardial wall motion, the LV wall was divided into seven segments. The ischemia-related coronary artery stenosis was calculated quantitatively and related to the quantitatively assessed mean regional left ventricular ejection fraction (RLVEF) of the ischemia-related segments. In 118 of 126 patients who received trial medication, we found that anistreplase/heparin therapy leads to a significantly (p < 0.01) greater reduction in coronary artery diameter stenosis than heparin-only therapy (n = 63, mean +/- SD, 11 +/- 22, vs n = 55, mean +/- SD, 3 +/- 11%). Anistreplase/heparin therapy was related to a larger significant improvement of the ischemia-related RLVEF than heparin-only therapy, although the latter association was not statistically significant (n = 63, mean +/- SD, 7 +/- 15, vs n = 55, mean +/- SD, 5 +/- 14%). The effects of change of coronary artery stenosis on regional LV wall motion were also determined. A paradoxical finding was that a persistently occluded vessel or a vessel showing an increase in coronary artery stenosis was associated with a greater improvement of the ischemia-related RLVEF than a reopened vessel or a vessel with a reduction in coronary artery stenosis (n = 15, mean +/- SD, 7 +/- 11, vs n = 41, mean +/- SD, 8 +/- 13, vs n = 15, mean +/- SD, 1 +/- 12, vs n = 47, mean +/- SD, 5 +/- 16%, NS). One day after the last attack of chest pain, the regional LV wall motion was still abnormal in about 20% of patients. CONCLUSION: In these patients with unstable angina, the LV wall motion improved both in the treated and the control group at follow-up angiography 1 day later. Improved coronary arterial anatomy was associated with a lesser improvement of the LV contractile function than when worsening of the coronary angiographic appearance occurred. There is no rational explanation of these results. This is a beginning of an effort to elucidate the clinical significance of the stunned and hibernating myocardium in humans.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH S_physiopathology_MeSH Angina__Unstable_physiopathology_MeSH S_radiography_MeSH Angina__Unstable_radiography_MeSH M_Anistreplase_MeSH S_therapeutic_use_MeSH Anistreplase_therapeutic_use_MeSH M_Chest_Pain_MeSH S_drug_therapy_MeSH Chest_Pain_drug_therapy_MeSH S_physiopathology_MeSH Chest_Pain_physiopathology_MeSH S_radiography_MeSH Chest_Pain_radiography_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Catheterization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Stunning_MeSH S_drug_therapy_MeSH Myocardial_Stunning_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Stunning_physiopathology_MeSH S_radiography_MeSH Myocardial_Stunning_radiography_MeSH M_Statistics__Nonparametric_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 7572650
----K E
----T Usefulness of heart rate variability in predicting drug efficacy (metoprolol vs diltiazem) in patients with stable angina pectoris.
----A We investigated whether analysis of heart rate (HR) variability may be used to predict the efficacy of drug treatment of myocardial ischemia. In a double-blind, crossover study, 28 patients with stable angina pectoris, proven coronary artery disease, and myocardial ischemia during Holter monitoring received metoprolol controlled-release 200 mg once daily and diltiazem 60 mg 4 times daily. After a placebo run-in phase and after each treatment period, 72-hour Holter recordings were obtained for HR variability and ST-segment analysis. At baseline, the total duration of myocardial ischemia was 11.4 +/- 13.9 minutes (mean +/- SD per 24 hours), and the total number of episodes was 2.2 +/- 2.3. Metoprolol significantly reduced the total duration of ischemia by -8.7 minutes (95% CI -14.5 to -2.8) and the total number of episodes by -1.9 (-2.9 to -0.8) in patients with a low SD of normal-to-normal intervals at baseline (SDNN), using the median value of 50 ms as a cut-off value. In contrast, significant treatment effects were not observed in patients with a high SDNN at baseline. Similar results were obtained using baseline total power or low-frequency power, but not when using baseline heart rate. Diltiazem reduced the total duration of ischemia by -4.9 minutes (-9.7 to -0.1), but not the number of episodes. Moreover, in contrast to metoprolol, efficacy of diltiazem was not related to baseline HR variability. In conclusion, patients with reduced HR variability at baseline responded to treatment with metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH P_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7551972
----K I
----T Pharmacological therapy for portal hypertension: rationale and results.
----A Drug therapy for acute variceal bleeding should be viewed as an adjunct to emergency sclerotherapy. Its role in preventing very early rebleeding (within days) following sclerotherapy needs to be established. The best candidates for such a role are somatostatin and octreotide, but glypressin and vasopressin and nitroglycerin combinations have therapeutic effects in the short-term. Propranolol is the drug for long-term prevention of rebleeding and prevention of the first variceal bleed. For primary prophylaxis it significantly reduces the rate of bleeding, and there is a trend towards reducing mortality. It should be used in cirrhotic patients with large varices. For secondary prophylaxis, propranolol significantly reduces rebleeding but does not improve survival. The reduction in rebleeding is similar to long-term sclerotherapy when compared in randomized studies. There is no value in adding beta-blockers to sclerotherapy compared with sclerotherapy alone, but few studies have evaluated the effects after the eradication of varices. beta-Blockers can be used as the first-line therapy to prevent variceal rebleeding. They also have been shown to reduce the frequency of rebleeding from congestive gastropathy. Many patients do not have a portal pressure reduction with propranolol. The addition of isosorbide mononitrate converts many nonresponders to responders. Current clinical trials are evaluating if therapeutic efficacy is improved by these drug combinations.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Hemostasis__Endoscopic_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Sclerotherapy_MeSH M_Vasoconstrictor_Agents_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 7557093
----K E
----T Continuous prazosin administration in cirrhotic patients: effects on portal hemodynamics and on liver and renal function.
----A BACKGROUND & AIMS: Hepatic vascular resistance is influenced by alpha-adrenergic tone. The aim of this study was to investigate the effects of continuous blockade of alpha-adrenoceptors with prazosin on hemodynamics, liver function, and renal function and whether the association of propranolol or furosemide enhances the portal pressure lowering effect of prazosin. METHODS: Cirrhotic patients with portal hypertension were studied at baseline and after a 3-month course of prazosin (n = 18) or placebo (n = 10). RESULTS: No changes were observed in the placebo group. Prazosin decreased the hepatic venous pressure gradient (HVPG) while increasing hepatic blood flow. Liver function improved as shown by an increase in hepatic and intrinsic hepatic clearances of indocyanine green and galactose elimination capacity. A significant reduction in mean arterial pressure and systemic vascular resistance was associated with increases in plasma renin activity and aldosterone concentration and a decrease in glomerular filtration rate. The plasma volume increased significantly, and 6 patients developed edema. The association of propranolol (n = 8) but not furosemide (n = 7) to prazosin increased the reduction in HVPG and attenuated the increase in plasma renin activity. CONCLUSIONS: In cirrhotic patients, continuous prazosin administration reduces portal pressure and improves liver perfusion and function but favors sodium and water retention. The association of propranolol enhances the decrease in portal pressure, suggesting a potential benefit from this combined therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Female_MeSH M_Furosemide_MeSH S_pharmacology_MeSH Furosemide_pharmacology_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Liver_MeSH S_drug_effects_MeSH Liver_drug_effects_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Liver_Cirrhosis_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_System_MeSH S_drug_effects_MeSH Portal_System_drug_effects_MeSH M_Prazosin_MeSH S_administration_&_dosage_MeSH Prazosin_administration_&_dosage_MeSH S_pharmacology_MeSH Prazosin_pharmacology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Venous_Pressure_MeSH S_drug_effects_MeSH Venous_Pressure_drug_effects_MeSH 
****** 7546992
----K I
----T Effects of beta receptor antagonists in patients with clinical evidence of heart failure after myocardial infarction: double blind comparison of metoprolol and xamoterol.
----A OBJECTIVE--To evaluate whether xamoterol, a partial agonist, would improve exercise time more than metoprolol in patients with mild to moderate heart failure after a myocardial infarction. DESIGN--Single-centre double blind randomised parallel group comparison of metoprolol 50-100 mg and xamoterol 100-200 mg twice daily. PATIENTS--210 patients aged 40-80 years (173 men) with clinical evidence of heart failure early after a myocardial infarction. 106 were given metoprolol and 104 xamoterol. MAIN OUTCOME MEASURES--Exercise test results and performance at three months; the exercise test, quality of life, and clinical assessments at baseline (5-7 days after the infarction) and after 3, 6, and 12 months. RESULTS--Exercise time increased at three months by 22% in the metoprolol group and 29% in the xamoterol group, but with no significant difference between the groups. Patients taking xamoterol showed overall non-significantly higher mean values of exercise time achieved with higher heart rates at rest and exercise. Improvements in quality of life, clinical signs of heart failure, and New York Heart Association functional class were seen in both treatment groups over one year, with minor benefits of xamoterol on breathlessness, peripheral oedema, and functional class. Eighteen patients taking metoprolol and 22 taking xamoterol withdrew from the study during one year, with a low mortality, reinfarction rate, and progress of heart failure in both treatment groups. Mean dose from baseline to 3 months was 135 mg metoprolol and 347 mg xamoterol. CONCLUSION--beta 1 Receptor antagonists with or without partial agonist activity are safe to use in mild to moderate heart failure after a myocardial infarction. Exercise tolerance, quality of life, and clinical signs and functional class of heart failure improve, and few patients show deterioration in their condition. Exercise tolerance is no better with xamoterol than metoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Xamoterol_MeSH S_therapeutic_use_MeSH Xamoterol_therapeutic_use_MeSH 
****** 7562888
----K E
----T Measurement of trough-to-peak ratios of four anti-hypertensive drugs on the basis of 24 h ambulatory blood pressure monitoring: different methods may give different results.
----A With 24 h ambulatory blood pressure monitoring (ABPM), the trough-to-peak (T/P) ratios (corrected for placebo) of atenolol 100 mg, cilazapril 2.5 mg, enalapril 20 mg and nifedipine-GITS 30 mg administered once daily for 4 weeks were determined in four groups of hypertensive patients. T/P ratios were calculated by three different methods: directly from the curves that averaged all individual 24 h profiles (A); averaging all individual T/P ratios after ABPM data were averaged for each patient over either 1 h intervals (B) or 3 h intervals (C). Methods B and C produced different values of T/P which, for each drug, were significantly higher with method C. With method A, nifedipine appeared to have the higher T/P. With methods B and C (which in contrast to method A, permitted statistical comparisons), differences between nifedipine and the other drugs were not significant. Meanwhile, method B appears to adhere most closely to FDA guidelines by taking more into account the interindividual variability of BP profile. Thus, we suggest that precise guidelines for measuring T/P on the basis of ABPM are needed, whereas for the comparison between drugs, both the mean value of the T/P and its variance must be determined.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 7549854
----K E
----T Propranolol or sclerotherapy to prevent variceal rebleeding.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH 
****** 7472698
----K I
----T Comparison of a lifestyle modification program with propranolol use in the management of diastolic hypertension.
----A OBJECTIVE: To compare the management of mild diastolic hypertension (90 to 104 mm Hg) using a nonpharmacologic intervention with that using propranolol or placebo. DESIGN: Randomized, placebo-controlled trial with a 2 x 2 factorial design. SETTING: University-based ambulatory care center. PARTICIPANTS: Two hundred seven men and 105 women, 22 to 59 years of age, 73% white, who had mild diastolic hypertension untreated for at least eight weeks. INTERVENTIONS: 1) a multicomponent lifestyle modification intervention (lifestyle focus group, or LFG) administered in eight weekly meetings + placebo, 2) LFG + propranolol, 3) propranolol alone, and 4) placebo alone, followed for 12 months. MEASUREMENTS: Systolic blood pressure (SBP), diastolic blood pressure (DBP), and self-reported adverse effects at each of nine follow-up visits; fasting total cholesterol, triglycerides, and glucose at baseline and 12 months; 24-hour urine sodium (Na+) and potassium (K+), three-day food records and physical activity questionnaire at three and 12 months; and a quality of life questionnaire at 12 months. MAIN RESULTS: The mean decreases in DBP at 12 months were: 8.5 mm Hg in the LFG + propranolol group; 7.7 mm Hg in the propranolol-only group; 5.9 mm Hg in the placebo-only group; and 5.4 mm Hg in the LFG + placebo group. Repeated-measures analysis of covariance showed that level of baseline DBP (p < 0.0001), time of follow-up (p < 0.0001), and propranolol use (p < 0.0001) were significantly associated with a decrease in DBP at 12 months. Despite reductions in urinary Na+ (-35 mEq; 95% CI = -50, -19), dietary Na+ (-521 mg; 95% CI = -710, -332), total calories ingested (-238; 95% CI = -335, -140), and weight (-1.4 lb; 95% CI = -3.7, +0.8), and significant increases in dietary K+ (+294 mg; 95% CI = +107, +480) and in mets-minutes of exercise (+43; 95% CI = +20, +67) at three months, assignment to the LFG intervention had no effect on DBP at three or 12 months. The subjects assigned to take propranolol more frequently reported fatigue during ordinary activities, sleep disturbance, decrease in sexual activity, and depressed feelings, when compared with the subjects taking placebo, but the numbers of study withdrawals did not differ by drug assignment. No significant difference in total cholesterol and glucose levels was observed by group assignment. Triglycerides increased significantly in the subjects assigned to propranolol (mean difference = +20 mg/dL; 95% CI of difference +1.5, +39). There was no difference in the responses to 21 quality of life items between the subjects assigned to propranolol and those assigned to placebo. CONCLUSIONS: This multicomponent lifestyle modification intervention was unable to promote persistent behavior changes and thus was inferior to propranolol therapy for the treatment for mild diastolic hypertension. Future research should focus on single modifiable factors to lower blood pressure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH 
****** 7546754
----K E
----T Desflurane controls the hemodynamic response to surgical stimulation more rapidly than isoflurane.
----A STUDY OBJECTIVE: To compare the control of hemodynamic response to surgical stimulus of desflurane to that of isoflurane. DESIGN: Prospective randomized study. SETTING: Operating room of a major U.S. teaching hospital. PATIENTS: 59 ASA status I, II, and III patients 18 to 80 years of age and were undergoing orthopedic or intra-abdominal surgical procedures of 1 or more hours in duration. INTERVENTIONS: Group 1 (n = 29) received desflurane in oxygen (O2) for their surgical procedure. Group 2 (n = 30) received isoflurane in O2 for their surgical procedure. Thiopental sodium 4 mg/kg and fentanyl 3 micrograms/kg provided induction; vecuronium 0.1 mg/kg facilitated intubation. Prior to incision the volatile anesthesia drug was titrated to maintain systolic blood pressure (SBP) within 20% of preinduction (baseline) values. Any time after incision, an SBP increase greater than 20% of baseline was treated with a 30% increase in inspired anesthetic concentration for 3 minutes, or until SBP was within 10% of baseline. Another three 30% increases were allowed at 3 minute intervals to return SBP to 10% of baseline. If four 30% increases did not return SBP to 10% of baseline, additional fentanyl up to 5 micrograms/kg or labetalol in 5 mg increments was given. MEASUREMENTS AND MAIN RESULTS: Measurement of hemodynamics and anesthetic concentration occurred every 2 minutes prior to skin incision and every 5 minutes thereafter. Measurement of hemodynamics and anesthetic concentration occurred every minute during treatment of blood pressure (BP) response to surgical stimulus. Desflurane allowed for more rapid control of BP response to surgical stimulus median 2 minutes (range 1 to 12 minutes) for desflurane versus 6 minutes (range 1 to 12 minutes, p = 0.011). The desflurane group required fewer 30% incremental anesthetic increases than the isoflurane group (1.8 versus 2.5, p = 0.016) to control increased SBP. End tidal/inspired drug concentration ratios were closer to unity in the desflurane patients both before (0.94 versus 0.80) and after (0.86 versus 0.70) changes in drug concentration to treat increased SBP. CONCLUSIONS: Anesthetic depth can be more rapidly titrated with desflurane compared to isoflurane. Alveolar/inspired concentration ratio approaches unity more rapidly with desflurane anesthesia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH P_Anesthesia__Inhalation_MeSH P_Anesthetics__Inhalation_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Intraoperative_Period_MeSH M_Isoflurane_MeSH S_analogs_&_derivatives_MeSH Isoflurane_analogs_&_derivatives_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Surgical_Procedures__Operative_MeSH S_adverse_effects_MeSH Surgical_Procedures__Operative_adverse_effects_MeSH 
****** 7553993
----K E
----T Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: a comparison of propofol and isoflurane.
----A The purpose of this study was to compare two anaesthetic protocols for haemodynamic instability (heart rate (HR) or mean arterial pressure (MAP) < 80 or > 120% of ward baseline values) measured at one-minute intervals during carotid endarterectomy (CEA). One group received propofol/alfentanil (Group Prop; n = 14) and the other isoflurane/alfentanil (Group Iso; n = 13). Periods of haemodynamic instability were correlated to episodes of myocardial ischaemia as assessed by Holter monitoring (begun the evening before surgery and ceasing the morning of the first postoperative day). In Group Prop, anaesthesia was induced with alfentanil 30 micrograms.kg-1 i.v., propofol up to 1.5 mg.kg-1 and vecuronium 0.15 mg.kg-1, and maintained with infusions of propofol at 3-12 mg.kg-1.hr-1 and alfentanil at 30 micrograms.kg-1.hr-1. In Group Iso, anaesthesia was induced with alfentanil and vecuronium as above, thiopentone up to 4 mg.kg-1 and maintained with isoflurane and alfentanil infusion. Phenylephrine was infused to support MAP at 110 +/- 10% of ward values during cross-clamp of the internal carotid artery (ICA) in both groups. Emergence hypertension and/or tachycardia was treated with labetalol, diazoxide or propranolol. Myocardial ischaemia was defined as ST-segment depression of > or = 1 mm (60 msec past the J-point) persisting for > or = one minute. For the entire anaesthetic course (induction to post-emergence), there was no difference between groups for either duration or magnitude outside the < 80 or > 120% range for HR or MAP. However, when the period of emergence from anaesthesia (reversal of neuromuscular blockade to post-extubation) was assessed, more patients were hypertensive (P = 0.004) and required vasodilator therapy in Group Iso (10/13 vs 5/14; P = 0.038 Fisher's Exact Test). The mean dose of labetalol was greater in Group Iso (P = 0.035). No patient demonstrated myocardial ischaemia during ICA cross-clamp. On emergence, 6/13 patients in Group Iso demonstrated myocardial ischaemia compared with 1/14 in Group Prop (P = 0.029). Therefore, supporting the blood pressure with phenylephrine, during the period of ICA cross-clamping, appears to be safe as we did not observe any myocardial ischaemia at this time. During emergence from anaesthesia, haemodynamic instability was associated with myocardial ischaemia. Under these specific experimental conditions, with emergence, hypertension and myocardial ischaemia were more prevalent with more frequent pharmacological interventions in patients receiving isoflurane.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH P_Anesthesia__Inhalation_MeSH P_Anesthesia__Intravenous_MeSH P_Anesthetics__Inhalation_MeSH P_Anesthetics__Intravenous_MeSH M_Blood_Pressure_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Electrocardiography__Ambulatory_MeSH M_Endarterectomy__Carotid_MeSH S_adverse_effects_MeSH Endarterectomy__Carotid_adverse_effects_MeSH M_Heart_Rate_MeSH P_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Intraoperative_Complications_MeSH S_etiology_MeSH Intraoperative_Complications_etiology_MeSH S_physiopathology_MeSH Intraoperative_Complications_physiopathology_MeSH P_Isoflurane_MeSH M_Middle_Aged_MeSH M_Monitoring__Intraoperative_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH P_Propofol_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia_MeSH S_etiology_MeSH Tachycardia_etiology_MeSH S_physiopathology_MeSH Tachycardia_physiopathology_MeSH 
****** 7547016
----K I
----T Metoprolol treatment for two years after coronary bypass grafting: effects on exercise capacity and signs of myocardial ischaemia.
----A OBJECTIVE--To evaluate whether prophylactic treatment with metoprolol for two years after coronary artery bypass grafting improves working capacity and reduces the occurrence of myocardial ischaemia in patients with coronary artery disease. METHODS--After coronary artery bypass grafting, patients were randomised to treatment with metoprolol or placebo for two years. Two years after randomisation, a computerised 12-lead electrocardiogram was obtained during a standardised bicycle exercise test in 618 patients (64% of all those randomised). RESULTS--The median exercise capacity was 140 W in the metoprolol group (n = 307) and 130 W in the placebo group (n = 311) (P > 0.20). An ST depression of > or = 1 mm at maximum exercise was present in 34% of the patients in the metoprolol group and 38% in the placebo group (P > 0.20) and an ST depression of > or = 2 mm at maximum exercise was present in 11% in the metoprolol group and 16% in the placebo group (P = 0.09). The median values for maximum systolic blood pressure were 200 mm Hg in the metoprolol group and 210 mm Hg in the placebo group (P < 0.0001), while the median values for maximum heart rate were 126 beats/min in the metoprolol group and 143 beats/min in the placebo group (P < 0.0001). The occurrence of cardiac and neurological clinical events two years postoperatively among exercised patients was comparable in the treatment groups. CONCLUSIONS--Treatment with metoprolol for two years after coronary artery bypass grafting did not significantly change exercise capacity or electrocardiographic signs of myocardial ischaemia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Postoperative_Period_MeSH 
****** 7487237
----K E
----T Should dihydropyridines be used as first-line drugs in the treatment of hypertension? The con side.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Dihydropyridines_MeSH S_adverse_effects_MeSH Dihydropyridines_adverse_effects_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 7549345
----K 4
----T [Multicenter double-blind study with 0.25% timolol in Gelrite (TG) once daily vs. 0.25% timolol solution (TS) twice daily. German Study Group]
----A In a 12-week double-masked trial we compared the ocular hypotensive effect of 0.25% timolol in Gelrite administered once daily (TG) to that of 0.25% timolol solution administered twice daily (TS). A second objective was to compare the tolerability and the safety of these treatments. Timolol in Gelrite is a new topical formulation of timolol in an anionic heteropolysaccharide gellan gum. A total of 156 patients entered the study after an appropriate wash-out. The medication schedule included one drop of test drug in each eye at 9 a.m. (active drug for both groups) and 9 p.m. (placebo for the TG group, active drug for the TS group). At trough, the mean decrease from baseline intraocular pressure (after appropriate wash-out) ranged from 5.7 to 6.3 mmHg for the TG group and from 5.9 to 6.2 mmHg for the TS group. The difference between the treatment group means ranged from -0.4 to 0.4 mmHg. At peak, the mean decrease from baseline IOP ranged from 5.3 to 6.2 mmHg for TG group and from 5.1 to 6.1 mmHg for the TS group. The difference between the treatment group means ranged from -0.7 to 0.4 mmHg. The results of this study support the hypothesis of a comparable hypotensive effect at peak and trough of 0.25% timolol in Gelrite q.d. to 0.25% timolol solution b.i.d. Furthermore, timolol in Gelrite has an acceptable tolerability profile. The incidence of blurred vision was higher in the Gelrite group, but this different was not statistically significant. The incidence of foreign body sensation was significantly higher in the Gelrite group (P < 0.022).(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Polysaccharides__Bacterial_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH M_Vehicles_MeSH 
****** 10155349
----K E
----T Efficacy of carvedilol in mild to moderate essential hypertension and effects on microalbuminuria: a multicenter, randomized, open-label, controlled study versus atenolol.
----A In this randomized, open-label, multicenter comparison, 140 adults with mild to moderate essential hypertension were treated with the nonselective beta blocker carvedilol (25 mg once daily) or the selective beta 1 blocker atenolol (100 mg once daily) orally for 2 months. Systolic and diastolic blood pressure and heart rate were measured monthly in the supine and standing positions. Urinary albumin levels and blood lipid profile were determined at baseline and at study end. The occurrence of cold extremities was monitored throughout the study. Both treatments significantly decreased systolic and diastolic blood pressure at a comparable level. At the final assessment, 88% of the carvedilol group achieved a supine diastolic blood pressure of 90 mm Hg or lower, compared with 82% of the atenolol group. Atenolol produced the greater decrease in heart rate, but between-group differences were significant only for standing measurements. With carvedilol, urinary albumin decreased in 25% of patients and increased in 2%; corresponding figures with atenolol were 13% and 12%. At study end, 10% of the carvedilol group and 37% of the atenolol group complained of cold extremities. No major between-group differences were observed in the percentage of patients with an increase in high-density lipoprotein or a decrease in low-density lipoprotein cholesterol. Triglycerides and total cholesterol tended to decrease in a greater percentage of patients taking carvedilol than atenolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Albuminuria_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Body_Temperature_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 7587995
----K I
----T Carvedilol for hypertension.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 7586246
----K I
----T Stroke after thrombolysis. Mortality and functional outcomes in the GUSTO-I trial. Global Use of Strategies to Open Occluded Coronary Arteries.
----A BACKGROUND: Stroke is the most feared complication of thrombolysis for acute myocardial infarction because of the resulting mortality and disability. We analyzed the incidence, timing, and outcomes of stroke in an international trial. METHODS AND RESULTS: Patients were randomly assigned to one of four thrombolytic strategies. Neurological events were confirmed clinically and anatomically and were adjudicated by a blinded committee. Stroke survivors, categorized by residual deficit and disability, assessed their quality of life with a time trade-off technique. Multivariable regression identified patient characteristics associated with intracranial hemorrhage. Over-all, 1.4% of the patients had a stroke (93% anatomic documentation). The risk ranged from 1.19% with streptokinase/subcutaneous heparin therapy to 1.64% with combination thrombolytic therapy (P = .007). Primary intracranial hemorrhage rates ranged from 0.46% with streptokinase/subcutaneous heparin to 0.88% with combination therapy (P < .001). Of all strokes, 41% were fatal, 31% were disabling, and 24% were nondisabling, with no significant treatment-related differences. Stroke subtype affected prognosis: 60% of patients with primary intracranial hemorrhage died and 25% were disabled versus 17% dead and 40% disabled with nonhemorrhagic infarctions. Patients with moderate or severe residual deficits showed significantly decreased quality of life. Advanced age, lower weight, prior cerebrovascular disease or hypertension, systolic and diastolic blood pressures, randomization to tissue plasminogen activator, and an interaction between age and hypertension were significant predictors of intracranial hemorrhage. CONCLUSIONS: Stroke remains a rare but catastrophic complication of thrombolysis. Additional studies should assess the net clinical benefit of thrombolysis in high-risk subgroups, particularly the elderly and patients with prior cerebrovascular events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Cerebral_Hemorrhage_MeSH S_chemically_induced_MeSH Cerebral_Hemorrhage_chemically_induced_MeSH S_epidemiology_MeSH Cerebral_Hemorrhage_epidemiology_MeSH S_psychology_MeSH Cerebral_Hemorrhage_psychology_MeSH M_Cerebral_Infarction_MeSH S_chemically_induced_MeSH Cerebral_Infarction_chemically_induced_MeSH S_epidemiology_MeSH Cerebral_Infarction_epidemiology_MeSH S_psychology_MeSH Cerebral_Infarction_psychology_MeSH M_Comparative_Study_MeSH M_Disability_Evaluation_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_administration_&_dosage_MeSH Fibrinolytic_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Fibrinolytic_Agents_adverse_effects_MeSH M_Heparin_MeSH S_administration_&_dosage_MeSH Heparin_administration_&_dosage_MeSH S_adverse_effects_MeSH Heparin_adverse_effects_MeSH M_Human_MeSH M_Incidence_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Quality_of_Life_MeSH M_Risk_Factors_MeSH M_Streptokinase_MeSH S_administration_&_dosage_MeSH Streptokinase_administration_&_dosage_MeSH S_adverse_effects_MeSH Streptokinase_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thrombolytic_Therapy_MeSH S_adverse_effects_MeSH Thrombolytic_Therapy_adverse_effects_MeSH M_Tissue_Plasminogen_Activator_MeSH S_administration_&_dosage_MeSH Tissue_Plasminogen_Activator_administration_&_dosage_MeSH S_adverse_effects_MeSH Tissue_Plasminogen_Activator_adverse_effects_MeSH 
****** 7475056
----K E
----T Insulin sensitivity in obese hypertensive dyslipidemic patients treated with enalapril or atenolol.
----A We evaluated the effects of enalapril [angiotensin converting enzyme (ACE) inhibitor] in comparison with atenolol (beta-blocker) on insulin sensitivity and serum lipoprotein concentration in obese hypertensive dyslipidemic patients. Twenty-eight hypertensive [mean blood pressure (MAP) 152 +/- 3/103 +/- 1 mm Hgl], obese [mean body mass index (BMI) 30 + 1 kg/m2A], dyslipidemic [total triglycerides 2.0 +/- 0.2 mM and/or high density lipoprotein (HDL) cholesterol 1.1 +/- 0.1 mM and low density lipoprotein (LDL) cholesterol 4.5 +/- 0.2 mM] outpatients were randomized in two groups receiving enalapril or atenolol for 12 weeks, in an investigator-blinded, parallel, comparative two-center trial. Insulin sensitivity was assessed by a modified insulin suppression test. Blood pressure (BP), insulin sensitivity, and serum lipoprotein concentrations were compared before and after each treatment and between the two treated groups. BP decreased significantly and comparably during enalapril and atenolol treatment (p < or = 0.01). The sensitivity to insulin improved by 15% (p = 0.03) in the enalapril group and worsened by 17% (p < or = 0.01) in the atenolol group. Serum lipoprotein concentrations were not modified by any treatment. The improvement in insulin sensitivity caused by enalapril treatment appears to be an advantage as compared with atenolol treatment in hypertensive obese and dyslipidemic patients, whereas the BP-lowering efficacy of the two drugs is similar. Because this effect has been reported with other ACE inhibitors, it appears to be characteristic of the entire class of ACE inhibitors.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_blood_MeSH Hyperlipidemia_blood_MeSH S_physiopathology_MeSH Hyperlipidemia_physiopathology_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Male_MeSH M_Obesity_MeSH S_blood_MeSH Obesity_blood_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8532943
----K I
----T [The effect of gallopamil and propranolol in patients with ischemic cardiopathy and moderate depression of ventricular function]
----A BACKGROUND: Calcium channel blockers have been wide and successfully used in the treatment of coronary heart disease. Gallopamil, a metoxylic derivative of verapamil, has many of its properties and so, caution is recommended when given to patients with depressed left ventricular function. Clinical studies about this effect are scarce, and we have assessed it in patients with coronary heart disease and diminished left ventricular function. METHODS: We studied 20 patients in a cross-over, randomized, double-blind study during three weeks active periods with two intercalating washout placebo periods of one week. Patients had history of previous myocardial infarction, positive exercise stress test and ejection fraction ranging from 30% to 50% by echocardiography. RESULTS: There were no significant differences between each drug and corresponding placebo on either systolic or diastolic function. When we compared both drugs, patients showed a milder increase in area under E after propranolol than after gallopamil (p < 0.008). Clinical episodes of cardiac failure were not reported, and ejection fraction did not change. CONCLUSIONS: Both gallopamil and propranolol can be used in patients with coronary heart disease and moderately depressed left ventricular ejection fraction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH S_drug_effects_MeSH Echocardiography__Doppler_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Echocardiography__Doppler_statistics_&_numerical_data_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Electrocardiography_statistics_&_numerical_data_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Gallopamil_MeSH S_therapeutic_use_MeSH Gallopamil_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Time_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 8574724
----K E
----T Effects of propranolol compared with clonidine on portal haemodynamics: a double-blind cross-over study using duplex-Doppler ultrasonography.
----A BACKGROUND: Patients with liver cirrhosis and large oesophageal varices run a high risk of digestive haemorrhage due to the rupture of oesophageal varices, an event associated with a high mortality. At present, the only treatment for the prevention of first bleeding from oesophageal varices on which there is general agreement is drug-based. In order to tailor drug treatment to the requirements of individual patients more precisely, an ever-increasing number of drugs is being investigated. DESIGN: Double-blind cross-over study. METHODS: Sixteen cirrhotic patients with large oesophageal varices were studied by means of duplex-Doppler ultrasonography to determine variations in portal haemodynamics after oral administration of 0.150 mg clonidine and to compare these with the variations observed after oral administration of 40 mg propranolol. RESULTS: Propranolol caused a significant reduction in maximum portal flow velocity (P < 0.001), whereas clonidine failed to cause any such variation (P = 0.194). Considering as responders those patients who exhibited at least a 10% decrease in maximum portal flow velocity, 11 patients responded to propranolol; of these, three also responded to clonidine. No patient responded only to clonidine. CONCLUSION: The absence of any effects on the parameters of portal haemodynamics would appear to deny clonidine any significant role in preventing first bleeding resulting from the rupture of oesophageal varices.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_alpha-Agonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Agonists_pharmacology_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Clonidine_MeSH S_pharmacology_MeSH Clonidine_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH S_ultrasonography_MeSH Liver_Cirrhosis_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_System_MeSH S_drug_effects_MeSH Portal_System_drug_effects_MeSH S_physiopathology_MeSH Portal_System_physiopathology_MeSH S_ultrasonography_MeSH Portal_System_ultrasonography_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Sympatholytics_MeSH S_pharmacology_MeSH Sympatholytics_pharmacology_MeSH M_Ultrasonography__Doppler__Duplex_MeSH 
****** 8522409
----K E
----T Left ventricular volume in thrombolysed patients with acute anterior myocardial infarction: the effect of captopril and xamoterol.
----A We measured left ventricular volume in 70 asymptomatic patients after first Q-wave anterior myocardial infarction in order to determine whether ventricular dilatation occurs and whether there is evidence for its attenuation or prevention by treatment with captopril or xamoterol--PRevention Of VEntricular Dilatation?: the PROVED? study. 77% of patients received thrombolytic treatment. Patients were randomised a mean of 11 days after infarction to receive either captopril 25 mg three times daily, xamoterol 200 mg twice daily or matching placebo. After 6 months of treatment, 6 patients from the placebo group (n = 24), 1 from the captopril group (n = 23) and 3 from the xamoterol group (n = 23) had been withdrawn from the study because of clinical complications. Left ventricular volume was measured using magnetic resonance imaging, before randomisation and after 6 months of treatment. Changes in left ventricular end-diastolic and end-systolic volume after 6 months of treatment were defined prospectively as the primary endpoints. Mean initial end-diastolic volume index was 85 (S.D. 19) ml/m2, mean end-systolic volume index was 45 (S.D. 18) ml/m2, and mean ejection fraction was 48 (S.D. 11)% for the whole group. There was no significant change in left ventricular volume index in the placebo or either treatment group after 6 months of treatment. Only minimal left ventricular dilatation was evident at 11 days. No further increase in left ventricular volume occurred after six months and there was no additional benefit from treatment with either captopril or xamoterol.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiac_Volume_MeSH S_drug_effects_MeSH Cardiac_Volume_drug_effects_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Dilatation__Pathologic_MeSH S_etiology_MeSH Dilatation__Pathologic_etiology_MeSH S_prevention_&_control_MeSH Dilatation__Pathologic_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Magnetic_Resonance_Imaging_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Placebos_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH M_Ventricular_Dysfunction__Left_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_prevention_&_control_MeSH Ventricular_Dysfunction__Left_prevention_&_control_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Xamoterol_MeSH S_therapeutic_use_MeSH Xamoterol_therapeutic_use_MeSH 
****** 8929232
----K E
----T Pharmacokinetic and pharmacodynamic properties and therapeutic use of bunazosin in hypertension. A review.
----A Bunazosin (CAS 52712-76-2), a quinazoline derivative, selectively blocks alpha1-receptors. In addition to its potent antihypertensive property, beneficial effects on lipid metabolism, glucose metabolism, vascular smooth muscle cell proliferation, it can be used in the presence of concomitant diseases, such as obstructive bronchitis, chronic renal insufficiency, peripheral arterial occlusive disease, and diabetes mellitus. In its extended-release formulation (bunazosin retard), it is generally a well-tolerated alpha1-blocker when compared to other agents in its class. Pharmacokinetic studies in normotensive volunteers showed that plasma peak concentration (Cmax) of bunazosin retard and bioavailability were approximately 50% and 81%, respectively, of the values of the standard non-retarded formulation. Bunazosin is metabolized mainly in the liver, and urine excretion accounts for only 10% of unchanged bunazosin. Following oral administration of 6 mg bunazosin retard to healthy volunteers, Cmax was 15 ng/ml, time to reach peak level (tmax) was 4 h and elimination half life was about 12 h. Bunazosin retard has Cmax and area underthe concentration curve (AUC) to be linearly related to the dose between 3 and 18 mg (r = 0.8). As expected, patients with impaired hepatic functions have shown an increase in AUC, Cmax, and elimination half live values. The hemodynamic effects of bunazosin are due to arterial vasodilation, reduced peripheral vascular resistance and cardiac afterload with moderate increase increase of cardiac output. Bunazosin was shown to decrease the systolic and diastolic blood pressure without a reflex tachycardia. In addition to its hypotensive effects bunazosin significantly increased the effective renal blood flow (by 34%) and creatinine clearance (by 37%) in patients with essential hypertension. In patients with impaired renal function bunazosin exhibits better increase in the effective renal plasma flow and glomerular filtration rate when compared to other alpha1-blockers (e.g. prazosin). Results of double-blind, randomized trials in 343 hypertensive patients showed bunazosin to be a equipotent hypertensive agent without multiple titration as usually necessary for other alpha-blockers. Diastolic blood pressure was normalized (< or equal 90 mmHg) or reduced by at least 10 mm Hg in 47% and 46% of patients, respectively. Results of two one-year long term studies in more than 600 young and elderly hypertensive patients gave no hint for tachyphylaxia. Bunazosin proved to be superior to prazosin in terms of orthostatic tolerance, as tested with the Schellong test. In conclusion due to its antihypertensive properties, beneficial effects on vascular smooth muscle cells, glucose metabolism , and lipid profile, and the less likelihood of orthostatic hypotension following treatment, bunazosin reard can be considered a useful antihypertensive agent.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_alpha-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Quinazolines_MeSH S_pharmacokinetics_MeSH Quinazolines_pharmacokinetics_MeSH S_pharmacology_MeSH Quinazolines_pharmacology_MeSH S_therapeutic_use_MeSH Quinazolines_therapeutic_use_MeSH M_Receptors__Adrenergic__alpha-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__alpha-1_antagonists_&_inhibitors_MeSH 
****** 8665975
----K E
----T Effects of lisinopril vs hydralazine on left ventricular hypertrophy and ambulatory blood pressure monitoring in essential hypertension.
----A In order to compare the long-term effects on ambulatory blood pressure and left ventricular hypertrophy of hydralazine and lisinopril we studied 30 patients, all males, still hypertensive (diastolic blood pressure > or = 95 mm Hg) despite combined beta-blocker/diuretic therapy and with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index > or = 1.31 g.m(-1)). They wer randomized to receive hydralazine slow release 50 mg/ chlorthalidone 12.5 mg) for 6 months. Casual blood pressure, non-invasive ambulatory blood pressure monitoring (ABPM), M-mode echocardiogram, plasma renin activity and plasma catecholamines were evaluated before the randomization and after 6 months of treatment. Both drugs significantly reduced casual as well as daytime systolic and diastolic blood pressure, without statistical differences between the two treatments. Lisinopril was significantly more effective than hydralazine in reducing night-time systolic and diastolic blood pressure. Plasma norepinephrine was significantly reduced by lisinopril and increased by hydralazine. Left ventricular mass was significantly reduced by lisinopril but not by hydralazine. The results of linear regression and multiple regression analysis suggested that the lisinopril-induced decrease in both day- and night-time blood pressure might account for the regression of left ventricular hypertrophy, whereas the lack of left ventricular hypertrophy regression during hydralazine treatment could be due mainly to the reflex sympathetic activation induced by the drug.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hydralazine_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_blood_MeSH Hypertrophy__Left_Ventricular_blood_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH 
****** 8576893
----K E
----T Results of combination anti-hypertensive therapy after failure of each of the components. Department of Veterans Affairs Cooperative Study Group on Anti-hypertensive Agents.
----A We randomised ambulatory men with diastolic blood pressure (BP) 95-109 mmHg without anti-hypertensive medication to single drug treatment with either hydrochlorothiazide 12.5-50 mg/day, atenolol 25-100 mg/day, captopril 25-100 mg/day, clonidine 0.2-0.6 mg/day, diltiazem-SR 120-360 mg/day, prazosin 4-20 mg/day or placebo in a double-blind prospective trial. The assigned drug was titrated to a goal BP of < 90 mm Hg. Patients not achieving goal BP were rerandomised to an alternative single active drug. Non-responders to the second drug received the first drug in combination with the second. Of the 102 non-responders to both drugs who qualified for the combination, 59 (57.8%) responded. The combination pairs that included a diuretic achieved diastolic goal BP in 69% and < 140 mm Hg systolic in 77% compared with 51% and 46%, respectively, for those combinations without a diuretic (P = 0.067; P = 0.002). Six of the eight terminations due to adverse drug reactions were in combinations containing prazosin; three of these six were hypotensive reactions. We conclude that two single drugs of insufficient efficacy to control BP individually have a high probability of achieving goal BP when combined, especially if the combination contains a diuretic.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 8535552
----K E
----T Effects of felodipine, metoprolol and their combination on blood pressure at rest and during exercise and on volume regulatory hormones in hypertensive patients.
----A The effects on blood pressure (BP) and heart rate (HR), at rest and during bicycle exercise, of the vascular selective calcium antagonist felodipine, the cardio-selective beta-blocker metoprolol, and of the two drugs in combination, were assessed in a double-blind, three-way cross-over study comprising 23 patients with essential, mild to moderate hypertension. All three treatment regimens were given to each patient in randomised order for 4 weeks after a 4 week placebo run-in period. Felodipine 10-20 mg daily, metoprolol 100-200 mg daily and the combination of felodipine 10-20 mg plus metoprolol 100 mg daily were all effective antihypertensive treatments both at rest and during exercise. The two drugs seemed to have additive effects and the effect on BP of the combination was greater than that of either drug given as monotherapy. The mean sitting BP was 148/103 mmHg at randomisation, after 4 weeks of placebo treatment, and 134/88, 134/94 and 121/84 mmHg, respectively, after 4 weeks' treatment with felodipine, metoprolol and the combination. Maximal exercise capacity was similar irrespective of treatment regimen, and the normal response to exercise BP and HR was maintained during all active treatments. Changes observed in volume regulatory hormones (PRA, aldosterone and ANP) were consistent with a direct tubular natriuretic-diuretic effect of felodipine and of beta-blocker attenuated release of renin. All treatment regimens were well tolerated and adverse events reported were usually mild and transient.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH P_Exercise_MeSH M_Exercise_Test_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8535541
----K E
----T Addition of urapidil or metoprolol to the treatment of hypertensive non-responders to nifedipine monotherapy: efficacy and metabolic effects. Italian Urapidil Study Group.
----A This study compared the effects on blood pressure and some metabolic variables of a 3-month period addition therapy of urapidil or metoprolol in 273 hypertensive non-responders to nifedipine sustained release (SR) monotherapy. This was a randomised, open-label, controlled, parallel-group comparative study, followed by another 3-month period during which all patients received the combination nifedipine SR-urapidil independently of the treatment they were previously randomized to. Both treatments caused significant falls in systolic (SBP) and diastolic blood pressure (DBP) when compared with the nifedipine SR monotherapy phase. The addition of urapidil to nifedipine SR caused a significant blood pressure reduction of 16.6/13.6 mmHg (p < 0.001), whereas after metoprolol the decrease was of 15.1/14 mmHg (p < 0.001). While in the overall population there was no statistically significant difference between the reduction caused by the two antihypertensive agents added to nifedipine SR, significant differences (DBP, p < 0.05; SBP, p < 0.01) were observed in the group of 51 patients aged at least 60 years. Total cholesterol and LDL-cholesterol were significantly reduced (p < 0.001) after the addition of urapidil to nifedipine SR, while, on the contrary, the addition of metoprolol to nifedipine SR was followed by a significant rise (p = 0.001). The changes caused by the two agents were statistically different among them (p < 0.01). The non-atherogenic HDL-cholesterol did not change during the addition of urapidil or metoprolol to nifedipine SR, while, the HDL/total cholesterol ratio was significantly increased after the addition of urapidil (p < 0.01) and unmodified after the addition of metoprolol. Between-group analysis showed a significant difference (p = 0.005). Serum triglycerides did not change in the urapidil plus nifedipine SR group but significantly increased in the metoprolol plus nifedipine SR group (p < 0.001); between-group difference was not statistically significant. Plasma glucose was unchanged after the addition of urapidil whereas it was significantly (p < 0.001) increased in the metoprolol-added group with a between-group difference statistically significant (p < 0.05). When metoprolol was substituted by urapidil during the second 3-month period, the negative effects on glucose, total cholesterol, LDL cholesterol and triglycerides were abolished while in the group already treated with urapidil plus nifedipine SR the favourable effects of urapidil plus nifedipine SR on total cholesterol, LDL-cholesterol and HDL/total cholesterol ratio were significantly increased compared with the end of the first 3-month treatment. The results of this study show that when urapidil and metoprolol are added to non-responders to nifedipine SR therapy there is a clinically and statistically relevant blood pressure reduction with both agents, with a therapeutic advantage for the combination urapidil + nifedipine SR in patients more than 60 years old. Moreover, the addition of urapidil was associated with a more favourable effect on serum lipids and glucose than that produced by the addition of metoprolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Piperazines_MeSH S_adverse_effects_MeSH Piperazines_adverse_effects_MeSH S_therapeutic_use_MeSH Piperazines_therapeutic_use_MeSH 
****** 8573993
----K E
----T Celiprolol. An evaluation of its pharmacological properties and clinical efficacy in the management of hypertension and angina pectoris.
----A Celiprolol is a beta 1-selective adrenoceptor antagonist (beta-blocker) which acts as a weak agonist at beta 2-adrenoceptors. The drug demonstrates vasodilator properties and does not depress heart rate to the same extent as propranolol, atenolol or metoprolol. Celiprolol has shown equivalent antihypertensive efficacy to other beta-blockers, notably propranolol, atenolol, metoprolol and pindolol, in patients aged 18 to 75 years with mild to moderate essential hypertension. The drug has also shown similar antihypertensive efficacy to the angiotensin converting enzyme inhibitor enalapril and to combination diuretic therapy with hydrochlorothiazide and amiloride. Celiprolol was equally effective in adult patients of all ages, although no data are available for patients aged over 75 years. Data from a small number of clinical trials indicate celiprolol to be as effective as both propranolol and atenolol in improving work capacity and reducing the frequency of anginal attacks in patients with stable effort angina. However, the drug has not yet been evaluated in postmyocardial infarction patients. Celiprolol offers advantages over other beta-blockers, including reduction of peripheral vascular resistance and maintenance of resting heart rate, cardiac output and renal perfusion. The drug is also associated with improvements in plasma lipid profiles and does not appear to adversely affect carbohydrate metabolism or lung function, although its use in patients with reversible obstructive pulmonary disease is not recommended. Celiprolol is therefore a highly cardioselective beta-blocker with ancillary characteristics which are potentially useful in patients with hypertension and angina complicated by other conditions commonly associated with advanced age. These include impaired glucose tolerance or diabetes mellitus, peripheral vascular disease and hyperlipidaemia. The drug may also be preferred to other beta-blockers in patients in whom a reduction in heart rate would be particularly undesirable. Further long term (> 12 months) clinical trials and pharmacoeconomic data are now required to confirm the clinical relevance of the pharmacodynamic advantages of celiprolol therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Administration__Oral_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8550251
----K E
----T The effect of beta-adrenergic blockade on non-esterified fatty acid uptake of exercising skeletal muscle during arm cranking.
----A beta-Adrenoceptor blocking agents impair endurance exercise performance in healthy subjects and in patients with hypertension. A possible explanation for the reduced exercise tolerance is a diminished availability of plasma non-esterified fatty acids (NEFA) for energy production during exercise. This study investigated the effect of beta-adrenoceptor blockade on NEFA uptake of exercising skeletal muscle at elevated blood NEFA concentrations. In 11 healthy volunteers a triacylglycerol emulsion was infused at increasing rate for 1 hour before and 1 hour during one-armed cranking exercise at 60% Wpeak with and without prior administration of the beta 1+2-adrenoceptor blocking agent propranolol (80 mg per os). Arteriovenous concentration differences of NEFA across the active forearm were measured and forearm blood flow was estimated using venous occlusion plethysmography. Heart rate and blood flow were significantly lower after propranolol (p < 0.05). Propranolol did not affect arterial NEFA concentration, arteriovenous NEFA difference or NEFA flux significantly. Net NEFA uptake increased with increasing arterial NEFA concentration or inflow in a similar manner with and without prior propranolol administration. Therefore, the results do not support the hypothesis that beta-adrenergic activity plays a role in the regulation of active skeletal muscle NEFA uptake under the conditions studied.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Arm_MeSH S_physiology_MeSH Arm_physiology_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Energy_Metabolism_MeSH S_drug_effects_MeSH Energy_Metabolism_drug_effects_MeSH M_Exercise_Tolerance_MeSH M_Exertion_MeSH S_physiology_MeSH Exertion_physiology_MeSH M_Fat_Emulsions__Intravenous_MeSH S_pharmacokinetics_MeSH Fat_Emulsions__Intravenous_pharmacokinetics_MeSH M_Fatty_Acids__Nonesterified_MeSH S_pharmacokinetics_MeSH Fatty_Acids__Nonesterified_pharmacokinetics_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Muscle__Skeletal_MeSH S_physiology_MeSH Muscle__Skeletal_physiology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH 
****** 8546341
----K E
----T Power spectral analysis of heart rate in elderly hypertensive subjects with or without silent coronary disease.
----A Much evidence indicates an involvement of the sympathetic nervous system in the genesis of silent myocardial ischemia. The authors assessed autonomic system activity by power spectrum analysis of heart rate variability in 21 elderly hypertensive men with and without angiographically confirmed coronary artery disease and compared the results with those from an age-matched control group. In the analysis an autoregressive algorithm was used to determine the power spectrum from an electrocardiographic recording of 512 consecutive RR intervals. The autonomic nervous system induces two distinct sinusoids: a low-frequency signal attributable to sympathetic activity and a high-frequency vagal response. In the hypertensive patients with coronary disease the authors also evaluated sympathetic activation after double-blind, placebo-controlled administration of metoprolol (100 mg/day), followed by amlodipine (10 mg/day), quinapril (20 mg/day), and amlodipine (5 mg/day) plus quinapril (10 mg/day).
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Aged_MeSH M_Algorithms_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_methods_MeSH Electrocardiography_methods_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isoquinolines_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH P_Signal_Processing__Computer-Assisted_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 8550773
----K E
----T Gastric emptying, glucose responses, and insulin secretion after a liquid test meal: effects of exogenous glucagon-like peptide-1 (GLP-1)-(7-36) amide in type 2 (noninsulin-dependent) diabetic patients.
----A The aim of the study was to investigate whether inhibition of gastric emptying of meals plays a role in the mechanism of the blood glucose-lowering action of glucagon-like peptide-1-(7-36) amide [GLP-1-(7-36) amide] in type 2 diabetes. Eight poorly controlled type 2 diabetic patients (age, 58 +/- 6 yr; body mass index, 30.0 +/- 5.2 kg/m2; hemoglobin A1c, 10.5 +/- 1.2%) were studied in the fasting state (plasma glucose, 11.1 +/- 1.1 mmol/L). A liquid meal of 400 mL containing 8% amino acids and 50 g sucrose (327 Kcal) was administered at time zero by a nasogastric tube. Gastric volume was determined by a dye dilution technique using phenol red. In randomized order, GLP-1-(7-36) amide (1.2 pmol/kg.min; Saxon Biochemicals) or placebo (0.9% NaCl with 1% human serum albumin) was infused between -30 and 240 min. In the control experiment, gastric emptying was completed within 120 min, and plasma glucose, insulin, C-peptide, GLP-1-(7-36) amide, and glucagon concentrations transiently increased. With exogenous GLP-1-(7-36) amide (plasma level, approximately 70 pmol/L), gastric volume remained constant over the period it was measured (120 min; P < 0.0001 vs. placebo), and plasma glucose fell to normal fasting values (5.4 +/- 0.7 mmol/L) within 3-4 h, whereas insulin was stimulated in most, but not all, patients, and glucagon remained at the basal level or was slightly suppressed. In conclusion, GLP-1-(7-36) amide inhibits gastric emptying in type 2 diabetic patients. Together with the stimulation of insulin and the inhibition of glucagon secretion, this effect probably contributes to the blood glucose-lowering action of GLP-1-(7-36) amide in type 2-diabetic patients when studied after meal ingestion. At the degree observed, inhibition of gastric emptying, however, must be overcome by tachyphylaxis, reduction in dose, or pharmacological interventions so as not to interfere with the therapeutic use of GLP-1-(7-36) amide in type 2 diabetic patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_metabolism_MeSH Diabetes_Mellitus__Type_II_metabolism_MeSH M_Female_MeSH P_Gastric_Emptying_MeSH M_Glucagon_MeSH S_blood_MeSH Glucagon_blood_MeSH S_pharmacology_MeSH Glucagon_pharmacology_MeSH M_Human_MeSH M_Insulin_MeSH S_secretion_MeSH Insulin_secretion_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptide_Fragments_MeSH S_blood_MeSH Peptide_Fragments_blood_MeSH S_pharmacology_MeSH Peptide_Fragments_pharmacology_MeSH M_Protein_Precursors_MeSH S_blood_MeSH Protein_Precursors_blood_MeSH S_pharmacology_MeSH Protein_Precursors_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8572849
----K 1
----T [Effects of bisoprolol and ramipril on short-term variability of systolic blood pressure during mental stress test: spectrum analysis]
----A The mid frequency component (MFC = 66-128 mHz) of blood pressure is an index of sympathetic vascular control. To investigate the effect of bisoprolol (B) and ramipril (R) treatment (TT) on the short-term variability of systolic blood pressure (SBP) diastolic blood pressure (DPB) and heart rate (HR) reactivity during mental stress, we studied 54 mild essential untreated hypertensive patients (24 men, 45 +/- 9.6 years, BP > 160/90 mmHg after a 15-days placebo run-in period) who were randomly assigned to double blind treatment (B: 10 mg/day: n = 28 and R: 5 mg/day: n = 26). A Stroop Word Color Conflict Test (SWCCT) was performed before and after 2 months of treatment. Hemodynamic parameters (BP and HR) were measured by a non invasive device (Finapres 2300E, Ohmeda-Maurepas) and underwent spectral analysis (SBP: mmHg.Hz-1/2, HR: beats/min.Hz-1/2, Anapres 1.2, Notocord-Orgametrie Systems, Igny-Lille) at rest and during SWCCT. The sympathetic vascular activity was assessed by calculating the area of the mid-frequency component (MFC = 66-128 Hz). RESULTS: [table: see text] CONCLUSION: The absolute variations in sympathetic activity during SWCCT as demonstrated by analysis of MFC of SBP and HR is not affected by chronic ramipril treatment, whereas bisoprolol attenuates sympathetic reactivity during SWCCT.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Prospective_Studies_MeSH M_Psychological_Tests_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Signal_Processing__Computer-Assisted_MeSH M_Spectrum_Analysis_MeSH P_Stress__Psychological_MeSH S_physiopathology_MeSH Stress__Psychological_physiopathology_MeSH M_Time_Factors_MeSH 
****** 8568162
----K 4
----T [Efficacy and tolerability of 2 presentations of eyedrops combining carteolol 2% and pilocarpine 2% in primary open-angle glaucoma and simple ocular hypertension]
----A PURPOSE: The aim of the study was to compare 2 combinations of eye drops containing 2% carteolol and 2% pilocarpine: LCM 1010: ready to use eye drops CBS 341A: eye drops to be reconstituted (freeze-dried powder + solvent). METHODS: Ninety-seven patients with primary open angle glaucoma or simple ocular hypertension were included in a randomized, double-blind multicentric study comparing 2 parallel groups of treatment. Intra-ocular pressure was greater than 21 mmHg with beta-blocker alone. One instillation of 2% carteolol-2% pilocarpine combination was given twice a day for one month. Before and after this treatment, intra-ocular pressure was measured at 9 am (12 hours after evening instillation) and at 11 am (2 hours after morning instillation). RESULTS: Both treatments reduced intra-ocular pressure by a comparable amount and there was no significant difference between groups at either measure: at 9 am: 2.11 +/- 2.39 mmHg (mean +/- SD) for LCM 1010 1.79 +/- 1.73 mmHg for CBS 341 A p = 0.25 at 11 am: 3.75 +/- 3.83 mmHg for LCM 1010 3.40 +/- 1.69 mmHg for CBS 341 A p = 0.42. Both eye drops were generally well tolerated. CONCLUSION: Efficacy and safety of ready to use eye drops 2% carteolol-2% pilocarpine combination proved to be comparable to that of eye drops to be reconstituted in the treatment of ocular hypertension poorly controlled by beta-blocker eye drops alone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carteolol_MeSH S_administration_&_dosage_MeSH Carteolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Carteolol_adverse_effects_MeSH S_therapeutic_use_MeSH Carteolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Hydrogen-Ion_Concentration_MeSH M_Male_MeSH M_Muscarinic_Agonists_MeSH S_administration_&_dosage_MeSH Muscarinic_Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Muscarinic_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Muscarinic_Agonists_therapeutic_use_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH P_Ophthalmic_Solutions_MeSH M_Pilocarpine_MeSH S_administration_&_dosage_MeSH Pilocarpine_administration_&_dosage_MeSH S_adverse_effects_MeSH Pilocarpine_adverse_effects_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH 
****** 8590535
----K I
----T Treatment of silent ischemia in unstable angina: a randomized comparison of sustained-release verapamil versus metoprolol.
----A Silent ischemia is a frequent finding in patients with unstable angina and portends a poor prognosis. We compared the efficacy of sustained-release (SR) verapamil and metoprolol in reducing silent ischemia in patients with unstable angina and assessed whether detection of silent ischemia was related to unfavorable outcomes in the contemporary setting of concurrent therapy with heparin and aspirin. Holter monitoring (leads a VF, V2, V5) for the first 72 h was used to assess the frequency and duration of ST-shift episodes. There were 37 patients in the verapamil-SR group and 40 patients in the metoprolol group, with both groups having similar baseline characteristics. There were more episodes of angina in the verampamil-SR group (29 vs. 12, p = 0.05). There was no difference between the two groups in the frequency (51 vs. 49 episodes, p = 0.9) or duration (23 +/- 48 vs. 18 +/- 50 min, p = 0.6) of ST-shift episodes. There were 20 unfavorable in-hospital outcomes distributed equally between the two groups (p = 0.9). Patients with unfavorable outcomes had ST shift more often (50 vs. 28%, p = 0.07) and for a longer duration (40 +/- 69 vs. 13 +/- 38 min, p = 0.03). Patients with ST shift > or = 60 min had a 60% probability of unfavorable outcome compared with 33% for ST shift of 1-59 min duration and 20% for no ST shift (p = 0.04). We conclude that metoprolol appears to reduce symptoms better than verapamil-SR, but no difference in silent ischemia or unfavorable outcomes was seen. Silent ischemia remains a common occurrence in these patients despite heparin and aspirin therapy and its detection continues to have prognostic value.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 8554206
----K E
----T United Kingdom Prospective Diabetes Study 17: a 9-year update of a randomized, controlled trial on the effect of improved metabolic control on complications in non-insulin-dependent diabetes mellitus.
----A PURPOSE: To report the progress (after 9-year follow-up) of a study designed to determine whether improved glucose control in patients with newly diagnosed non-insulin-dependent diabetes mellitus (NIDDM) is effective in reducing the incidence of clinical complications. DATA SOURCE: A multicenter, randomized, controlled trial of different therapies for NIDDM. After initial diet therapy, 4209 asymptomatic patients who remained hyperglycemic (fasting plasma glucose levels, 6.0 to 15.0 mmol/L) were assigned to either a conventional therapy policy, primarily with diet alone, or to an intensive therapy policy, aiming for fasting plasma glucose levels of less than 6.0 mmol/L, with assignment to primary therapy with sulfonylurea or insulin (which increased insulin supply) or metformin (which enhanced insulin sensitivity). RESULTS: All three modes of pharmacologic therapy in the intensively treated group-sulfonylurea, insulin, and metformin-had similar efficacy in reducing the fasting plasma glucose and glycated hemoglobin levels. Over 9 years, patients assigned to intensive therapy with sulfonylurea or insulin had lower fasting plasma glucose levels (median, 7.3 and 9.0 mmol/L, respectively) than patients assigned to conventional therapy. Regardless of the assigned therapy, however, the fasting plasma glucose and hemoglobin A1c levels increased, and maintaining near-normal glycemia was, in general, not feasible. Even insulin therapy did not achieve the therapeutic goal of near-normal glycemia because of the difficulty in treating marked hyperglycemia and the risk for hypoglycemic episodes. Nine years after the diagnosis of diabetes, 29% of the patients had had a diabetes-related clinical end point, 20% had had a macrovascular complication, and 9% had had a microvascular complication. CONCLUSIONS: A report will be published in 1998 after a median duration from randomization of 11 years (range, 6 to 20 years) with an 81% power at a 1% level of significance of detecting whether the obtained improvement in glucose control causes a 15% decrease or increase in the incidence of major complications and whether any specific therapy is advantageous or disadvantageous.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Body_Weight_MeSH M_Combined_Modality_Therapy_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_diet_therapy_MeSH Diabetes_Mellitus__Type_II_diet_therapy_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Fasting_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_metabolism_MeSH Hemoglobin_A__Glycosylated_metabolism_MeSH M_Human_MeSH M_Hypoglycemia_MeSH S_chemically_induced_MeSH Hypoglycemia_chemically_induced_MeSH M_Hypoglycemic_Agents_MeSH S_adverse_effects_MeSH Hypoglycemic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Islets_of_Langerhans_MeSH S_physiopathology_MeSH Islets_of_Langerhans_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8575234
----K E
----T Effect of perindopril and metoprolol on left ventricular hypertrophy and performance in essential hypertension.
----A The effects of perindopril and metoprolol on left ventricular hypertrophy (LVH) and function were studied in 47 essential hypertensive patients with LVH. Previous antihypertensive drugs were discontinued for at least 2 weeks, after which patients were randomly divided into 2 groups. 25 subjects were treated with perindopril 4 to 8 mg once daily in the morning (Group A) and 22 subjects with metoprolol 25 to 62.5 mg twice daily (Group B). The subjects were evaluated before and after 4 and 8 weeks of treatment by use of echocardiography. Before treatment LV mass indexes (LVMI) of two groups were respectively 143.2 +/- 21.3 g/m2 and 140.6 +/- 23.7 g/m2 (P > 0.05). In Group A, reduction of LVMI occurred after 4 weeks of treatment, and more pronounced after 8 weeks (from 143.2 +/- 21.3 g/m2 to 126.6 +/- 15.3 g/m2, P < 0.001), whereas reduction of LVMI occurred only after 8 weeks in Group B (from 140.6 +/- 23.7 g/m2 to 133.4 +/- 13.2 g/m2, P < 0.001). In addition, there was a significant (P < 0.05) difference in LVMI between the two groups after 8 weeks. LV systolic function remained unchanged, whereas E/A increased significantly (P < 0.001) in two groups after 8 weeks. In conclusion, antihypertensive treatment with perindopril and metoprolol induced a significant regression of LVH associated with improvement in LV diastolic performance. Perindopril, compared with metoprolol, was more effective in reversing LVH.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH 
****** 8553333
----K 1
----T [Effect of 1-alpha blockader on maximal oxygen consumption and physical endurance in hypertensive men]
----A The effect of alpha 1 adrenoceptor blockade (doxazosin, 4 mg daily) on maximal oxygen uptake (VO2 max) and physical endurance capacity in 16 mildly hypertensive, athletic men was investigated in a randomized, placebo-controlled, double-blind, two-period of 4 weeks, cross-over study. The maximal work load obtained during graded bicycle ergometer exercise and the VO2 max were reduced by 16 +/- 3 W (mean +/- SE) and 3 +/- 1 ml x kg-1 x min-1 on doxazosin (p < 0.001 for both), and the running time on 5000 m track increased by 43 +/- 12 sec (p < 0.05). Thus, alpha 1-blockade moderately reduces VO2 max and physical endurance capacity in mildly hypertensive athletic men. However, lower systolic blood pressure (9 +/- 4 mm Hg, p < 0.05) immediately after running, and unchanged heart rate suggest a safer performance of exercise.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_administration_&_dosage_MeSH Doxazosin_administration_&_dosage_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Physical_Endurance_MeSH S_drug_effects_MeSH Physical_Endurance_drug_effects_MeSH M_Running_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8557899
----K I
----T Combination therapy with metoprolol and nifedipine versus monotherapy in patients with stable angina pectoris. Results of the International Multicenter Angina Exercise (IMAGE) Study.
----A OBJECTIVES. This study was designed to investigate whether combination therapy with metoprolol and nifedipine provides a greater anti-ischemic effect than does monotherapy in individual patients with stable angina pectoris. BACKGROUND. Combination therapy with a beta-adrenergic blocking agent (which reduces myocardial oxygen consumption) and a dihydropyridine calcium antagonist (which increases coronary blood flow) is a logical approach to the treatment of stable angina pectoris. However, it is not clear whether, in individual patients, this combined therapy is more effective than monotherapy. METHODS. Two hundred eighty patients with stable angina pectoris were enrolled in a double-blind trial in 25 European centers. Patients were randomized (week 0) to metoprolol (controlled release, 200 mg once daily) or nifedipine (Retard, 20 mg twice daily) for 6 weeks; placebo or the alternative drug was then added for a further 4 weeks. Exercise tests were performed at weeks 0, 6 and 10. RESULTS. At week 6, both metoprolol and nifedipine increased the mean exercise time to 1-mm ST segment depression in comparison with week 0 (both p < 0.01); metoprolol was more effective than nifedipine (p < 0.05). At week 10, the groups randomized to combination therapy had a further increase in time to 1-mm ST segment depression (p < 0.05 vs. placebo). Analysis of the results in individual patients revealed that 7 (11%) of 63 patients adding nifedipine to metoprolol and 17 (29%) of 59 patients (p < 0.0001) adding metoprolol to nifedipine showed an increase in exercise tolerance that was greater than the 90th percentile of the distribution of the changes observed in the corresponding monotherapy + placebo groups. However, among these patients, an additive effect was observed only in 1 (14%) of the 7 patients treated with metoprolol + nifedipine and in 4 (24%) of the 17 treated with nifedipine + metoprolol. CONCLUSIONS. The mean additive anti-ischemic effect shown by combination therapy with metoprolol and nifedipine in patients with stable angina pectoris is not the result of an additive effect in individual patients. Rather, it may be attributed to the recruitment by the second drug of patients not responding to monotherapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8586825
----K I
----T A randomized comparison of the effect of four antihypertensive monotherapies on the subjective quality of life in previously untreated asymptomatic patients: field trial in general practice. The OCAPI Study Group. Optimiser le Choix d'un Anti-hypertenseur de Premiere Intention.
----A OBJECTIVE: To assess the equivalence of four antihypertensive treatments in patients with mild-to- moderate hypertension, and to compare the effects of those drugs on the subjective quality of life and clinical safety. DESIGN, SETTING AND PATIENTS: 653 patients aged > or = 18 years with untreated hypertension were randomly allocated to receive a combination of two diuretics (altizide and spironolactone), a beta-blocker (bisoprolol), a calcium antagonist (verapamil), or an angiotensin converting enzyme (ACE) inhibitor (enalapril). Follow-up lasted for 1 year. MAIN OUTCOME MEASURES: A composite outcome of the following measures was used to define success: attendance at the 12-month visit; at least nine supine DBP measurements during the study; and median supine DBP < 90 mmHg and a reduction of at least 10 mmHg compared with the baseline value. Failure was defined as one or more of those criteria not being fulfilled. Equivalence was concluded if the 95% confidence interval for the success rates differed between two groups by less than +/- 10%. Clinical safety and subjective quality of life were also assessed. RESULTS: No statistically significant differences in the change in DBP or systolic blood pressure were observed between the groups. The success rates were 43.9, 42.0, 32.5 and 43.9% in diuretic, beta-blocker, calcium antagonist and ACE inhibitor groups, respectively. Equivalence between the treatments could not be concluded, although analysis with a larger equivalence interval showed that some comparisons indicated equivalence. Significant improvement in satisfaction was observed for certain items for subjective quality of life at 1 month in the calcium antagonist treatment group, and significant differences in the responses to the clinical safety questionnaire were observed after 1-month follow-up in calcium antagonist and beta-blocker groups. Differences were no longer significant after 9 months. CONCLUSIONS: These results do not provide evidence on the basis of efficacy of blood pressure lowering or ability to increase short-term (1-year) safety and quality of life favouring any particular treatment among the studied drugs for newly diagnosed patients with mild-to-moderate hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 8600607
----K E
----T A comparison of the metabolic effects of captopril and atenolol on glucose, insulin and lipoproteins in patients with mild-to-moderate essential hypertension.
----A The metabolic effects of captopril 25 mg twice daily and atenolol 50 mg daily on glucose, insulin and lipids were compared in 83 otherwise healthy mild-to-moderate hypertensive between the ages of 25 and 60 years in a randomised double-blind trial. Hourly glucose and insulin levels were measured during a 2-hour 75 g oral glucose tolerance test at baseline and after 12 weeks of treatment. Lipid profiles including total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2, HDL3, triglycerides, apoprotein (Apo)A1, ApoB, and Apo(a) were obtained before and after the treatment period. Blood pressure decreased significantly and equivalently in both treatment groups. The glucose and insulin levels and glucose x insulin product at 2 hours after the glucose load increased after 12 weeks of treatment with atenolol compared with the baseline values, but these parameters all decreased after the treatment period with captopril compared with their baseline values. These results indicate an improvement in insulin sensitivity with captopril and a deterioration with atenolol. HDL-cholesterol and HDL3 decreased in the atenolol group but increased in the captopril group. We conclude that captopril has more favourable effects than atenolol on glucose, insulin and lipid metabolism in the treatment of mild-to-moderate hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Insulin_MeSH S_metabolism_MeSH Insulin_metabolism_MeSH M_Lipoproteins_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH S_metabolism_MeSH Lipoproteins_metabolism_MeSH M_Middle_Aged_MeSH 
****** 8562234
----K E
----T Effect of low dose beta blockers on atrial and ventricular (B type) natriuretic factor in heart failure: a double blind, randomised comparison of metoprolol and a third generation vasodilating beta blocker.
----A OBJECTIVES--This study examines the acute effects of two differing beta adrenergic blocking agents (metoprolol and a third generation vasodilating beta blocker) on plasma concentrations of atrial natriuretic factor (ANF), brain (ventricular) natriuretic factor (BNF), and haemodynamic variables in patients with heart failure. SETTING--University teaching hospital. METHODS--20 patients with impaired left ventricular systolic function [ejection fraction 32 (SEM 2.3)%] were randomised in a double blind manner to receive either oral metoprolol 6.25 mg twice daily or celiprolol 25 mg daily. Haemodynamic variables were evaluated by Swan-Ganz pulmonary artery catheter over 24 hours. ANF and BNF concentrations were measured at baseline, 5 h, and 24 h by radioimmunoassay. RESULTS--At baseline ANF and BNF concentrations were considerably raised compared to the normal range. Treatment with metoprolol caused ANF to rise further to 147% of the basal level at 5 h (P = 0.017) and 112% at 24 h (P = 0.029). This was associated with a small but non-significant rise in pulmonary capillary wedge pressure. Cardiac output and systemic vascular resistance were unchanged at 24 h. In contrast, after celiprolol ANF fell to 90% of basal levels at 5 h and to 74% of basal level at 24 h (P = 0.019), associated with a small but non-significant fall in pulmonary capillary wedge pressure [-3.3 (2.7) mm Hg] and systemic vascular resistance, and rise in cardiac output from 3.2 (0.2) to 4.0 (0.4) l/min (P = 0.04). BNF concentrations rose to 112% of baseline at 5 h (P = 0.09) after metoprolol but fell slightly, to 91% of baseline values, after celiprolol (NS). CONCLUSIONS--Metoprolol, even in very low doses (6.25 mg), produced a rise in ANF and BNF, although minimal haemodynamic changes were detected. In contrast, a vasodilating beta blocker was associated with a significant fall in ANF and BNF and a small rise in cardiac output. This study confirms both the advantages of vasodilating beta blockers over metoprolol for initial treatment of heart failure and the usefulness of ANF and BNF measurements for the assessment of drug effects in heart failure compared to traditional haemodynamic measurements.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH S_drug_effects_MeSH Atrial_Natriuretic_Factor_drug_effects_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Natriuretic_Peptide__Brain_MeSH M_Nerve_Tissue_Proteins_MeSH S_blood_MeSH Nerve_Tissue_Proteins_blood_MeSH S_drug_effects_MeSH Nerve_Tissue_Proteins_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8579030
----K E
----T Changes in plasma endothelin-1 levels reflect clinical response to beta-blockade in chronic heart failure.
----A Plasma levels of endothelin-1 are elevated in patients with chronic heart failure; however, it is unknown whether changes in plasma endothelin-1 levels accurately reflect clinical response to therapy in these patients. To determine this, we measured plasma endothelin-1 in addition to functional, hemodynamic, and other neurohormonal parameters as part of a double-blind, placebo-controlled study of the beta-blocker vasodilator carvedilol in patients with moderate to severe chronic heart failure. Patients were assigned (2:1 randomization) to receive carvedilol (25 mg twice daily, n = 10) or placebo (n = 5) for 14 weeks, with evaluations made before and after therapy. Compared to patients receiving placebo, patients receiving carvedilol improved significantly as assessed by the parameters described. These changes were paralleled by significant falls in endothelin-1 with carvedilol (-2.1 + 3.8 pg/ml) in comparison to placebo (2.2 + 3.9 pg/ml; p < 0.05 for between-group differences). Changes in endothelin-1 after treatment in both groups correlated significantly with changes in symptom severity, New York Heart Association class, 6-minute walk distance (r = 0.64 to 0.80; p < 0.05), hemodynamic parameters (ejection fraction, right atrial pressure, pulmonary artery diastolic pressure, pulmonary wedge pressure, right atrial pressure, and stroke volume index; r = 0.54 to 0.86; p < 0.05), and neurohormonal parameters (serum aldosterone and plasma norepinephrine (r = 0.74 to 0.76; p < 0.05). By stepwise regression analysis, change in endothelin-1 was an independent, noninvasive predictor of functional and hemodynamic responses to therapy in these patients. These findings suggest that endothelin-1 accurately reflects functional, hemodynamic, and neurohormonal responses to beta-blocker therapy in patients with congestive heart failure. Measurement of endothelin-1 may therefore be a useful, noninvasive approach to the evaluation of clinical response to drug therapy in these patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Endothelins_MeSH S_blood_MeSH Endothelins_blood_MeSH M_Female_MeSH M_Free_Radical_Scavengers_MeSH S_therapeutic_use_MeSH Free_Radical_Scavengers_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8556689
----K E
----T Diet in the prevention and treatment of atherosclerosis. A perspective for the elderly.
----A Atherosclerosis is the leading cause of coronary heart disease among older persons. With an increasing elderly population, cardiovascular disease has become an urgent public health concern. Diet plays an important role in atherogenesis with known beneficial effects on major risk factors among the younger population--cholesterol, hypertension, and diabetes. Intervention studies are needed to establish the benefits of diet therapy in the elderly segment of the population. Efforts are also needed to educate the elderly and health professionals about the benefits of a healthy Step I diet.
----P Journal_Article Review Review__Multicase 
----M M_Age_Distribution_MeSH M_Aged_MeSH M_Arteriosclerosis_MeSH S_epidemiology_MeSH Arteriosclerosis_epidemiology_MeSH S_etiology_MeSH Arteriosclerosis_etiology_MeSH S_prevention_&_control_MeSH Arteriosclerosis_prevention_&_control_MeSH M_Cholesterol__Dietary_MeSH S_adverse_effects_MeSH Cholesterol__Dietary_adverse_effects_MeSH M_Coronary_Disease_MeSH S_diet_therapy_MeSH Coronary_Disease_diet_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH P_Diet__Fat-Restricted_MeSH M_Human_MeSH M_Intervention_Studies_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Sex_Distribution_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8573224
----K 1
----T Different hemodynamic effects of celipropol and atenolol in patients with mild to moderate hypertension.
----A The hemodynamic effects of celiprolol (CAS 56980-93-9), a betablocker with beta 1 antagonist and beta 2 agonist properties, were compared with those of atenolol (CAS 29122-68-7) in 12 patients with mild to moderately severe hypertension (diastolic BP 95-110 mmHg). Celiprolol and atenolol lead to a similar and significant reduction of systolic and diastolic blood pressure (p < 0.005). However, with celiprolol heart rate at rest was significantly less depressed then with atenolol (p = 0.004) and showed a distinctly less pronounced depression of heart rate with exercise (p = 0.004). Cardiac output at rest was reduced by 19% under atenolol, but was increased by 9% under celiprolol treatment; in this respect, the two medications differed significantly (p = 0.03). The adaptation of heart rate and cardiac output to exercise was better with celipropol as compared to atenolol treatment. The difference between arm arterial pressure and ankle occlusion pressure at rest was not significantly influenced by atenolol, whereas celiprolol treatment increased this difference by a mean of up to 16 mmHg (p = 0.009). This different effect on peripheral arterial circulation was even more pronounced after exercise. Both celiprolol and atenolol increased blood cell flow velocity in the nailfold capillaries, but this increases was statistically only significant with celiprolol (p = 0.047). These results demonstrate that the hemodynamic effects of celiprolol were significantly different from those of atenolol; celiprolol produces less bradycardia, increases cardiac output at rest and decreases peripheral arterial resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Microcirculation_MeSH S_drug_effects_MeSH Microcirculation_drug_effects_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Respiratory_Function_Tests_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8580671
----K E
----T Portal-systemic encephalopathy and gastrointestinal bleeding after cardioselective beta-blocker (metoprolol) administration to patients with portal hypertension.
----A The use of the non-selective beta-blocker propranolol has been widely recommended to prevent gastrointestinal bleeding in patients with portal hypertension. We conducted a prospective, randomized controlled trial of metoprolol, a selective beta-blocker for prevention of gastrointestinal bleeding from portal hypertension in 29 non-selected patients with liver disease and previous gastrointestinal bleeding. Fifteen patients received placebo treatment for 40 +/- 18 months and 14 patients received metoprolol for 31 +/- 17 months. A sustained reduction in resting pulse was observed in those patients treated with metoprolol. There was no significant difference in acute re-bleeding episodes between the two groups. Of the 14 patients treated with metoprolol, three (21%) re-bled, all three requiring blood transfusion. Four (26.5%) of the 15 patients treated with the placebo re-bled, two cases with acute bleeding and the remaining two cases presented a positive stool guaiac test. All cases who bled during the metoprolol therapy required exclusion from the trial, and surgical procedures or sclerotherapy as well. After both metoprolol or placebo treatments, similar deterioration of standard liver function tests was observed. Further, at the end of the trial, 11 patients on metoprolol (78%) and four of the patients treated with the placebo (27%) required treatment for clinical portal-systemic encephalopathy (p < 0.01). The risk of poor sympathomimetic response after cardioselective beta 1-blocker during acute bleeding episodes and the appearance of hepatic encephalopathy deserve further investigation. The selective beta-blocker metoprolol seems to be an inadequate choice to prevent gastrointestinal re-bleeding in patients with portal hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_chemically_induced_MeSH Gastrointestinal_Hemorrhage_chemically_induced_MeSH M_Hepatic_Encephalopathy_MeSH S_chemically_induced_MeSH Hepatic_Encephalopathy_chemically_induced_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Placebos_MeSH M_Prospective_Studies_MeSH 
****** 8604962
----K E
----T Change in depression as a precursor of cardiovascular events. SHEP Cooperative Research Group (Systoloc Hypertension in the elderly).
----A OBJECTIVE: To determine the relationship between increasing depressive symptoms and cardiovascular events or mortality. DESIGN: Cohort analytic study of data from randomized placebo-controlled double-blind clinical trial of antihypertensive therapy. Depressive symptoms were assessed semi-annually with the Center for Epidemiological Studies-Depression (CES-D) scale during an average follow-up of 4.5 years. SETTING: Ambulatory patients in 16 clinical centers of the Systolic Hypertension in the Elderly Program. PATIENTS: Generally healthy men and women aged 60 years or older randomized to active antihypertensive drug therapy or placebo who were 70% white and 53% women and had follow-up CES-D scores and no outcome events during the first 6 months (N=4367). MAIN OUTCOME MEASURES: All-cause mortality, fatal or nonfatal stroke, or myocardial infarction. RESULTS: Baseline depressive symptoms were not related to subsequent events; however, an increase in depression was prognostic. Cox proportional hazards regression analyses with the CES-D scale as a time-dependent variable, controlling for multiple covariates, indicated a 25% increased risk of death per 5-unit increase in the CES-D score (relative risk [RR], 1.25;95% confidence interval [CI], 1.15 to 1.36). The RR for stroke or myocardial infarction was 1.18(95%CI,1.08 to 1.30). Increase in CES-D score was an independent predictor in both placebo and active drug groups, and it was strongest as a risk factor for stroke among women (RR,1.29;95%CI,1.07 to 1.34). CONCLUSIONS: Among elderly persons, a significant and substantial excess risk of death and stroke or myocardial infarction was associated with an increase in depressive symptoms over time, which may be a marker for subsequent major disease events and warrants the attention of physicians to such mood changes. However, further studies of casual pathways are needed before wide-spread screening for depression in clinical practice is to be recommended.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_complications_MeSH Cardiovascular_Diseases_complications_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_psychology_MeSH Cardiovascular_Diseases_psychology_MeSH M_Cohort_Studies_MeSH M_Depression_MeSH S_complications_MeSH Depression_complications_MeSH S_epidemiology_MeSH Depression_epidemiology_MeSH S_psychology_MeSH Depression_psychology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 8608285
----K E
----T Is the cognitive function of older patients affected by antihypertensive treatment? Results from 54 months of the Medical Research Council's trial of hypertension in older adults.
----A OBJECTIVE--To establish whether initiation of treatment with diuretic or beta blocker is associated over 54 months with change in cognitive function. DESIGN--A cognitive substudy, nested within a randomised, placebo controlled, single blind trial. SETTING--226 general practices from the Medical Research Council's general practice research framework. SUBJECTS--A subset of 2584 subjects sequentially recruited from among the 4396 participants aged 65-74 in the trial of treatment of hypertension in older adults. The 4396 subjects were randomised to receive diuretic, beta blocker, or placebo. Subjects had mean systolic pressures of 160-209 mm Hg and mean diastolic pressures <115 mm Hg during an eight week run in. OUTCOME MEASURES--The rate of change in paired associate learning test (PALT) and trail making test part A (TMT) scores (administered at entry and at 1, 9, 21, and 54 months) over time. RESULTS--There was no difference in the mean learning test coefficients (rate of change of score over time) between the three treatments: diuretic -0.31 (95% confidence interval -0.23 to -0.39), beta blocker -0.33 (-0.25 to -0.41), placebo -0.30, (-0.24 to -0.36). There was also no difference in the mean trail making coefficients (rate of change in time taken to complete over time) between the three groups: diuretic -2.73 (95% confidence interval -3.57 to -1.88), beta blocker -2.08 (-3.29 to -0.87), placebo -3.01, (-3.69 to -2.32). A less conservative protocol analysis confirmed this negative finding. CONCLUSION--Treating moderate hypertension in older people is unlikely to influence, for better or for worse, subsequent cognitive function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Cognition_Disorders_MeSH S_chemically_induced_MeSH Cognition_Disorders_chemically_induced_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Psychological_Tests_MeSH M_Psychometrics_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8610612
----K E
----T Effects of bisoprolol on heart rate variability in heart failure.
----A Analysis of heart rate variability (HRV) provides a non-invasive index of autonomic nervous system activity. HRV has been shown to be reduced in heart failure. Preliminary data indicate that beta blockers improve clinical status in patients with heart failure, but HRV improvement remains to be demonstrated. Fifty-four patients from the randomized double-blind, placebo-controlled Cardiac Insufficiency Bisoprolol Study were included in the HRV study. The bisoprolol daily dose was 5 mg once daily. We assessed HRV during 24-hour Holter recordings before randomization and after 2 months of treatment. HRV as measured in the time domain by root-mean-square successive differences (rMSSD), the percentage of adjacent RR differences >50 ms (pNN50), and the SD of RR intervals (SDNN), and in the frequency domain by high-frequency (0.16 to 0.40 Hz) and low-frequency (0.04 to 0.15 Hz) power. Most patients were in New York Heart Association functional class III. The mean left ventricular ejection fraction was 27 +/- 7%, and heart failure was idiopathic or ischemic. After 2 months, the patients receiving bisoprolol had a reduced mean heart rate compared with that in placebo patients (p=0.0004). Bisoprolol increased 24-hour rMSSD (p=0.04) and 24-hour pNN50 (p=0.04), daytime SDNN (p=0.05), and daytime high-frequency power (p=0.03) power. Bisoprolol induced a significant increase in HRV parameters related to parasympathetic activity in heart failure. Increased vagal tone may contribute to the protective effect of beta blockers and may have prognostic implications.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 8602055
----K E
----T Risk of gastrointestinal haemorrhage with calcium antagonists in hypertensive persons over 67 years old.
----A BACKGROUND: Calcium antagonists are used frequently in management of hypertension. In addition to their cardiovascular effects, these drugs inhibit platelet aggregation. Therefore we examined whether the use of calcium antagonists was associated with an increased risk of gastrointestinal haemorrhage (GIH). METHODS: A prospective cohort study was conducted from 1985 through 1992 on 1636 hypertensive persons aged > or = 68 years living in three communities. The participants were taking beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, or calcium antagonists; those taking combinations of these drugs were excluded. The incidence of GIH was assessed by surveying hospital discharge diagnoses and deaths. Age, gender, disability, arterial pressure, other drugs, and comorbid conditions were examined as confounders. FINDINGS: Compared with beta-blockers (4819 person-years, 65 events), after adjustment for confounders the relative risk for GIH associated with ACE inhibitor (772 person-years, 13 events) was 1.23 (95% CI 0.66-2.28) and with calcium antagonists (1510 person-years, 42 events) it was 1.86 (1.22-2.82). The risks for verapamil, diltiazem, and nifedipine did not differ significantly. The results were unchanged when the analyses were restricted to severe events (GIH in conjunction with blood transfusion or death). INTERPRETATION: Calcium antagonists were associated with an increased risk of GIH in this population. Therefore caution is needed in prescription of these agents to old patients who have other risk factors for gastrointestinal bleeding.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_chemically_induced_MeSH Gastrointestinal_Hemorrhage_chemically_induced_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8607401
----K I
----T Effect of quinapril or metoprolol on heart rate variability in post-myocardial infarction patients.
----A The effect of quinapril or metoprolol on heart rate variability (HRV) indexes was studied in patients who had recovered from acute myocardial infarction. Patients with stable coronary artery disease and normal volunteers were used as controls. Sixty patients with uncomplicated myocardial infarction (aged 32 to 74 years [mean 56.7]) were randomized to quinapril (n = 25), metoprolol (n = 25), and placebo (n = 10). HRV was assessed 5 days (baseline) and 35 days after the onset of acute myocardial infarction. After the baseline studies, the post-myocardial infarction patients were treated with metoprolol (50 to 100 mg/day), quinapril (5 to 10 mg/day), or placebo. Twenty patients with stable coronary artery disease and 20 healthy volunteers, age- and sex-matched to myocardial infarction patients, were used as controls. Compared with placebo, quinapril and metoprolol increased HRV indexes significantly 35 days after the onset of myocardial infarction. HRV indexes were not statistically different between the 2 treatment groups. At baseline and after therapy, HRV was similar in patients with anterior or inferior wall myocardial infarction. HRV 35 days after the onset of myocardial infarction was not different from HRV in patients with stable coronary artery disease, but was decreased when compared with that in normal volunteers. Data suggest that quinapril has the same beneficial effect on HRV indexes as metoprolol in patients who have recovered from uncomplicated acute myocardial infarction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Isoquinolines_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Prospective_Studies_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 8607723
----K E
----T Efficacy and tolerance of antihypertensive treatment in men and women with stage 1 diastolic hypertension. Results of the Treatment of Mild Hypertension Study.
----A OBJECTIVE: To explore the sex-specific benefits and risks of treatment of stage 1 diastolic hypertension. METHODS: Participants were African-American and white hypertensive men (n = 557) and women (n = 345) (age range, 45 to 69 years) with a diastolic blood pressure less than 100 mm Hg. Participants were randomized to treatment with placebo, chlorthalidone (15 mg/d), acebutolol hydrochloride (400 mg/d), doxazosin mesylate (2 mg/d), amlodipine besylate (5 mg/d), or enalapril maleate (5 mg/d); all were given nutritional-hygienic intervention. RESULTS: After 4 years, women who were randomized to lifestyle intervention only were less likely to be receiving step 1 therapy alone (placebo) than men who were randomized to placebo therapy (46% vs 66%, respectively, P < .01). There were significantly greater decreases in the mean systolic blood pressure in both men and women who were assigned to treatment with active drugs compared with those participants who were receiving placebo therapy; differences among treatments with active drugs were similar between men and women. Men experienced larger falls in their total and low-density lipoprotein cholesterol and triglyceride levels regardless of the treatment assignment than did women; however, there were no significant sex-by-treatment interactions. Quality-of-life indexes were generally improved with active drug treatment compared with placebo therapy in both sexes; there was a sex-by-treatment interaction for the general health index. The relative risk (RR) for combined clinical events was similar in women (RR, 0.64; 95% confidence interval [CI], (0.36 to 1.16) and in men (RR, 0.67; 95% CI, 0.40 to 1.14) who were assigned to treatment with all active drugs combined, compared with those who were receiving placebo therapy. CONCLUSION: In these exploratory analyses, men and women who were assigned to treatment with active drugs experienced greater and generally similar benefits from treatment than those participants who were assigned to lifestyle intervention only.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hygiene_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nutrition_MeSH P_Patient_Education_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 8608620
----K E
----T Impaired heart rate response to graded exercise. Prognostic implications of chronotropic incompetence in the Framingham Heart Study.
----A BACKGROUND: Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample. METHODS AND RESULTS: In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise ("chronotropic response index"). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P <.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors. CONCLUSIONS: An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence.
----P Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Exercise_Test_MeSH P_Exertion_MeSH M_Follow-Up_Studies_MeSH P_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Survival_Analysis_MeSH 
****** 8605839
----K 1
----T [Decreasing the antihypertensive dosage during longterm treatment and complete regression of left ventricular hypertrophy]
----A AIM OF STUDY: To discover whether in hypertensives with left ventricular hypertrophy (LVH) the increased muscle mass will completely regress under antihypertensive treatment and drug dosage can in consequence be reduced. PATIENTS AND METHOD: Prospectively 22 previously untreated hypertensives (20 men, 2 women; mean age 43.6 +/- 9 years) with echocardiographically confirmed LVH were investigated. The observation period was 102 +/- 5 months. All patients initially received metoprolol, 100 mg daily, after 14 days 200 mg daily (additionally hydrochlorothiazide in five patients). In all patients the blood pressure became normal at rest and on exercise within 6 weeks. RESULTS. After one year the mean left ventricular muscle mass index (LVMI) had fallen from 151 +/- 29 to 117 +/- 26 g/m2 (P < 0.001), and after 7 years to 82 +/- 14 g/m2 (P < 0.001; - 45.7%). Complete remission of LVH was demonstrated in 21 Patients. The drug dosage could either be reduced or the drug completely discontinued in 11 patients (group 1): after 102 +/- 5 months four patients took no drug, while seven were on 100 mg metoprolol. This was not possible in the other 11 patients (group 2), five of whom had been on both metoprolol and hydrochlorothiazide. The two groups differed with respect to loss of body weight (group 1: from 81.+/- 12 to 79.1 +/- 13 kg; P < 0.05; group 2: 85.7 +/- 8 to 88.1 +/- 10 kg; P < 0.05), but not regarding reduction of LVMI and blood pressure. CONCLUSION: Antihypertensive treatment for several years leads to regression in LVH in nearly all patients. In half of them the drug dosage can be reduced or the drug even discontinued. Weight loss may play an important part in this development.
----P Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Weight_Loss_MeSH 
****** 8615482
----K E
----T Hemodilution tolerance in patients with coronary artery disease who are receiving chronic beta-adrenergic blocker therapy.
----A Hemodilution tolerance is not well defined in patients with coronary artery disease receiving beta-adrenergic blockers chronically. Ninety patients scheduled for coronary artery bypass graft (CABG) surgery were randomized to a hemodilution (n = 60) and a control group (n = 30). During midazolam-fentanyl anesthesia, hemodynamic variables, ST segment deviation, and O2 consumption were determined prior to and after 6 and 12 mL/kg isovolemic exchange of blood for 6% hydroxyethyl starch. Hemoglobin decreased from 12.6 +/- 0.2 to 9.9 +/- 0.2 g/dL (mean +/- SEM, P < 0.05). With stable filling pressures, cardiac index increased from 2.05 +/- 0.05 to 2.27 +/- 0.05 L.min-1.m-2(P < 0.05) and O2 extraction from 27.4% +/- 0.6% to 31.2% +/- 0.7% (P < 0.05), resulting in stable O2 consumption. No alterations in ST segments were observed in leads II and V5 during hemodilution. Individual increases in cardiac index and O2 extraction were not linearly related to age and left ventricular (LV) ejection fraction (P = 0.841, P = 0.799). We conclude that isovolemic hemodilution to a hemoglobin value of 9.9 +/- 0.2 g/dL is well tolerated and fully compensated in patients with coronary artery disease receiving beta-adrenergic blockers chronically. Within the investigated ranges, the compensatory mechanisms during hemodilution are largely independent of age (35-81 yr) and LV ejection fraction (26%-83%).
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Cardiac_Output_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH P_Hemodilution_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Oxygen_Consumption_MeSH M_Regression_Analysis_MeSH M_Vascular_Resistance_MeSH 
****** 8614419
----K I
----T The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group.
----A BACKGROUND. Controlled clinical trials have shown that beta-blockers can produce hemodynamic and symptomatic improvement in chronic heart failure, but the effect of these drugs on survival has not been determined. METHODS. We enrolled 1094 patients with chronic heart failure in a double-blind, placebo-controlled, stratified program, in which patients were assigned to one of the four treatment protocols on the basis of their exercise capacity. Within each of the four protocols patients with mild, moderate, or severe heart failure with left ventricular ejection fractions < or = 0.35 were randomly assigned to receive either placebo (n = 398) or the beta-blocker carvedilol (n = 696); background therapy with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor remained constant. Patient were observed for the occurrence death or hospitalization for cardiovascular reasons during the following 6 months, after the beginning (12 months for the group with mild heart failure). RESULTS. The overall mortality rate was 7.8 percent in the placebo group and 3.2 percent in the carvedilol group; the reduction in risk attributable to carvedilol was 65 percent (95 percent confidence interval, 39 to 80 percent; P < 0.001). This finding led the Data and Safety Monitoring Board to recommend termination of the study before its scheduled completion. In addition, as compared with placebo, carvedilol therapy was accompanied by a 27 percent reduction in the risk of hospitalization for cardiovascular causes (19.6 percent vs. 14.1 percent, P = 0.036), as well as a 38 percent reduction in the combined risk of hospitalization or death (24.6 percent vs, 15.8 percent, P < 0.001). Worsening heart failure as an adverse reaction during treatment was less frequent in the carvedilol than in the placebo group. CONCLUSIONS. Carvedilol reduces the risk or death as well as the risk of hospitalization for cardiovascular causes in patients with heart failure who are receiving treatment with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH M_Chronic_Disease_MeSH M_Disease-Free_Survival_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Free_Radical_Scavengers_MeSH S_therapeutic_use_MeSH Free_Radical_Scavengers_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8629589
----K E
----T Combined alpha-beta blockade (doxazosin plus metoprolol) compared with beta blockade alone in chronic congestive heart failure.
----A There has been growing evidence for the benefits of beta blockers, but alpha blockers have not shown sustained benefits in chronic congestive heart failure (CHF). Thirty patients with moderate to severe CHF (New York Heart Association class II to IV) were sequentially assigned to receive metoprolol 6.25 mg with the alpha-1 antagonist doxazosin 4 mg/day or metoprolol alone. The dose of metoprolol was gradually increased to a target dose of 50 mg orally twice daily. Hemodynamic measurements were obtained before drug therapy, 2 hours after the first dose of combined alpha-beta therapy or metoprolol alone, and after 3 months of continuous treatment. Nuclear ejection fraction, plasma norepinephrine, and submaximal and maximal exercise capacity were also measured before and after chronic therapy. With initial combined drug administration, mean arterial pressure, left ventricular filling pressure, and systemic vascular resistance decreased significantly compared with results after metoprolol alone. However, after 3 months of continuous therapy, both treatment groups showed similar and significant reductions in systemic vascular resistance and heart rate, with significant increases in cardiac index, stroke volume index, stroke work index, ejection fraction, and exercise capacity. Furthermore, the next dose of chronic combined medication no longer showed vasodilating effects. Chronic therapy with fixed-dose doxazosin and increasing doses of metoprolol produced identical effects as those seen in patients receiving metoprolol alone.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 8621132
----K E
----T The effect of long-term treatment with spironolactone on variceal pressure in patients with portal hypertension without ascites.
----A The effect of spironolactone on esophageal variceal pressure (VP) in patients without ascites was investigated. VP was assessed using a noninvasive endoscopic gauge. Spironolactone was administered during a 6-week period at a dosage of 100 mg/d. This treatment decreased VP from 16.8 +/- 1.9 (SD) to 14.1 +/- 2.7 mm Hg (P < .001) in a group of 12 patients and from 18.6 +/- 2.1 to 13.7 +/- 4.1 mm Hg (P < .01) in another group of 8 patients who still had high VP despite chronic intake of propranolol. In both groups, placebo administration to 12 and 8 comparable patients did not significantly alter VP. Spironolactone induced a significant reduction of plasma volume (42.1 +/- 5.5 to 36.1 +/- 6.6 mL/kg body weight, P < .01) and of the concentration of alpha-atrial natriuretic peptide (alpha-ANP) (39.8 +/- 22 to 27.7 +/- 20 pg/mL, P < .01); in addition, a pronounced increase in plasma renin activity (PRA) (1.1 +/- 0.9 to 7.5 +/- 3.4 ng/mL/h, P < .001) was induced by the treatment. No significant changes in systemic hemodynamics were observed during the studies. Severe side effects were not observed except for a high incidence (55%) of painful gynecomasty in the male patients. In conclusion, chronic spironolactone administration effectively lowers VP, even in patients under chronic propranolol therapy. The combination of propranolol and spironolactone deserves further study as a prophylactic therapy of variceal hemorrhage, but development of gynecomasty might be a problem. Finally, we confirmed the reproducibility of VP measurements with the noninvasive gauge in chronic conditions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Ascites_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Plasma_Volume_MeSH S_drug_effects_MeSH Plasma_Volume_drug_effects_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Reproducibility_of_Results_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH 
****** 8643883
----K E
----T Statistical reporting of clinical trials with individual changes from allocated treatment.
----A We consider clinical trials in which information is available about subjects' treatment changes after randomization. To understand whether any difference between randomized groups in the intention-to-treat analysis can be explained by such treatment changes, we need analysis strategies which take account of treatment actually received. Selection bias is then a potentially serious problem. We relate risk in a time-dependent proportional hazards model to current treatment, with treatment combinations coded in two alternative ways. To reduce selection bias, treatment history (number of treatments dropped) and baseline covariates can be added to the model. Including current risk markers would also reduce selection bias but makes interpretation difficult. The methods are illustrated using data from the British Medical Research Council (MRC) elderly hypertension trial, with time to cardiovascular death as an outcome. Results for the comparison of diuretic and beta-blocker treatment are similar in all analyses, suggesting that selection bias is small and adding support to the hypothesis that the observed treatment differences are due to the randomized treatments themselves.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH P_Data_Collection_MeSH P_Data_Interpretation__Statistical_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Proportional_Hazards_Models_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Risk_MeSH M_Selection_Bias_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 8622227
----K E
----T Reversal of left ventricular hypertrophy in essential hypertension. A meta-analysis of randomized double-blind studies.
----A OBJECTIVE: To determine the ability of various antihypertensive agents to reduce left ventricular hypertrophy, a strong, blood pressure-independent cardiovascular risk factor, in persons with essential hypertension. DATA SOURCES: MEDLINE, DIMDI, RINGDOC, ADES, EMBASE, and review articles through July 1995 (English-language and full articles only). STUDY SELECTION: Meta-analysis of all published articles including only double-blind, randomized, controlled clinical studies with parallel-group design. DATA EXTRACTION: Intensive literature search and data extraction according to a prefixed scheme performed independently by 2 investigators. Reduction of left ventricular mass index after antihypertensive therapy with placebos, diuretics, beta-blockers, calcium channel blockers, or angiotensin-converting enzyme (ACE) inhibitors was the principal parameter. DATA SYNTHESIS: Of 471 identified references describing the effects of antihypertensive drugs on left ventricular hypertrophy, only 39 clinical trials fulfilled the inclusion criteria of our study. We found that the decrease in left ventricular mass index was more marked the greater was the decline in blood pressure (systolic r=0.46, P<.001; diastolic r=0.21, P=.08) and the longer was the duration of therapy (r=0.38, P<.01). After adjustment for different durations of treatment (mean duration of treatment, 25 weeks), left ventricular mass decreased 13% with ACE inhibitors, 9% with calcium channel blockers, 6% with beta-blockers, and 7% with diuretics. There was a significant difference between drug classes (P<.01): ACE inhibitors reduced left ventricular mass more than beta-blockers (significant, P<.05) and diuretics (tendency, P=.08). Similar differences between drug classes were found with regard to effect on left ventricular wall thickness (P<.05). CONCLUSIONS: The database of articles published through July 1995 is small and incomplete, and most of the articles are of poor scientific quality. In this first meta-analysis including only double-blind, randomized, controlled clinical studies, decline in blood pressure, duration of drug treatment, and drug class determined the reductions in left ventricular mass index. The ACE inhibitors seemed to be more potent than beta-blockers and diuretics in the reduction of left ventricular mass index; calcium channel blockers were somewhat in the intermediate range. The ACE inhibitors and, to a lesser extent, calcium channel blockers emerged as first-line candidates to reduce the risk associated with left ventricular hypertrophy.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Heart_Ventricles_MeSH S_anatomy_&_histology_MeSH Heart_Ventricles_anatomy_&_histology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 8621989
----K E
----T Can treatment that is helpful on average be harmful to some patients? A study of the conflicting information needs of clinical inquiry and drug regulation.
----A Randomized controlled trials are conducted with heterogeneous groups of patients, and the trial results represent an estimate of the average difference in the responses of the treatment groups. Clinicians, however, engage in a process of clinical inquiry, assembling data that will allow an assessment of the appropriate choice of treatment according to more narrowly defined clinical features. We describe a method of clinical inquiry within RCTs that can enhance the applicability of results to clinical decision making. Our methods included the use of data from the Beta-Blocker Heart Attack Trial, which enrolled 3837 subjects in 31 clinical centers. The 31 centers were divided into 21 dominant centers (mortality rates higher for placebo than propranolol) and 10 divergent centers (higher mortality rates for patients randomized to propranolol). Overall, compared to placebo, propranolol reduced the risk of dying for the "average" patient from 9.8 to 7.2%. Results for patients in dominant centers (RR = 0.50) were significantly different from those in divergent centers (RR = 1.33). We identified two cotherapies--aspirin use and coronary artery surgery--that subsequently affected the benefits of propranolol in divergent centers. For patients in divergent centers, propranolol reduced the risk of dying for patients treated with aspirin and/or coronary surgery (RR = 0.39), but not for patients not receiving these therapies (RR = 1.42). We conclude that differences in results across centers of a multicenter RCT may reflect important distinctions in the clinical conditions of enrolled subjects. These distinctions help to identify subgroups of patients in which treatment that has an average overall benefit may be harmful for some patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Drug_Approval_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 8622245
----K E
----T Long-term effects on plasma lipids of diet and drugs to treat hypertension. Treatment of Mild Hypertension Study (TOMHS) Research Group.
----A OBJECTIVE.- To compare long-term plasma lipid changes among 6 antihypertensive treatment interventions for stage I (mild) hypertension. DESIGN.- Multicenter, randomized, double-blind, parallel-group clinical trial. SETTING.- Four academic clinical research units in the United States. PARTICIPANTS.- A total of 902 men and women, aged 45 to 69 years, with stage I diastolic hypertension (diastolic blood pressure <100 mm Hg), recruited from 11914 persons screened in their communities. INTERVENTIONS.- Participants were randomized to 1 of 6 treatment groups: (1) placebo, (2) beta-blocker (acebutolol), (3) calcium antagonist (amlodipine), (4) diuretic (chlorthalidone), (5) alpha1-antagonist (doxazosin), and (6) angiotensin-converting enzyme inhibitor (enalapril). All groups received intensive lifestyle counseling to achieve weight loss, dietary sodium and alcohol reduction, and increased physical activity. MAIN OUTCOME MEASURES.- Changes in plasma total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides from baseline to annual visits through 4 years. RESULTS.- Mean changes in all plasma lipids were favorable in all groups. The degree of weight loss with fat-modified diet and exercise was significantly related to favorable lipid changes. Significant differences (P<.01) among groups for average changes during follow-up in each lipid were observed. Decreases in plasma total cholesterol and LDL cholesterol were greater with doxazosin and acebutolol (for plasma total cholesterol, 0.36 and 0.30 mmol/L [13.8 and 11.7 mg/dL], respectively), less with chlorthalidone and placebo (0.12 and 0.13 mmol/L [4.5 and 5.1 mg/dL], respectively). Decreases in triglycerides were greater with doxazosin and enalapril, least with acebutolol. Increases in HDL cholesterol were greater with enalapril and doxazosin, least with acebutolol. Significant relative increases in plasma total cholesterol with chlorthalidone compared with placebo at 12 months were no longer present at 24 months and beyond, when mean plasma total cholesterol for the chlorthalidone group fell below baseline. Analyses of participants continuing to receive chlorthalidone throughout the 4 years of follow-up indicated this was not due solely to an increasing percentage of participants changing or discontinuing use of medication during follow-up. CONCLUSIONS.- Weight loss with a fat-modified diet plus increased exercise produces favorable long-term effects on blood pressure and all plasma lipid fractions of adults with stage I hypertension; blood pressure reduction is enhanced to a similar degree by addition of a drug from any one of 5 classes of antihypertensive medication. These drugs differ quantitatively in influencing the degree of long-term favorable effects on blood lipids obtained with nutritional-hygienic treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_pharmacology_MeSH Acebutolol_pharmacology_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_pharmacology_MeSH Chlorthalidone_pharmacology_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Diet__Fat-Restricted_MeSH M_Diet__Reducing_MeSH M_Diet__Sodium-Restricted_MeSH M_Diuretics_MeSH S_pharmacology_MeSH Diuretics_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Enalapril_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_MeSH M_Female_MeSH M_Health_Behavior_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_diet_therapy_MeSH Hypertension_diet_therapy_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Linear_Models_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH M_Weight_Loss_MeSH 
****** 8642189
----K E
----T Prostacyclin biosynthesis in essential hypertension before and during treatment.
----A Protacyclin biosynthesis was investigated in 133 untreated newly diagnosed patients with uncomplicated essential hypertension. Urinary excretion of 6-oxo-prostaglandin F1 alpha and of 2,3-dinor-6-oxo-prostaglandin F1 alpha, stable breakdown products of prostacyclin, was measured following a 1 month run-in period. To determine whether lowering blood pressure (BP) influenced prostacyclin biosynthesis, 106 consenting patients with diastolic pressure 90-120 mm Hg were allocated randomly to treatment with bendrofluazide, metoprolol, quinapril or amlodipine in an open parallel group design. Dose was increased to reduce diastolic arterial pressure to <90 mm Hg. Terazosin was added if this target BP was not achieved, and its dose increased if necessary. Urinary excretion rates of prostaglandins were measured after 1 year in patients in whom the target diastolic pressure was achieved. Mean arterial pressure varied from 106-168 mm Hg in untreated patients and excretion of both prostacyclin-derived products varied from <5 to >350 ng/g creatinine. Arterial pressure and prostaglandin excretion were not significantly correlated. In 57 patients in whom target pressure was achieved, BP before treatment was 166 +/- 2/100 +/- 1 at baseline and 144 +/- 2/86 +/- 1 mm Hg at 1 year. Excretion rates of each prostacyclin-derived product were similar before treatment and at 1 year, with no significant differences between the drugs. These findings do not support the hypothesis that deficient prostacyclin biosynthesis contributes to the pathogenesis of essential hypertension, or that increased prostacyclin biosynthesis plays a part in the response to treatment with antihypertensive medication.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_6-Ketoprostaglandin_F1_alpha_MeSH S_analogs_&_derivatives_MeSH 6-Ketoprostaglandin_F1_alpha_analogs_&_derivatives_MeSH S_urine_MeSH 6-Ketoprostaglandin_F1_alpha_urine_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Epoprostenol_MeSH S_biosynthesis_MeSH Epoprostenol_biosynthesis_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Isoquinolines_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH P_Tetrahydroisoquinolines_MeSH M_Thromboxane_A2_MeSH S_metabolism_MeSH Thromboxane_A2_metabolism_MeSH M_Thromboxane_B2_MeSH S_urine_MeSH Thromboxane_B2_urine_MeSH 
****** 8636540
----K E
----T Persistent transient myocardial ischemia despite beta-adrenergic blockade predicts a higher risk of adverse cardiac events in patients with coronary artery disease.
----A OBJECTIVES: We evaluated the prevalence and prognostic significance of transient myocardial ischemia despite beta-adrenergic blockade in patients with coronary artery disease. BACKGROUND: Persistence of transient ischemia despite therapy may correspond to a subset of high risk patients with coronary disease. The impact of beta-blocker withdrawal in these patients remains unknown. METHODS: Patients (n = 313) with documented coronary artery disease and beta-blocker therapy, with (group I, n = 84) or without (group II, n = 229) transient ischemia on ambulatory electrocardiographic monitoring, were followed up during 21 +/- 9 months for cardiac events (death, myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass surgery and worsening angina). Occurrence of events was compared by log-rank test. RESULTS: The number of coronary stenoses did not differ significantly between groups I and II. Beta-blocker therapy was discontinued more frequently during follow-up in group II (25% vs. 14% in group I, p = 0.04). Cumulative percentage of death or myocardial infarction, or both, tended to be higher in group I a 30 months (17% vs. 5% in group II, p = 0.09). Coronary angioplasty and bypass surgery were significantly more frequent in group I (p = 0.01 and 0.0008, respectively). Transient ischemia was associated with a higher cumulative probability of adverse events (p = 0.004). The number of coronary stenoses, presence of transient ischemia and beta-blocker withdrawal were the only significant prognostic factors of cardiac events in the Cox model. In group I patients, the relative hazard of cardiac events was increased threefold when beta-blocker therapy was interrupted. CONCLUSIONS: These data suggest that 1) the occurrence of transient ischemia despite beta-blocker therapy identifies a subset of high risk patients with coronary artery disease, and 2) the interruption of beta-blocker therapy increases the risk of adverse cardiac events.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Disease-Free_Survival_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH M_Prognosis_MeSH M_Risk_Assessment_MeSH M_Treatment_Failure_MeSH 
****** 8638023
----K I
----T Management of patients with life-threatening sustained ventricular tachyarrhythmias--the role of guided antiarrhythmic drug therapy.
----A Two recent studies have evaluated the utility of electrophysiologic (EP) testing in the treatment of patients with serious ventricular arrhythmias. The first study compared electrophysiologically guided antiarrhythmic drug therapy with nonguided beta-blocker therapy. Patients without inducible arrhythmias were assigned to oral metoprolol; patients with inducible arrhythmias were randomly assigned to receive either oral metoprolol or EP-guided drug therapy with propafenone, flecainide, disopyramide, sotalol, or amiodarone. Antiarrhythmic drugs were tested in a random order, but amiodarone was always tested last. A total of 170 patients were evaluated; 115 patients had inducible arrhythmias, and 61 patients were randomly assigned to serial drug testing, 54 to metoprolol without invasive testing, and the remainder who were noninducible to empiric metoprolol. The best outcome was observed in patients without inducible arrhythmias, all of whom received metoprolol. There was no difference in outcome between the two groups with inducible arrhythmias, either treated with metoprolol or with EP-guided serial antiarrhythmic drug testing. The second study evaluated survivors of out-of-hospital ventricular fibrillation (VF) without new myocardial infarction. Patients received assessment of left ventricular ejection fraction, Holter monitoring (HM), and EP testing. Only patients with inducible sustained ventricular arrhythmias or with sufficient ambulatory ventricular ectopy were included in the study. Therapy was randomized either to empiric amiodarone or conventional drug therapy guided by EP testing and/or HM. A total of 228 patients were treated, 113 with amiodarone and 115 with conventional antiarrhythmic drug therapy. The composite primary end points were total mortality, documented out-of-hospital resuscitation from recurrent VF, or syncopal implantable cardioverter/defibrillator shock followed by return of consciousness. Patients treated with empiric amiodarone had a better outcome than did patients treated with guided conventional drug therapy. In those patients in whom an implantable cardioverter/defibrillator was used, patients treated with amiodarone had fewer total shocks and fewer syncopal shocks than did patients treated with conventional therapy. Patients with a history of out-of-hospital VF or sustained ventricular tachycardia without inducible ventricular arrhythmias at EP study have the best outcome. Empiric metoprolol is equivalent to conventional antiarrhythmic drug therapy guided by EP testing. Empiric amiodarone is superior to conventional antiarrhythmic drug therapy guided by HM and/or EP testing.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Defibrillators__Implantable_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 8659199
----K 1
----T [Are beta-blockers generally contraindicated in patients with peripheral arterial occlusive disease?]
----A Ninety patients with chronic ischemic heart disease and stage IIb peripheral arterial occlusive disease were investigated to determine the effect of celiprolol, atenolol and isosorbide dinitrate on peripheral arterial blood flow. Walking distance and the resistance index in the femoral artery were measured before and after 3 months medication and compared with the findings in controls (30 patients with chronic ischemic heart disease and stage IIb peripheral arterial occlusive disease) who received placebo. Patients with peripheral arterial occlusive disease who were treated with atenolol 50 mg/day demonstrated significant decreases in both pain-free and maximal walking distance. In contrast, the walking distances in those given celiprolol 200 mg/day and those who received isosorbide dinitrate 80 mg/day did not differ from the distances in control subjects. The Doppler flow through the femoral artery, as measured by color duplex sonography, showed a significant decrease in resistance index, both in patients given celiprolol and in those given isosorbide dinitrate. In patients treated with atenolol the resistance index rose significantly. The results of this study confirm that the beta-adrenoceptor blocker celiprolol exerts a supplementary vasodilatory action resembling that of nitrates and hence can be used in patients with chronic ischemic heart disease and impaired peripheral arterial perfusion.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Arterial_Occlusive_Diseases_MeSH S_drug_therapy_MeSH Arterial_Occlusive_Diseases_drug_therapy_MeSH M_Atenolol_MeSH S_contraindications_MeSH Atenolol_contraindications_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Celiprolol_MeSH S_contraindications_MeSH Celiprolol_contraindications_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Ischemia_MeSH S_drug_therapy_MeSH Ischemia_drug_therapy_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Leg_MeSH S_blood_supply_MeSH Leg_blood_supply_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8628357
----K E
----T Nadolol plus isosorbide mononitrate compared with sclerotherapy for the prevention of variceal rebleeding.
----A BACKGROUND: Patients who have bleeding from esophageal varices are at high risk for rebleeding and death. We compared the efficacy and safety of endoscopic sclerotherapy with the efficacy and safety of nadolol plus isosorbide mononitrate for the prevention of variceal rebleeding. METHODS: Eighty-six hospitalized patients with cirrhosis and bleeding from esophageal varices diagnosed by endoscopy were randomly assigned to treatment with repeated sclerotherapy (43 patients) or nadolol plus isosorbide-5-mononitrate (43 patients). The primary outcomes were rebleeding, death, and complications. The hepatic venous pressure gradient was measured at base line and after three months. RESULTS: Base-line data were similar in the two groups, and the median follow-up was 18 months in both. Eleven patients in the medication group and 23 in the sclerotherapy group had rebleeding. The actuarial probability of remaining free of rebleeding was higher in the medication group for all episodes related to portal hypertension (P = 0.001) and variceal rebleeding (P = 0.002). Four patients in the medication group and nine in the sclerotherapy group died (P = 0.07 for the difference in the actuarial probability of survival). Seven patients in the medication group and 16 in the sclerotherapy group had treatment-related complications (P = 0.03). Thirty-one patients in the medication group underwent two hemodynamic studies; 1 of the 13 patients with more than a 20 percent decrease in the hepatic venous pressure gradient had rebleeding, as compared with 8 of the 18 with smaller decreases in the pressure gradient (P = 0.04) for the actuarial probability of rebleeding at two years). CONCLUSIONS: As compared with sclerotherapy, nadolol plus isosorbide mononitrate significantly decreased the risk of rebleeding from esophageal varices.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Actuarial_Analysis_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_adverse_effects_MeSH Nadolol_adverse_effects_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH S_adverse_effects_MeSH Sclerotherapy_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8641743
----K E
----T A diuretic is more effective than a beta-blocker in hypertensive patients not controlled on amlodipine and lisinopril.
----A The combination of an angiotensin-converting enzyme inhibitor and a calcium antagonist has a synergistic effect in patients with more severe hypertension. However, when this combination fails to control blood pressure, it is not clear which drug is then additive. The aim of this work was to study in a double-blind, randomized, crossover design the effect on blood pressure of the addition of either a thiazide diuretic (bendrofluazide, 5 mg once daily) or a beta-blocker (atenolol, 100 mg once daily) or placebo each for a month in hypertensive patients who are not adequately controlled on the combined treatment of amlodipine 5 mg once daily and lisinopril 5 mg twice daily. Eighteen patients with a supine diastolic pressure of more than 90 mm Hg after at least 1 month on the combined treatment of amlodipine and lisinopril were enrolled in the study. The results show that in patients whose blood pressures are not controlled by the combination of amlodipine and lisinopril, the addition of bendrofluazide 5 mg once daily causes a significant fall in blood pressure compared with placebo and a significantly greater fall than 100 mg atenolol once daily.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Failure_MeSH 
****** 8640972
----K E
----T Sex differences in myocardial infarction and coronary deaths in the Scottish MONICA population of Glasgow 1985 to 1991. Presentation, diagnosis, treatment, and 28-day case fatality of 3991 events in men and 1551 events in women.
----A BACKGROUND: Scottish MONICA used medical and medico-legal records and World Health Organization MONICA Project criteria to register coronary events in 25- to 64-year-old residents of the high-incidence area of north Glasgow from 1985 to 1991. METHODS AND RESULTS: Age-standardized data from 3991 episodes of nonfatal definite myocardial infarction and coronary deaths in men (mean age, 55.5 years) were compared with 1551 in women (57.0 years). Many results, such as the overall 28-day fatality rates of 49.8% in men and 48.5% in women, showed insignificant differences. However, 74.3% of deaths in men occurred out of hospital versus 67.8% in women (P = .0004). After admission to hospital, fatality rates in women were 14% higher (P = .07) and after admission to coronary care, 22% higher (P = .04). Women were more often widowed. Fewer had a history of previous myocardial infarction, but the prevalence of angina pectoris, of smoking, and of chest pain in the attack was the same as in men; more had shock, syncope, and breathlessness. More consulted a doctor before admission to hospital, which delayed their coming under care. More men had ECG Q-wave progression, and more women had smaller ECG changes. This, and marginally reduced chances of direct admission to coronary care, of thrombolysis, of aspirin, and of beta-blockers, did not explain women's excess hospital fatality. CONCLUSIONS: Acute coronary events appear to be recognized and treated fairly equally in men and women 25 to 64 years old in Glasgow, so differences are small but subtle. More men die suddenly out of hospital; the reason why more women die after arrival may be because the equivalent number of men have already died outside.
----P Journal_Article 
----M M_Acute_Disease_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Angioplasty_MeSH S_utilization_MeSH Angioplasty_utilization_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Attitude_of_Health_Personnel_MeSH M_Cardiopulmonary_Resuscitation_MeSH S_utilization_MeSH Cardiopulmonary_Resuscitation_utilization_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH S_utilization_MeSH Coronary_Angiography_utilization_MeSH M_Coronary_Care_Units_MeSH S_statistics_&_numerical_data_MeSH Coronary_Care_Units_statistics_&_numerical_data_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Inpatients_MeSH S_statistics_&_numerical_data_MeSH Inpatients_statistics_&_numerical_data_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Myocardial_Revascularization_MeSH S_utilization_MeSH Myocardial_Revascularization_utilization_MeSH M_Outpatients_MeSH S_statistics_&_numerical_data_MeSH Outpatients_statistics_&_numerical_data_MeSH M_Scotland_MeSH S_epidemiology_MeSH Scotland_epidemiology_MeSH P_Sex_Characteristics_MeSH M_Sex_Factors_MeSH M_Socioeconomic_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Survival_Rate_MeSH M_Thrombolytic_Therapy_MeSH S_utilization_MeSH Thrombolytic_Therapy_utilization_MeSH M_Treatment_Outcome_MeSH M_World_Health_Organization_MeSH 
****** 8693706
----K E
----T [Treatment of hypertension with a fixed combination of bopindolol and chlorthalidone (Sandoretic)]
----A A multicentric, prospective, 16-week open study evaluated the effectivity and tolerance of the fixed combination of the beta-blocking agent bopindolol with the diuretic chlorthalidone--Sandoretic in 81 patients with mild to moderate hypertension. The combination of these two drugs is appropriate, since both drugs have long-term effects. Sandoretic induced a decrease of the mean sitting initial systolic blood pressure of 162.5 +/- 16.5 mmHg to 134.2 +/- 12.8 mmHg at the end of the study, a decrease of 28.3 mmHg. Diastolic blood pressure decreased after 16 weeks of treatment from the initial value of 103.9 +/- 4.9 mmHg to 85.3 +/- 6.0, a decrease of 18.6 mmHg. Changes of the standing systolic and diastolic blood pressures were of similar magnitude. Sandoretic treatment led to a normalization of the diastolic blood pressure (90 mmHg and lower) in 80.3% of patients. In 49.4% of patients treatment with Sandoretic led even to a diastolic blood pressure of 85 mmHg and lower and 29.6% patients had at the end of treatment diastolic blood pressure 80 mmHg and lower. Tolerance of the drug was excellent in 75.3% patients. Sandoretic induced a mild, however, significant decrease of potassium plasma levels. The increase of the uric acid plasma level was also significant. Monitoring of potassium plasma levels is therefore necessary during the treatment with Sandoretic. In patients showing a decrease of the potassium plasma level, potassium sparing diuretic-amiloride should be added or the dosage of the drug should be halved.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH M_Drug_Combinations_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Pindolol_analogs_&_derivatives_MeSH M_Prospective_Studies_MeSH 
****** 8800982
----K E
----T Early continuous ST segment monitoring in unstable angina: prognostic value additional to the clinical characteristics and the admission electrocardiogram.
----A BACKGROUND AND OBJECTIVE: In unstable angina, clinical characteristics, resting electrocardiography, and early continuous ST segment monitoring have been individually reported to identify subgroups at increased risk of adverse outcome. It is not known, however, whether continuous ST monitoring provides additional prognostic information in such a setting. DESIGN: Observational study of 212 patients with unstable angina without evidence of acute myocardial infarction admitted to district general hospitals, who had participated in a randomised study comparing heparin and aspirin treatment versus aspirin alone. METHODS: Clinical variables and a 12 lead electrocardiogram (ECG) were recorded at admission, and treatment was standardised to include aspirin, atenolol, diltiazem, and intravenous glyceryl trinitrate, in addition to intravenous heparin (randomised treatment). Continuous ST segment monitoring was performed for 48 h and all inhospital adverse events were recorded. RESULTS: The admission ECG was normal in 61 patients (29%), showed ST depression in 59 (28%) (17 > or = 0.1 mV), and T wave changes in a further 69 (33%). The remaining 23 had Q waves (18), right bundle branch block (four), or ST elevation (one). During 8963 h of continuous ST segment monitoring (mean 42.3 h/patient), 132 episodes of transient myocardial ischaemia (104 silent) were recorded in 32 patients (15%). Forty patients (19%) had an adverse event (cardiac deaths (n = 3), non-fatal myocardial infarction (n = 6) and, emergency revascularisation (n = 31)). Both admission ECG ST depression (P = 0.02), and transient ischaemia (P < 0.001) predicted an increased risk of non-fatal myocardial infarction or death, while no patients with a normal ECG died or had a myocardial infarction. Adverse outcome was predicted by admission ECG ST depression (regardless of severity) (odds ratio (OR) 3.41) (P < 0.001), and maintenance beta blocker treatment (OR 2.95) (P < 0.01). A normal ECG predicted a favourable outcome (OR 0.38) (P = 0.04), while T wave or other ECG changes were not predictive of outcome. Transient ischaemia was the strongest predictor of adverse prognosis (OR 4.61) (P < 0.001), retaining independent predictive value in multivariate analysis (OR 2.94) (P = 0.03), as did maintenance beta blocker treatment (OR 2.85) (P = 0.01) and admission ECG ST depression, which showed a trend towards independent predictive value (OR 2.11) (P = 0.076). CONCLUSIONS: Patients with unstable angina and a normal admission ECG have a good prognosis, while ST segment depression predicts an adverse outcome. Transient myocardial ischaemia detected by continuous ST segment monitoring in such patients receiving optimal medical treatment provides prognostic information additional to that gleaned from the clinical characteristics or the admission ECG.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_complications_MeSH Angina__Unstable_complications_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH S_physiopathology_MeSH Angina__Unstable_physiopathology_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Electrocardiography_MeSH P_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Monitoring__Physiologic_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Outcome_Assessment_(Health_Care)_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8673763
----K E
----T Follow up after spontaneous coronary artery dissection: a report of five cases.
----A Five cases of spontaneous coronary artery dissection (SCAD) are reported, three in women and two in men (mean age 44 years; range 28-65), all of whom suffered a myocardial infarction. Common risk factors for coronary artery disease were present in the two men; in the female group one patient was taking an oral contraceptive, one was in the postpartum period, and the third was a smoker. Only the three women received intravenous alteplase and their ejection fraction was normal; both men had impaired left ventricular function. Two patients had SCAD of the left anterior descending coronary artery and three of the right coronary artery. Only the two men had angiographic features of coronary atherosclerotic involvement. No patients required surgical revascularisation or percutaneous transluminal coronary angioplasty. At a mean follow up of 27 months (range 6 to 40) all patients were alive and all but one were asymptomatic.
----P Case_Reports Journal_Article 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aneurysm__Dissecting_MeSH S_complications_MeSH Aneurysm__Dissecting_complications_MeSH S_radiography_MeSH Aneurysm__Dissecting_radiography_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH 
****** 8703663
----K E
----T The effects of rilmenidine and atenolol on mental stress, dynamic exercise and autonomic function in mild to moderate hypertension.
----A 1. The effects of 4 week treatment with rilmenidine or atenolol on tests of mental stress, dynamic exercise, autonomic function and psychometric tests were evaluated in a randomized, double-blind, placebo-controlled, cross-over study. 2. After a 4 week placebo run-in, 12 patients with essential hypertension (blood pressure [BP] 160/95 +/- 15/7 mmHg) received rilmenidine 1-2 mg day-1, and atenolol 50-100 mg day-1, each for 4 weeks, with a 4 week placebo wash-out between drug treatments. 3. Both agents produced a comparable reduction in supine and erect BP. During the mental arithmetic test, BP and heart rate (HR) responses were similar for rilmenidine and atenolol. 4. During bicycle exercise, the increase in HR was significantly greater after rilmenidine (+50 vs 41 beats min-1, P = 0.04). During recovery, the areas under the curve for diastolic BP (46,450 vs 51,400 mmHg s, P = 0.02) and HR (49,445 vs 63,597 beats min-1 s, P = 0.001) were significantly less with atenolol than rilmenidine. 5. Neither rilmenidine nor atenolol affected mental performance as judged by arithmetic and psychomotor tests. Physiological responses to autonomic function tests (deep breathing, facial immersion, isometric handgrip and cold pressor) were preserved with both drugs. The standing to lying ratio was higher on atenolol (P = 0.01) and Valsalva ratio was higher on rilmenidine (P = 0.03). 6. In conclusion, rilmenidine and atenolol exerted comparable antihypertensive effects both at rest and during mental and dynamic stress. Atenolol attenuated HR responses to dynamic exercise and the Valsalva manoeuvre; rilmenidine did not interfere with the physiological responses of BP and HR during autonomic function tests.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxazoles_MeSH S_pharmacology_MeSH Oxazoles_pharmacology_MeSH S_therapeutic_use_MeSH Oxazoles_therapeutic_use_MeSH M_Stress__Psychological_MeSH M_Supine_Position_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8651108
----K E
----T Meta-analysis of the use of low-dose beta-adrenergic blocking therapy in idiopathic or ischemic dilated cardiomyopathy.
----A We concluded that low-dose beta-adrenergic blocking agents are beneficial in the treatment of patients with ischemic or idiopathic cardiomyopathy. Low-dose beta blockers appear to improve NYHA functional class and LVEF.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Human_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH 
****** 8644056
----K 1
----T [Losartan and the LIFE-study. Antihypertensive treatment with AT1-receptor antagonist]
----A The renin-angiotensin system, through the effects of angiotensin II, may be involved in the pathogenesis of essential hypertension and associated left ventricular hypertrophy. Treatment with angiotensin-converting enzyme inhibition (ACEI) lowers blood pressure and reduces left ventricular hypertrophy. ACEI, however, may not completely inhibit the production of angiotensin II and its effects, and adverse effects like cough and rise in creatinine have been associated with ACEI and reduced degradation of bradykinin. The first selective antagonist of the angiotensin II-1 (AT1) receptor, losartan, has recently been approved. The LIFE study has been started, in which 8,300 hypertensive patients with left ventricular hypertrophy in Scandinavia and the USA will be randomized to blinded treatment with either atenolol or losartan to compare the effects on cardiovascular morbidity and mortality over a period of five years.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Angiotensin_I_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_I_antagonists_&_inhibitors_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Imidazoles_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Scandinavia_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_United_States_MeSH 
****** 8656168
----K E
----T Number-needed-to-treat analysis of the prevention of myocardial infarction and death by antidyslipidemic therapy.
----A BACKGROUND. Atherosclerosis of the coronary arteries is the most common cause of death in the United States for persons over the age of 45. Dyslipidemia is one of the risk factors for the development of coronary atherosclerosis. Recent studies suggest that treating dyslipidemia in persons with coronary atherosclerosis may decrease morbidity and mortality. METHODS. A meta-analysis of 33 studies on the clinical and angiographic benefits of treating dyslipidemia in the prevention of morbidity and mortality from cardiovascular disease was performed. These benefits are quantitated in the form of "number needed to treat" (NNT) as an estimate of the public health benefit. The NNT is defined as the number of people that need to be treated to prevent one event. RESULTS. Treatment of dyslipidemia in persons with multiple atherosclerosis risk factors alone, ie, primary prevention, was effective in preventing myocardial infarction and all-cause death. In six trials of primary prevention, excluding the British cooperative trial using clofibrate, the NNT was 53 to prevent a nonfatal MI and 190 to prevent all-cause death (4.8 years treatment with total cholesterol reduction of 15%). Treatment of dyslipidemia in people with known atherosclerosis, ie, secondary and tertiary prevention, was also effective in preventing myocardial infarctions and death from all causes. For 23 trials of secondary and tertiary prevention, the NNT was 37 to prevent death from any cause (4.9 years treatment with total cholesterol reduction of 18%). In the trials with quantitative angiography, the NNT was 7 to prevent progression of coronary atherosclerosis and 10 to induce regression of coronary atherosclerosis (2.5 years treatment with a low-density lipoprotein cholesterol reduction of 28%). Similar benefits were observed in those trials employing HMG CoA reductase inhibitors. Benefits may be similar with niacin or dietary therapy, but these therapies did not reach significance in all categories of benefits, potentially due to beta error. These treatment benefits are comparable to other secondary prevention measures such as aspirin or beta blockers. The benefits appeared to extend to persons over 65, with less clearly defined benefits for women. CONCLUSIONS. These results support the overall clinical benefit of treating dyslipidemia, both in persons with and without known atherosclerosis.
----P Journal_Article Meta-Analysis 
----M M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Coronary_Angiography_MeSH M_Coronary_Arteriosclerosis_MeSH S_complications_MeSH Coronary_Arteriosclerosis_complications_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH M_Disease_Progression_MeSH M_Female_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Niacin_MeSH S_therapeutic_use_MeSH Niacin_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 8706768
----K E
----T How informed general practitioners manage mild hypertension: a survey of readers of drug bulletins in 7 countries. International Society of Drug Bulletins (ISDB).
----A OBJECTIVE. To determine whether general practitioners (GP) who are readers of independent drug bulletins can be used as an international epidemiological observatory of the criteria adopted by "well informed" doctors in various countries in the management of mild hypertension. DESIGN. Questionnaire study of GPs' diagnostic criteria for mild hypertension, routine investigation and management of patients with this diagnosis. PARTICIPANTS. 206 GPs readers of independent drug bulletins in 7 countries, comprising 95 known systematic readers of a local bulletin and 111 randomly selected regular subscribers. MAIN OUTCOME MEASURES. Response rate to the questionnaire. Diagnostic criteria, routine investigations, and treatment used for patients with mild hypertension. RESULTS. The study required two months for planning and implementation. Four countries out of eleven had a response rate < or = 50% and were excluded; the frequency of responses from other countries was 69%. The average diastolic blood pressure (DBP) considered diagnostic of mild hypertension range from 94 mm Hg (lower threshold) to 106 (upper threshold). A minority (17%) of GPs routinely request the minimum recommended laboratory tests to assess patients. GPs routinely advise non-drug measures before starting a drug. Most would not start drug treatment in patients without other risk factors and a DBP below 100 mmHg. The top first choice drugs were diuretics and beta-adrenoceptor blockers. Half of the doctors were able to quote some published guide to the management of mild hypertension, and 18% cited a relevant trial. Attitudes in diagnosing and treating mild hypertension differed widely between GPs and countries. CONCLUSIONS. GP readers of drug bulletins can be used quickly and inexpensively to assess the extent to which recommended diagnostic and therapeutic practices are accepted by "well informed" doctors. The results suggest that attitudes in managing mild hypertension vary widely among GPs and countries and differ remarkably from the recommendations of published guidelines.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Diet_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Family_Practice_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Guidelines_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_International_Cooperation_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Questionnaires_MeSH M_World_Health_Organization_MeSH 
****** 8777472
----K I
----T Quality of life in hypertensive patients treated with either carvedilol or enalapril.
----A An important aspect of antihypertensive drug treatment is quality of life (QL) which should at least not be negatively affected. In this study, the QL during treatment with carvedilol (C), a beta-blocker with vasodilating properties due to alpha-1-receptor blockade, was compared to that of enalapril (E) in patients who had responded to the treatment. PATIENTS AND METHODS: Patients with mild to moderate hypertension (diastolic blood pressure 95-115 mmHg) were randomised to receive either E(n = 119) of C(n = 129) in a double-blind multicenter study. The starting doses were 12.5 (C) and 10 (E) mg with doubling of the dose if necessary at 3-week intervals. If insufficient blood pressure (BP) control was found at 50 mg C or 40 mg E, 12.5 mg of hydrochlorothiazide was added. After having reached the goal BP the patients entered a 5-months maintenance period. General well-being was evaluated by the "Goteborg Quality of Life Questionnaire". RESULTS: Equally many patients in the respective treatment groups responded at the different dose levels. Diastolic BP after 5 months in the maintenance period was similar on C and E, respectively. For most items, QL was not affected by the treatments. An increased incidence of cough was perceived in the E group (p < 0.001). None of the C treated patients reported frequent cough at the end of the study compared with 12% of E treated patients. CONCLUSION: C and E had similar BP lowering effects. Neither treatment seemed to affect the patients QL adversely. Cough, although seldom leading to withdrawal from the therapy, may be more common than is commonly recognised during treatment with ACE-inhibitors.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cough_MeSH S_chemically_induced_MeSH Cough_chemically_induced_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH P_Quality_of_Life_MeSH 
****** 8695026
----K E
----T Changes in frequency of orthostatic hypotension in elderly hypertensive patients under medications.
----A To evaluate changes in frequency of orthostatic blood pressure (BP) reduction (orthostatic hypotension; OH) in elderly hypertensive patients (HT) before and after treatment for hypertension, we measured BP after supine for 10 min and standing position for 2 min, before and after treatment for 2 years by five kinds of antihypertensive drugs in 50 elderly normotensive subjects (NT) and each of 50 HT in double-blind study. Orthostatic hypotension was defined as 10% or more decline of supine mean BP, and the frequency of OH was in 27% of HT following BP reduction by any kinds of antihypertensive drugs. In conclusion, the reducing or normalized BP by treatment for hypertension in elderly HT decreases the prevalence of orthostatic hypotension.
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypotension__Orthostatic_MeSH S_blood_MeSH Hypotension__Orthostatic_blood_MeSH S_physiopathology_MeSH Hypotension__Orthostatic_physiopathology_MeSH M_Japan_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Posture_MeSH M_Prevalence_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8667090
----K E
----T Implementation of local guidelines for cost-effective management of hypertension. A trial of the firm system.
----A OBJECTIVE. To evaluate the effects of an intensive intervention to implement guidelines for cost-effective management of hypertension on medication use and cost, blood pressure control, and other resource use. DESIGN. Retrospective cohort trial based on the Cleveland Veterans' Affairs Medical Center Firm System. SETTING. General internal medicine teaching clinic in a large university-affiliated Department of Veterans Affairs Medical Center. PARTICIPANTS. All patients seen in the intervention firm (n = 1273) and control firm (n = 884) clinics in the 3-month period following the introduction of the guidelines. INTERVENTIONS. The control firm received guidelines and usual education for the cost-effective outpatient management of hypertension. The intervention firm received guidelines plus intensive guideline-based education and supervision. MEASUREMENTS AND MAIN RESULTS. The use of guideline medications was greater in the intervention firm as compared with the control. The intervention firm initiated more hydrochlorothiazide (HCTZ), 17.4% (95% confidence interval [CI] 14.8, 20.1) of patients versus 11.9% (CI 9.3, 14.8) in the control firm (p = .002). Atenolol was initiated in 7.2% (CI 5.6, 9.0) in intervention firm versus 4.7% (CI 3.2, 6.6) in the control (p = .03). In addition, the use of nonguideline medications was less in the intervention firm. The intervention firm initiated less long-acting nifedipine, 7.8% (CI 6.0, 9.8) versus 10.6% (CI 8.2, 13.5) in the control (p = .04). Blood pressure control demonstrated greater improvement in the intervention firm (p = .02). Use of guidelines was associated with decreased costs for antihypertensive medications in the intervention firm as a whole as compared with the control firm. There was no increased use in other measured resources in the intervention firm including the number of outpatient laboratory services obtained, clinic visits, emergency room visits, or hospitalizations. CONCLUSIONS. Intensive implementation of guideline-based education and supervision was associated with an increased use of guideline medications, decreased use of costly alternative agents, and no decrement in the measured outcomes of care.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Female_MeSH M_Health_Education_MeSH M_Hospitals__Veterans_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Ohio_MeSH P_Practice_Guidelines_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 8677865
----K E
----T Usefulness of beta-blocker therapy in patients with non-insulin-dependent diabetes mellitus and coronary artery disease. Bezafibrate Infarction Prevention (BIP) Study Group.
----A The benefit of beta-blocker therapy in patients after myocardial infarction is well established. The use of beta blockers in the high-risk subgroup of patients with combined diabetes mellitus (DM) and coronary artery disease (CAD) remains controversial. From a database of 14,417 patients with chronic CAD who had been screened for participation in the Bezafibrate Infarction Prevention (BIP) study, 2,723 (19%) had non-insulin-dependent DM. Baseline characteristics and 3-year mortality were analyzed in patients with DM receiving (n = 911; 33%) and not receiving (n = 1,812; 67%) beta blockers. Total mortality during a 3-year follow-up was 7.8% in those receiving beta blockers compared with 14.0% in those who were not (a 44% reduction). A reduction in cardiac mortality of 42% between the 2 groups was also noted. Three-year survival curves showed significant differences in mortality with increasing divergence (p = 0.0001). After multiple adjustment, multivariate analysis identified beta-blocker therapy as a significant independent contributor to improved survival (relative risk = 0.58; 90% confidence interval 0.46 to 0.74). Within the diabetic population, the main benefit associated with beta-blocker therapy was observed in older patients, in those with a history of myocardial infarction, those with limited functional capacity, and those at lower risk. Thus, therapy with beta blockers appears to be associated with improved long-term survival in the high-risk subpopulation of patients with DM and CAD.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Actuarial_Analysis_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Bezafibrate_MeSH S_therapeutic_use_MeSH Bezafibrate_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Databases__Factual_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_mortality_MeSH Diabetes_Mellitus__Type_II_mortality_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH 
****** 8677870
----K E
----T Comparison of subgroups assigned to medical regimens used to suppress cardiac ischemia (the Asymptomatic Cardiac Ischemia Pilot [ACIP] Study).
----A This report focuses on the subset of 235 patients from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study receiving randomly assigned medical therapy to treat angina and suppress ischemia detected on ambulatory electrocardiography: 121 patients received the sequence of atenolol and nifedipine, and 114 diltiazem and isosorbide dinitrate. After 12 weeks of therapy, the primary end point (absence of ambulatory electrocardiographic (ECG) ischemia and no clinical events) was reached in 47% of atenolol/nifedipine- versus 31% of diltiazem/isosorbide dinitrate-treated patients (adjusted p = 0.03). A trend to increased exercise time to ST depression was seen in the atenolol and nifedipine versus diltiazem and isosorbide dinitrate regimens (median treadmill duration 5.8 vs 4.8 minutes; p = 0.04). However, when adjusted for baseline imbalances in ambulatory ECG ischemia, the 2 medical combinations were similar in suppression of ambulatory ECG ischemia. In both medication regimens, an association between mean heart rate and ischemia on ambulatory electrocardiography after 12 weeks of treatment was observed so that patients on either regimen with a mean heart rate > 80 beats/min had ischemia detectable almost twice as often as those with a mean heart rate < 70 beats/min (p < 0.001).
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Pilot_Projects_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH 
****** 8664529
----K E
----T Evaluation and treatment of nonsustained ventricular tachycardia.
----A The clinical significance of nonsustained ventricular tachycardia continues to undergo reevaluation as clinicians attempt to optimize screening strategies for identifying high-risk patients and to evaluate the efficacy of therapeutic interventions. The utility of ambulatory monitoring and programmed stimulation as screening tools in the patient who has suffered an infarction remains unsettled; ongoing clinical trials may help resolve these issues. New data suggest that the survival benefit associated with angiotensin-converting enzyme inhibition is unrelated to effects on spontaneous arrhythmias, similar to results previously reported for beta-blockers. Randomized clinical trials of prophylactic amiodarone in patients with congestive heart failure and nonsustained ventricular tachycardia have produced conflicting results. A strong relationship between polymorphic nonsustained ventricular tachycardia and sudden death in patients without structural heart disease or QT prolongation has been reported. The significance of nonsustained ventricular tachycardia in dilated cardiomyopathy and hypertrophic cardiomyopathy has also been reassessed.
----P Journal_Article Review Review__Tutorial 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Cardiomegaly_MeSH S_complications_MeSH Cardiomegaly_complications_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_diagnosis_MeSH Cardiomyopathy__Congestive_diagnosis_MeSH M_Electrocardiography_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Tachycardia__Ventricular_MeSH S_complications_MeSH Tachycardia__Ventricular_complications_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8656666
----K E
----T Effects of angiotensin-converting enzyme inhibition versus beta-adrenergic blockade on aortic stiffness in essential hypertension.
----A We assessed the effects of 6 months of treatment with an angiotensin-converting enzyme (ACE) inhibitor (cilazapril) or a beta 1-adrenergic blocker (atenolol) on aortic stiffness in essential hypertension. Forty patients (16 women) aged 47 +/- 9 years (mean +/- SD) with baseline systolic and diastolic blood pressures of 162 +/- 15 and 105 +/- 5 mm Hg, respectively, were entered into a double-blind, parallel-group study with cilazapril, 5 mg once daily, or atenolol, 100 mg once daily. The treatment period was preceded by a 4-week placebo washout phase. Aortic elastic modulus (Ep) was determined by cine magnetic resonance imaging (MRI) and indirect brachial artery blood pressure measurements prior to and after 3 weeks and 6 months of therapy. The reductions in systolic and diastolic blood pressures from baseline to 6 months averaged -17 +/- 13 and -10 +/- 6 mm Hg, respectively, with cilazapril and -23 +/- 16 and -14 +/- 6 mm Hg with atenolol. Concomitantly, Ep of the ascending aorta decreased with cilazapril from a median of 2,234 10(3)dyn/cm2 (interquartile range, 866-3,740) to 868 10(3)dyn/cm2 (515-1,486) and with atenolol from a median of 1,611 10(3)dyn/cm2 (895-2,790) to 1,054 10(3)dyn/cm2 (616-1,860). In repeated-measurements analysis of variance, the change in Ep with time was statistically significant (p < 0.001) but the group x time interaction was not. We conclude that 6 months of treatment with either cilazapril or atenolol reduces the stiffness of the ascending aorta in essential hypertension. No statistically significant differences between the effects of the two drugs were observed. The mechanisms and clinical significance of improved aortic distensibility with antihypertensive therapy deserve further study.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Aorta__Thoracic_MeSH S_drug_effects_MeSH Aorta__Thoracic_drug_effects_MeSH S_physiopathology_MeSH Aorta__Thoracic_physiopathology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH M_Comparative_Study_MeSH M_Compliance_MeSH S_drug_effects_MeSH Compliance_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 8998247
----K E
----T Effect of atenolol and reserpine on selected events in the systolic hypertension in the elderly program (SHEP).
----A The effect of atenolol and reserpine on incidence of strokes, coronary heart disease (CHD), cardiovascular disease (CVD), and mortality was assessed in 4736 persons aged 60 years and older with isolated systolic hypertension. Participants were randomized to either chlorthalidone (2371), with step-up to atenolol, or reserpine if needed, or placebo (2365). The average baseline SBP/DBP was 170/77 mm Hg. In the active treatment group, step 1, dose 1 was chlorthalidone, 12.5 mg/day; dose 2 was 25 mg/day. For step 2, dose 1 was atenolol 25 mg/day (or reserpine 0.05 mg/day if atenolol was contraindicated); dose 2 was 50 mg/day (reserpine, 0.10 mg/day). During 4.5 years average follow-up, 32% (757) of the active treatment group were on atenolol, with an average exposure of two years and 8% (193) were on reserpine with an average exposure of 1.7 years. Overall there were 96 strokes, 140 CHD events and 289 CVD events among the 2365 active group participants. Using time-dependent lifetable regression with adjustment for several variables, the addition of either atenolol or reserpine to chlorthalidone did not substantially alter the risk ratios for chlorthalidone alone. The relative risk for CHD events for atenolol versus no atenolol was 1.04 (95% confidence interval: 0.58, 1.86) and for reserpine versus no reserpine was 0.93 (95% confidence interval: 0.29, 2.96). The relative risk for atenolol were 0.84 (95% confidence interval: 0.54, 1.30) for death, 1.34 (95% confidence interval: 0.80, 2.28) for stroke, and 1.07 (95% confidence interval: 0.71, 1.61) for CVD. For reserpine, the corresponding relative risks and confidence intervals were 0.65 (0.26, 1.59) for death, 0.27 (0.04, 2.26) for stroke, and 0.55 (0.20, 1.49) for CVD. Thus, the beneficial effects in several outcomes in Systolic Hypertension in the Elderly Program (SHEP) were due to the treatment regimen of lowering blood pressure based on low-dose chlorthalidone (plus atenolol or reserpine as required to meet blood pressure criteria). Additional (independent) benefits attributable to atenolol or to reserpine were not identified. However, a greater number of patients might have been necessary to adequately evaluate potential differential effects of these drugs, especially for reserpine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Reserpine_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Risk_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH 
****** 8680629
----K E
----T Correlates of leukocyte counts in men.
----A Because of previously reported associations between a high leukocyte count and risk of ischemic heart disease (IHD), we examined the relation of leukocyte counts to various characteristics among 3591 white and 506 black 31- to 45-year-old men. The mean leukocyte count was approximately 1000 cells/microL higher among whites than among blacks, and approximately 1900 cells/microL higher among current smokers than among nonsmokers. The leukocyte count was also higher among men who had recently stopped smoking and among men who reported their general health as poor or fair. Independent of these relations, the leukocyte count was associated positively with the platelet count (r = 0.29), triglyceride level (r = 0.21), heart rate (r = 0.15), and use of corticosteroids and beta-blockers; and inversely with alcohol consumption and prothrombin time (r = -0.10). The examined characteristics could together account for 37% of the variability in leukocyte counts. These relatively strong associations indicate that it may be difficult to disentangle the relation of the leukocyte count to IHD from that of other risk factors.
----P Journal_Article 
----M M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Cause_of_Death_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_ethnology_MeSH Coronary_Disease_ethnology_MeSH S_immunology_MeSH Coronary_Disease_immunology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH P_European_Continental_Ancestry_Group_MeSH M_Human_MeSH M_Hypertension_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_immunology_MeSH Hypertension_immunology_MeSH S_mortality_MeSH Hypertension_mortality_MeSH P_Leukocyte_Count_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH S_immunology_MeSH Smoking_immunology_MeSH S_mortality_MeSH Smoking_mortality_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_Veterans_MeSH S_statistics_&_numerical_data_MeSH Veterans_statistics_&_numerical_data_MeSH M_Vietnam_MeSH 
****** 8674173
----K E
----T Comparison of d,l-sotalol and implantable defibrillators for treatment of sustained ventricular tachycardia or fibrillation in patients with coronary artery disease.
----A BACKGROUND: Implantable cardioverter-defibrillators (ICDs) and d,l-sotalol are widely used to treat ventricular tachyarrhythmia and ventricular fibrillation (VT/VF). The purpose of this study was to compare the long-term efficacy of d,l-sotalol and ICDs in patients with coronary artery disease. METHODS AND RESULTS: In a case-control study, 50 patients treated with oral d,l-sotalol were matched to 50 patients treated with ICDs. Both groups were matched for sex (82 men), age (58 +/- 10 years), ejection fraction (40 +/- 12%), extent of coronary artery disease, presenting arrhythmia, and year that treatment began. In all patients in the sotalol group, VT/VF was inducible in the drug-free electrophysiological study. Induction of sustained VT/VF was suppressed by d,l-sotalol (438 +/- 95 mg/d). In the ICD group, either VT/VF was not inducible (n = 5) or inducible sustained VT/VF was refractory to antiarrhythmic drug treatment (n = 45). Sotalol treatment led to a marked reduction in arrhythmic events. Whereas 83% of the patients in the sotalol group were free of sudden death and nonfatal VT at 3 years, only 33% of the ICD patients did not receive appropriate ICD therapies (P < .005). Actuarial rates for absence of sudden death at 3 years were 85% in the sotalol group and 100% in the ICD group (P < .005). Actuarial rates for overall survival at 3 years were 75% in the sotalol group and 85% in the ICD group (P = .02). CONCLUSIONS: In this case-control study, ICD therapy was more effective tha electrophysiologically guided antiar-rhythmic treatment with d,l-sotalol in prevention of sudden death and reduction of total morality in patients with coronary artery disease. Prospective studies are needed to confirm these results.
----P Journal_Article 
----M M_Administration__Oral_MeSH M_Case-Control_Studies_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH P_Defibrillators__Implantable_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Ventricular_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Fibrillation_MeSH S_therapy_MeSH Ventricular_Fibrillation_therapy_MeSH 
****** 8752790
----K I
----T Prognostic significance of transient ischemic episodes: response to treatment shows improved prognosis. Results of the Total Ischemic Burden Bisoprolol Study (TIBBs) follow-up.
----A OBJECTIVES: The Total Ischemic Burden Bisoprolol Study (TIBBS) follow-up examined cardiac event rates in relation to transient ischemia and its treatment. BACKGROUND: It is unclear whether transient ischemia on the ambulatory electrocardiogram has prognostic implications in stable angina and whether medical treatment can improve the prognosis. METHODS: The TIBBS trial was an 8-week, randomized, controlled comparison of the effects of bisoprolol and nifedipine on transient ischemic episodes in patients with stable angina pectoris. Of the 545 patients screened, 520 (95.4%) could be followed up. Rates of cardiac and noncardiac death, nonfatal acute myocardial infarction, hospital admission for unstable angina and need for coronary artery bypass graft surgery or percutaneous transluminal coronary angioplasty were recorded. RESULTS: A total of 145 events occurred in 120 (23.1%) of 520 patients. Patients with more than six episodes had an event rate of 32.5% compared with 25.0% for patients with two to six episodes and 13.2% for patients with less than two episodes (p < 0.001). Hard events (death, acute myocardial infarction, hospital admission for unstable angina pectoris) were more frequent in patients with two or more ischemic episodes (12.2% vs. 4.7%, p = 0.0049). Patients with a 100% response rate of transient ischemic episodes during the TIBBS trial had a 17.5% event rate at 1 year compared with 32.3% for non-100% responders (p = 0.008). Patients receiving bisoprolol during the TIBBS tria had a lower event rate (22.1%) at 1 year than patients randomized to nifedipine (33.1%, p = 0.033). CONCLUSIONS: In patients with stable angina pectoris, frequent episodes of transient ischemia are a marker for an increased event rate. A 100% response to medical treatment reduces the event rate. The greater reduction of ischemia with bisoprolol than nifedipine during the TIBBS trial translated into an improved outcome at 1 year.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Disease-Free_Survival_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_epidemiology_MeSH Myocardial_Ischemia_epidemiology_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Patient_Selection_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8682000
----K E
----T Pointers from recent multicentre trials using ambulatory monitoring--placing placebo in perspective.
----A The primary role of interventional procedures in the management of some congenital heart diseases is established and their clinical utility broadens every day. Yesterday's relatively crude procedures have been replaced by safe and more effective techniques. Improvements and new developments in specifically designed paediatric equipment have played a significant role. In order to meet the cardiologist's drive to refine existing techniques and develop new ones, further investment into paediatric cardiac catheterization equipment is mandatory. More and more "heart operations' will be performed in cardiac catheterization laboratories in the future, and this will have clear implications on costs, as most non-surgical techniques are cheaper than surgery, and hospitalization is much shorter. New methods, tested within research protocols in specialized centres, combined with continuous critical evaluation of established techniques will ensure improved and sustained results. The primary consideration of practising paediatric cardiologists should not be whether it is possible to perform such techniques, but whether their clinical utility, morbidity and mortality justifies a non-surgical approach for their centre. Interventional catheterization, in other words has to "compete' with the results of surgery prior to new techniques being recommended for general use. Despite this "competition' it has been welcome to see a collaboration between paediatric cardiologists and paediatric cardiac surgeons in planning staged repairs of complex congenital heart disease. A typical example of this is the fenestrated Fontan procedure, in which the immediate post-operative course has dramatically improved due to the deliberate placement of a residual atrial shunt, which is then closed with an umbrella in the catheter laboratory. This type of cooperation is bound to increase further and is already contributing to a far better outcome for many of the complex congenital heart lesions.
----P Clinical_Trial Comment Editorial Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Human_MeSH M_Placebo_Effect_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8682014
----K I
----T Effect of metoprolol on death and cardiac events during a 2-year period after coronary artery bypass grafting. The MACB Study Group.
----A PURPOSE: To evaluate the effect of long-term treatment with metoprolol after coronary bypass grafting on death and cardiac events. METHODS: Patients in western Sweden on whom coronary artery bypass grafting was performed between June 1988 and June 1991 were evaluated for inclusion during the first 3 weeks after surgery. Major exclusion criteria were age > 75 years, concomitant valve surgery, traditional contraindications to beta-blockers and unwillingness to participate. Patients were randomized in a double-blind fashion to 100 mg of metoprolol/placebo daily for 2 weeks and thereafter 200 mg daily for 2 years. RESULTS: Of 2365 patients who were operated on, 967 were randomized to either metoprolol (n = 480) or placebo (n = 487). Primary end points (death, non-fatal myocardial infarction, unstable angina pectoris, need for coronary artery bypass grafting or percutaneous transluminal angioplasty), were reached by 42 patients in the metoprolol group (8.8%), as compared with 39 in the placebo group (8.0%) (P = 0.73). Of all the patients randomized to metoprolol, 34% withdrew from blind treatment prematurely compared with 44% for placebo (P < 0.01). CONCLUSION: Prophylactic treatment with metoprolol over a 2-year period after coronary artery bypass grafting did not reduce death or the development of cardiac events. However, the 95% confidence limits ranged from the possibility of a 30% reduction in events to a 68% increase in events if patients were treated with metoprolol as compared with placebo.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH S_surgery_MeSH Angina_Pectoris_surgery_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH M_Recurrence_MeSH M_Survival_Rate_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH 
****** 8682134
----K I
----T Effects of metoprolol vs verapamil in patients with stable angina pectoris. The Angina Prognosis Study in Stockholm (APSIS)
----A OBJECTIVE: To study long-term treatment effects of metoprolol or verapamil on combined cardiovascular end points and psychological variables in patients with stable angina pectoris. DESIGN: Randomized, double-blind, double-dummy trial. PATIENTS: The study included 809 patients under 70 years of age with stable angina pectoris. The mean age of the patients was 59 +/- 7 years and 31% were women. Exclusion criteria were myocardial infarction within the previous 3 years and contraindications to beta-blockers and calcium antagonists. The patients were followed between 6 and 75 months (median 3.4 years and a total of 2887 patient years). INTERVENTION: The patients were treated with either metoprolol (Seloken ZOC 200 mg o.d.) or verapamil (Isoptin Retard 240 b.i.d.). Acetylsalicylic acid, ACE inhibitors, lipid lowering drugs and long acting nitrates were allowed in the study. END POINTS: Death, non-fatal cardiovascular events including acute myocardial infarction, incapacitating or unstable angina, cerebrovascular or peripheral vascular events. Psychological variables reflecting quality of life i.e. psychosomatic symptoms, sleep disturbances and an evaluation of overall life satisfaction. RESULTS: Combined cardiovascular events did not differ and occurred in 30.8% and 29.3% of metoprolol and verapamil treated patients respectively. Total mortality in metoprolol and verapamil treated patients was 5.4 and 6.2%, respectively. Cardiovascular mortality was 4.7% in both groups. Non-fatal cardiovascular events occurred in 26.1 and 24.3% of metoprolol and verapamil-treated patients, respectively. Psychosomatic symptoms and sleep disturbances were significantly improved in both treatment groups. The magnitudes of change were small and did not differ between treatments. Life satisfaction did not change on either drug. Withdrawals due to side effects occurred in 11.1 and 14.6% respectively. CONCLUSION: This long term study indicates that both drugs are well tolerated and that no difference was shown on the effect on mortality, cardiovascular end points and measures of quality of life.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Sweden_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 8682138
----K I
----T The Total Ischaemic Burden European Trial (TIBET). Effects of atenolol, nifedipine SR and their combination on the exercise test and the total ischaemic burden in 608 patients with stable angina. The TIBET Study Group.
----A OBJECTIVES: To determine the effects of atenolol, nifedipine and their combination on exercise parameters and ambulatory ischaemic activity in patients with mild chronic stable angina. SETTING: Multicentre, multinational study involving 608 patients from 69 centres in nine countries. DESIGN: Placebo washout followed by double-blind parallel-group study comparing atenolol 50 mg bd, nifedipine SR 20 mg bd, and their combination. Patients underwent maximal exercise testing using either a bicycle (n = 289) or treadmill (n = 319) and 48 h of ambulatory ST segment monitoring outside the hospital environment at the end of the placebo washout period and after 6 weeks of active therapy. RESULTS: Both medications alone and in combination caused significant improvements in exercise parameters and significant reductions in ischaemic activity during daily activities, when compared with placebo. There were, however, no significant differences between groups, for any of the measured ischaemic parameters although combination therapy resulted in a greater fall in resting systolic and diastolic blood pressure than either treatment alone. CONCLUSIONS: In the management of mild chronic stable angina there appears to be little advantage gained from using combination therapy for ischaemia reduction.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Europe_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8682116
----K I
----T Total Ischaemic Burden European Trial (TIBET). Effects of ischaemia and treatment with atenolol, nifedipine SR and their combination on outcome in patients with chronic stable angina. The TIBET Study Group.
----A OBJECTIVE: To study the relationship between presence or absence of ischaemic events on Holter monitoring and occurrence of a hard or hard+soft endpoint. DESIGN: A randomized double-blind parallel group study of atenolol, nifedipine and their combination, with ambulatory monitoring off-treatment and after 6 weeks of randomized treatment and prospective follow-up of 2 years on average. SETTING: Europe. SUBJECTS: 682 men and women with a diagnosis of chronic stable angina and who were not being considered for surgery. MAIN OUTCOME: Hard endpoints were cardiac death, nonfatal myocardial infarction and unstable angina; soft endpoints were coronary artery bypass surgery, coronary angioplasty and treatment failure. RESULTS: The study showed no evidence of an association between the presence, frequency or total duration of ischaemic events on Holter monitoring, either on or off treatment, and the main outcome measures. There was a non-significant trend to a lower rate of hard endpoints in the group receiving combination therapy. Compliance, as measured by withdrawal from trial medication, was clearly poorest in the nifedipine group with similar withdrawal rates in the atenolol and combination therapy groups. CONCLUSION: The recording of ischaemic events in 48 h Holter monitoring failed to predict hard or hard+soft endpoints in patients with chronic stable angina.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Europe_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 8728305
----K E
----T Prediction of patient responses to antihypertensive drugs using genetic polymorphisms: investigation of renin-angiotensin system genes.
----A OBJECTIVE: To investigate whether the M235T polymorphism of the angiotensinogen (AGT) gene and the insertion/deletion (I/D) polymorphism of the angiotensin-1 converting enzyme (ACE) gene predict blood pressure response to different antihypertensive agents. DESIGN: Sixty-three patients with untreated essential hypertension were randomly assigned in a placebo-controlled crossover comparison to atenolol 50 mg once daily, lisinopril 10 mg once daily and nifedipine SR 20 mg twice daily, and the effect on blood pressure was assessed by ambulatory blood pressure monitoring (ABPM). In a further 44 patients, placebo-controlled ABPM data were available after treatment with a single agent (atenolol 50 mg once daily in 16 cases and lisinopril 10mg once daily in 28 cases). The change in systolic and diastolic blood pressure achieved by each agent was analysed for association with genotypes at the AGT and ACE gene loci. METHODS: Polymerase chain reaction (PCR) amplification of genomic DNA from each individual was used to identify the I/D polymorphism of the ACE gene. The M235T polymorphism of the AGT gene was detected by Tth111I digestion of PCR product. RESULTS: There was no significant association between response to any drug and either the AGT M235T or ACE I/D polymorphisms. CONCLUSIONS: The large variability between individuals in the observed blood pressure response to these agents cannot be attributed to the polymorphisms analysed at the ACE and AGT loci.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Alleles_MeSH M_Analysis_of_Variance_MeSH M_Angiotensinogen_MeSH S_genetics_MeSH Angiotensinogen_genetics_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Cross-Over_Studies_MeSH M_DNA_MeSH S_analysis_MeSH DNA_analysis_MeSH M_Female_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_genetics_MeSH Peptidyl-Dipeptidase_A_genetics_MeSH M_Polymerase_Chain_Reaction_MeSH M_Polymorphism_(Genetics)_MeSH S_genetics_MeSH Polymorphism_(Genetics)_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8728306
----K E
----T Comparative effects of combination drug therapy regimens commencing with either losartan potassium, an angiotensin II receptor antagonist, or enalapril maleate for the treatment of severe hypertension.
----A OBJECTIVE: To compare the efficacy and safety of a regimen of losartan potassium (losartan) and a regimen of enalapril maleate (enalapril) in a randomized trial of patients with severe hypertension in which the initial treatments were blinded. DESIGN AND METHODS: Seventy-five patients, 23-74 years of age, with sitting diastolic blood pressure of 115-130mmHg, were enrolled in a 12-site multicenter study. The primary efficacy parameters were the change in trough systolic and diastolic blood pressure, as well as response to treatment in terms of categories of hypertensive response. RESULTS: A gradual reduction in mean sitting diastolic blood pressure was observed in all patients treated from week 1 to 12 (10-29mmHg for the losartan regimen and 14-32 mmHg for the enalapril regimen). At week 4, a substantial number of patients remained on monotherapy at either the initial dose or double the dose of losartan (52%) or enalapril (72%). The blood pressure curves for each treatment were parallel over time. The enalapril-based regimen elicited a statistically significantly greater reduction in blood pressure than the losartan-based regimen, although the mean differences in the blood pressure response between the two treatment groups was small. Based on sitting diastolic blood pressure < 90 mmHg or a reduction in blood pressure of at least 10 mmHg, 98% of the patients assigned to the losartan regimen and 100% of the patients assigned to the enalapril regimen had a satisfactory response with a regimen of one to three antihypertensive drugs. Headache was the most common adverse experience in both treatment groups (occurring in 22% of patients assigned to the losartan regimen and 20% of patients assigned to the enalapril regimen). CONCLUSIONS: In this study, the losartan-based regimen effectively lowered blood pressure, was generally well tolerated, and was generally similar to the enalapril-based regimen in the treatment of patients with severe hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Imidazoles_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 8707022
----K 1
----T [Propafenone and sotalol: long-term efficacy and tolerability in the prevention of paroxysmal atrial fibrillation. A placebo-controlled double-blind study]
----A BACKGROUND. Atrial fibrillation is a relatively frequent atrial arrhythmias activated with increased morbidity and mortality. METHODS. To assess the propafenone and sotalol efficacy in the prevention of paroxysmal atrial fibrillation (FA) we enrolled, in a double blind placebo controlled study over 1 year, 300 patients (168 males); mean age 52.3 +/- 17.2 years, randomized to receive orally, three times daily, either propafenone (mean daily dose of 13 +/- 1.5 mg/Kg; Group A: 102 patients) or sotalol (mean daily dose of 3 +/- 0.4 mg/Kg; Group B: 106 patients) or placebo (Group C: 92 patients). All subjects experienced in previous 12 months at least 4 FA episodes. During follow-up we considered atrial tachyarrhythmia (TAA) onset: FA recurrences and/or the onset of atrial flutter (FIA). Three patients (3%) of Group A and 5 (5%) of Group B interrupted therapy for side effects; 5 patients (5.5%) of Group C with supraventricular tachycardia interrupted the double blind therapy; 11 were lost to follow-up. RESULTS. Of the remaining 276 patients, TAA were observed in 43 (44.8%) of 96 patients in Group A, 28 (29.5%) of 95 patients in Group B and 62 (72.9%) of 85 patients in Group C. TAA were significantly less in A and B groups than in Group C (p < 0.005); a significant TAA reduction was also observed in patients treated with sotalol compared with those treated with propafenone (p < 0.05). TAA were: FA-118 (88.7%) and FIA-15 (11.3%). The arrhythmia free time was significantly shorter in Group C. CONCLUSIONS. Sotalol seems to be more effective than propafenone and therefore represents a valid alternative for FA prevention.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propafenone_MeSH S_administration_&_dosage_MeSH Propafenone_administration_&_dosage_MeSH S_adverse_effects_MeSH Propafenone_adverse_effects_MeSH S_therapeutic_use_MeSH Propafenone_therapeutic_use_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Time_Factors_MeSH 
****** 8707025
----K E
----T [Efficacy and tolerability of felodipine and nifedipine in stable angina refractory to beta-blocker therapy]
----A BACKGROUND. Medical therapy of stable angina contemplates beta-blockers as a first line. The combination of dihydropyridines with beta-blocking drugs enhances the effectiveness of both single therapies. Nifedipine, in the usual formulation (AR), is burdened by an unsatisfactory tolerability, and this is the main reason to study new dihydropyridines. AIM. To compare efficacy and tolerability of felodipine ER 10 mg o.d. with that of nifedipine AR 20 mg b.d. in patients with stable angina pectoris refractory to beta-blocker therapy. PATIENTS AND METHODS. Of 15 initial patients, 14 were entirely evaluable for the study, the design of which was double blind, double dummy, random cross over and placebo controlled. All patients showed reproducible threshold of ischemia at exercise testing. In constancy of beta-blocker therapy, they were given placebos for 2 weeks, then one of the active drugs with a placebo of the other one for 4 weeks, followed by the cross-over period of 4 weeks. Efficacy and tolerability of treatments were evaluated by clinical observation and rest and exercise radionuclide angiography. At the end of each individual study, it was decided blindly if and which of the 2 drugs seemed preferable, considering symptoms, undesired collateral effects and the results of exercise procedures. RESULTS. The efficacy on angina of the 2 active treatments was not different. More patients suffered undesired side effects on nifedipine than on felodipine. Left ventricular ejection fraction (LVEF) at rest was 65.3 +/- 4.3% (s.e.) on placebo, 64.6 +/- 2.6% on felodipine and 67.5 +/- 2.5% on nifedipine (p n.s.). A significant reduction in resting LV function (that is, a decrease of LVEF > or = 5%) was observed in 2 patients on felodipine and 3 on nifedipine, but in both groups other 3 patients showed improvement in LVEF. During exercise, LVEF decreased 6.1 +/- 2.0% on placebo and 3.3 +/- 3.2% on nifedipine, while it increased 1.0 +/- 2.6% on felodipine (p < 0.01 vs. placebo). At the end of the study, felodipine was blindly judged superior to nifedipine in 10 patients, nifedipine was superior in 1 case, in the other 3 there was no clear difference (p < 0.02). CONCLUSIONS. In 14 patients with stable angina refractory to beta-blockers, the addition of felodipine or nifedipine has similar antiischemic effects. However, felodipine showed better results in LVEF response to exercise and less side effects, and this leaded to a more frequent blind choice of felodipine versus nifedipine to add to beta-blocker therapy.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Placebos_MeSH M_Stroke_Volume_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8730344
----K E
----T Calcium channel blockers versus ACE inhibitors as antihypertensives in polycystic kidney disease.
----A The effects of calcium channel blockers (CCBs) and angiotensin converting enzyme (ACE) inhibitors on blood pressure and the progression of renal dysfunction were compared in hypertensive patients with polycystic kidney disease (PKD). Twenty-six patients with PKD and hypertension who had been treated with other antihypertensive agents, such as diuretics, beta-blockers, or alpha-methyldopa, were followed up for two years, during which their blood pressure and renal function were monitored. Patients were divided into two groups classified according to the type of antihypertensive agents given. Group 1 (n = 14) received CCBs, while group 2 (n = 12) received ACE inhibitors. No significant differences were found in their blood pressure control and serum creatinine levels throughout the study. The creatinine clearances were decreased in both groups. However, the decreases in creatinine clearance were smaller (p < 0.05) in the group treated with CCBs. In addition, two patients in group 2 showed rapid increases in serum creatinine. Our data suggest that CCBs reduced blood pressure effectively and preserved renal function in PKD patients at least as well as ACE inhibitors.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nicardipine_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Polycystic_Kidney_Diseases_MeSH S_complications_MeSH Polycystic_Kidney_Diseases_complications_MeSH 
****** 8725417
----K E
----T The effect of midazolam at two plasma concentrations of hemodynamics and sufentanil requirement in coronary artery surgery.
----A OBJECTIVES: In this study, the hemodynamics and sufentanil requirement were compared at two midazolam target plasma concentrations in patients undergoing coronary artery bypass grafting (CABG). DESIGN: Prospective, randomized study. SETTING: University hospital, single institution. PARTICIPANTS: Patients undergoing CABG. INTERVENTIONS: Patients were randomly assigned to receive midazolam at a target plasma concentration of 150 ng/mL (group 1; n = 10) or 300 ng/mL (group 2; n = 10). Sufentanil infusion was titrated to maintain hemodynamic stability, defined as mean arterial pressure within 15% of baseline values. All patients received preoperative beta-blocking agents. Arterial blood samples of midazolam and sufentanil were analyzed by high-performance liquid chromatography and radioimmunoassay, respectively. MEASUREMENTS AND MAIN RESULTS: The mean dose of sufentanil (7.5 +/- 1.7 microgram/kg in group 1 v 7.2 +/- 2.5 micrograms/kg in group 2) did not differ. There were no significant differences in hemodynamics between the groups in the period before or after cardiopulmonary bypass (CPB). Before CPB, in two patients in each group, hypertension was controlled with sufentanil only. One patient in group 1 required a vasodilator in addition to sufentanil. No ischemic events occurred before CPB. After CPB, one patient in group 2 required a vasodilator to control hypertension. Two patients in group 2 required treatment with nitroglycerin for myocardial ischemia. Stable plasma concentrations of sufentanil and midazolam were obtained during and after CPB. The midazolam infusion was continued in both groups at a rate of 1.25 micrograms/kg/min during the first 4 postoperative hours. The time to awakening did not differ between the groups (100 +/- 58 minutes in group 1 v 173 +/- 147 minutes in group 2) nor did the plasma concentrations of midazolam (96 +/- 28 ng/mL v 108 +/- 42 ng/mL) at the time of awakening. Intraoperative awareness was not reported. CONCLUSION: In patients undergoing CABG, good hemodynamic control with a similar incidence of hemodynamic interventions was observed at midazolam target plasma concentrations of 150 and 300 ng/mL when coadministered with sufentanil. The sufentanil requirement was identical in both groups. This study suggests that a midazolam plasma concentration of 150 ng/mL is sufficient to provide satisfactory hemodynamic control and to avoid intraoperative awareness.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adjuvants__Anesthesia_MeSH S_administration_&_dosage_MeSH Adjuvants__Anesthesia_administration_&_dosage_MeSH S_blood_MeSH Adjuvants__Anesthesia_blood_MeSH S_pharmacology_MeSH Adjuvants__Anesthesia_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Analgesics__Opioid_MeSH S_administration_&_dosage_MeSH Analgesics__Opioid_administration_&_dosage_MeSH S_blood_MeSH Analgesics__Opioid_blood_MeSH S_pharmacology_MeSH Analgesics__Opioid_pharmacology_MeSH M_Anesthesia_Recovery_Period_MeSH M_Anesthetics__Intravenous_MeSH S_administration_&_dosage_MeSH Anesthetics__Intravenous_administration_&_dosage_MeSH S_blood_MeSH Anesthetics__Intravenous_blood_MeSH S_pharmacology_MeSH Anesthetics__Intravenous_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiopulmonary_Bypass_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Midazolam_MeSH S_administration_&_dosage_MeSH Midazolam_administration_&_dosage_MeSH S_blood_MeSH Midazolam_blood_MeSH S_pharmacology_MeSH Midazolam_pharmacology_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Sufentanil_MeSH S_administration_&_dosage_MeSH Sufentanil_administration_&_dosage_MeSH S_blood_MeSH Sufentanil_blood_MeSH S_pharmacology_MeSH Sufentanil_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Wakefulness_MeSH S_drug_effects_MeSH Wakefulness_drug_effects_MeSH 
****** 8767350
----K 1
----T [Antihypertensive effect and adverse effects of isradipine in patients with sever hypertension. Results of an open multicenter study]
----A Antihypertensive Efficacy and Tolerability of Isradipine in Patients with Severe Hypertension/Results of an open multicenter study. In this open multicentre study 55 patients (mean age 51.2 years) with severe hypertension (diastolic blood pressure > 115 mmHg) were treated for seven weeks with the calcium antagonist of the dihydropyridine type isradipine (CAS 75695-93-1, Lomir). If necessary, metoprolol or enalapril were added to the regimen. Before inclusion into the active treatment phase, responsiveness of the patients to a single administration of isradipine (5 mg) was compared with placebo. Preexisting antihypertensive therapy (18 patients) was to be maintained during the study period. Blood pressure was recorded with an automatic device. During the 7-week period blood pressure decreased from 173.7/124.8 mmHg to 143.2/97.8 mmHg. Both the group with isradipine monotherapy (n = 32) and the combination group (n = 11) showed a significant reduction in systolic and diastolic blood pressure. Diastolic blood pressure response, defined as a decline of more than 15 mmHg, was noted in 87.5% (monotherapy) and 72.7% (combination group) of patients. On the whole, blood pressure was normalized in 27.9% of the participants. Nineteen patients experienced 43 adverse events, most of which were rated mild to moderate. Therapy was withdrawn in only one patient (due to ankle edema). The most frequent adverse event was headache (20.9%).
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isradipine_MeSH S_administration_&_dosage_MeSH Isradipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Isradipine_adverse_effects_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 8706070
----K 1
----T [Glycemia increases during treatment of hypertension. 13 years' experience in the treatment of middle-aged men, randomized for treatment with beta blockers and diuretics]
----A BACKGROUND: Hypertension can no longer be evaluated only with regard to the increase of blood pressure; its clinical picture must comprise also metabolic changes with originate from insulin resistance. METHODS AND RESULTS: The authors submit some incentives from a 13-year long therapeutic follow-up of hypertension in a group of 54 middle-aged men suffering from essential hypertension. From a control group of 38 men they differed as regards blood pressure (174.2 +/- 13.2/112.9 +/- 7.0 mm Hg vs. 126.4 +/- 13.9/77.6 +/- 7.4 mm Hg, p < 0.001), body build (BMI = 28.0 +/- 3.4 kg/m2 vs 23.9 +/- 2.5 kg/m2, p < 0.001), waist/hip ratio 0.98 +/- 0.04 vs 0.94 +/- 0.04, p < 0.05, as well as uric acid serum levels (413.7 +/- 111.0 mumol vs. 362.6 +/- 65.9 mumol/l, p < 0.05) and HDL cholesterol (1.36 +/- 0.30 mmol/l vs. 1.51 +/- 0.48 mmol/l, p < 0.05). However, the fasting blood sugar levels did not differ (5.2 +/- 0.7 mmol/l vs 5.1 +/- 0.6 mmol/l). Although the index of insulin resistance was elevated (6.6 +/- 2.1 vs. 2.84 +/- 1.6, p < 0.01). The blood sugar level rose steadily and reached a level of 18.7% +/- 14.8% (p < 0.01). The increments of the blood sugar level correlated with changes in body weight (1.2% +/- 6.1% r = 0.535, p < 0.001), TAG (4.0% +/- 5.6% r = 0.332, p < 0.05) and the fasting baseline blood sugar levels (r = 0.551, p < 0.001). The mentioned variables contributed to the prediction of increments of the blood sugar level in multiple regression (determined coefficient R2 = 0.51). No relationship with the type of treatment was revealed. 11% of the patients developed during the investigation period symptoms of type 2 diabetes. The development of diabetes could be predicted on the basis of three baseline variables- the BMI, the index of insulin resistance and the basal blood sugar level (logistic regression, r = 0.790. CONCLUSIONS: Hypertension is a constituent of the metabolic syndrome, although the rise of the blood sugar does not directly correlate with manifestation of type 2 diabetes, it is a warning that insulin resistance can influence the effectiveness of provisions of the therapeutic regimen, and last not least, also the development of type 2 diabetes.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8729308
----K 1
----T [Prevention of increase of blood pressure and intracranial pressure during endotracheal intubation in neurosurgery: esmolol versus lidocaine]
----A OBJECTIVES: To compare the preventive effects of esmolol and lidocaine on the increase in mean arterial pressure (MAP) and intracranial pressure (ICP) during endotracheal intubation in neurosurgery. STUDY DESIGN: Comparative, randomised, double-blind study. PATIENTS: Twenty-two patients, physical status ASA I or II, undergoing neurosurgery, and randomised into two groups (esmolol group and lidocaine group). METHODS: After induction of anaesthesia with thiopentone, vecuronium, fentanyl and isoflurane, one group received iv esmolol 1.5 mg.kg-1 and the other iv lidocaine 1.5 mg.kg-1, 130 sec before endotracheal intubation. The MAP measured with a radial catheter, the ICP obtained with a lumbar subarachnoid catheter and the cerebral perfusion pressure (CPP, calculated from MAP and ICP) were assessed before induction of anaesthesia, before esmolol or lidocaine injection, and before intubation, during the maximal change in MAP, as well as 2 and 5 minutes after intubation. RESULTS: The time course of MAP, ICP and CCP were similar throughout the study in the two groups, with a significant decrease (P < 0.05) of the CPP from 92 +/- 12 to 62 +/- 8 mmHg after esmolol, and from 96 +/- 12 to 68 +/- 15 mmHg after lidocaine. Following intubation, CPP increased significantly (P < 0.05) to 99 +/- 23 mmHg after esmolol and to 99 +/- 17 mmHg after lidocaine. The ICP increased also significantly (P < 0.05) after intubation from 11 +/- 6 to 17 +/- 10 mmHg in the esmolol group, and from 10 +/- 6 to 16 +/- 9 mmHg in the lidocaine group. CONCLUSIONS: Esmolol or lidocaine as an iv bolus of 1.5 mg.kg-1 before laryngoscopy and intubation do not completely prevent the increase in MAP and ICP.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Anesthetics__Local_MeSH S_pharmacology_MeSH Anesthetics__Local_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Intracranial_Pressure_MeSH S_drug_effects_MeSH Intracranial_Pressure_drug_effects_MeSH P_Intubation__Intratracheal_MeSH S_adverse_effects_MeSH Intubation__Intratracheal_adverse_effects_MeSH M_Lidocaine_MeSH S_pharmacology_MeSH Lidocaine_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neurosurgery_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH 
****** 8763003
----K 1
----T [Prognostic factors after sustained ventricular fibrillation or tachycardia. A multivariate study apropos of 160 cases]
----A The authors analysed survival of 160 patients (121 men and 31 women; average age 57.2 +/- 12.5 years; follow-up 29 +/- 20 months) treated for malignant ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation, syncope with inducible ventricular tachycardia). The therapeutic evaluation was frequently invasive (145 patients underwent at least programmed ventricular stimulation, 108 patients underwent full endocavitary electrophysiological studies) and non-pharmacological therapy was widely used (defibrillator n = 44; antiarrhythmic surgery n = 28; ablative procedures n = 19; transplantation n = 7). The following underlying pathologies were observed: ischaemic heart disease n = 120; non-ischaemic left heart disease n = 19; right heart cardiac disease n = 4; and apparently normal hearts n = 17). The average ejection fraction was 40.5 +/- 15.5% and 29 patients were in the NYHA functional classes III or IV. Fifty-five patients had life-threatening arrhythmias whilst receiving amiodarone. At 2 years, the actuarial sudden death rate was 5.9 +/- 2.1% and the actuarial total cardiac mortality rate was 13.1 +/- 2.9%. Univariate analysis showed age, the presence of underlying cardiac disease, the presence of dilated cardiomyopathy, the absence of an invasive approach, the need for basal pacing in electrical cardioversion, the absence of betablocker therapy, a decreased left ventricular ejection fraction and a high NYHA functional class, to be predictive of sudden death. In multivariate analysis, age, the NYHA class for total cardiac mortality and the NYHA class for sudden death, were the only independent predictive factors. The authors conclude that in the era of invasive methods of evaluation and widespread use of non-pharmacological therapeutic methods, the symptomatology of cardiac failure assessed by the NYHA classification remains the most powerful independent prognostic factor after an episode of malignant ventricular arrhythmia.
----P Journal_Article Review Review__Tutorial 
----M M_Actuarial_Analysis_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Cardiac_Pacing__Artificial_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Tachycardia__Ventricular_MeSH S_complications_MeSH Tachycardia__Ventricular_complications_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Fibrillation_MeSH S_complications_MeSH Ventricular_Fibrillation_complications_MeSH S_mortality_MeSH Ventricular_Fibrillation_mortality_MeSH S_therapy_MeSH Ventricular_Fibrillation_therapy_MeSH M_Ventricular_Function__Left_MeSH 
****** 8732729
----K E
----T Cost-effective therapy for hypertension.
----A The costs of treating hypertension are out of control. The Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure and others recommend the use of diuretics and beta-blockers as first-line agents. Newer drugs such as calcium channel blockers, alpha-blockers, and angiotensin-converting-enzyme inhibitors have improved metabolic profiles, but have not been proved in long-term, randomized, controlled trials to reduce morbidity and mortality. Our General Medicine Clinic has gradually shifted toward prescribing the newer agents. We reviewed our drug use, evaluated the literature, and made recommendations in the form of guidelines. Clinicians' concerns included quality-of-life issues, sexual dysfunction, metabolic changes--lipids, potassium, insulin resistance--and others. These concerns were addressed, and a consensus was reached. Our goal is to streamline therapy, reduce costs, and provide proven effective medication.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cost_Control_MeSH M_Cost-Benefit_Analysis_MeSH M_Diabetes_Mellitus_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH S_economics_MeSH Diabetes_Mellitus_economics_MeSH M_Drug_Costs_MeSH P_Drug_Utilization_Review_MeSH S_economics_MeSH Drug_Utilization_Review_economics_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Michigan_MeSH M_Practice_Guidelines_MeSH M_Quality_of_Life_MeSH M_United_States_MeSH 
****** 8733214
----K E
----T A longitudinal study of factors predicting change in cognitive test scores over time, in an older hypertensive population.
----A This study aims to describe factors associated with cognitive decline among 2584 subjects, aged 65-74, who were followed up for 54 months in the Medical Research Council Elderly Hypertension Trial (1982-1989). The subjects completed a cognitive test, the Paired Associate Learning Test (PALT), five times over this period. Decline on the PALT was associated with advanced age, male sex, rural residence, depression and low intelligence. These effects were modified by gender and level of pre-morbid intelligence. Advanced age, rural residence and number of cigarettes smoked daily were only associated with PALT decline among women of below median intelligence. The association between depression and PALT decline was only apparent in women of below median intelligence and men of above median intelligence. While these findings are consistent with other research into cognitive decline, they differ in some ways from reported risk factors for dementia, suggesting aetiological separateness. That women were more vulnerable than men to the effects of age and smoking raises the question of the impact on cognition of accelerated atherosclerosis after the menopause.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amiloride_MeSH S_adverse_effects_MeSH Amiloride_adverse_effects_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cognition_Disorders_MeSH S_diagnosis_MeSH Cognition_Disorders_diagnosis_MeSH S_psychology_MeSH Cognition_Disorders_psychology_MeSH M_Dementia_MeSH S_diagnosis_MeSH Dementia_diagnosis_MeSH S_psychology_MeSH Dementia_psychology_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Neuropsychological_Tests_MeSH S_statistics_&_numerical_data_MeSH Neuropsychological_Tests_statistics_&_numerical_data_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH S_psychology_MeSH Smoking_psychology_MeSH 
****** 8733032
----K E
----T Does high salt intake cause hyperfiltration in patients with essential hypertension?
----A In animal models of salt-dependent hypertension, hyperfiltration is associated with a faster decline in renal function and there is evidence that in hypertensive man, increased creatinine clearance is a marker of early hypertensive nephropathy. We have studied the influence of salt intake on the glomerular filtration rate (GFR) (Creatinine Clearance) in 14 patients with mild hypertension. Each patient was studied in random order and according to a crossover design, at habitual salt intake, at high salt intake (ie habitual +50/100 mmol/day) and at low salt intake (habitual -50/100 mmol/day). Protein, calcium and potassium intake was fixed across the three study periods. The control group was formed by seven healthy subjects. High salt intake, caused a significant (P < 0.01) increase in 24 h mean arterial pressure (MAP) and the expected suppression in plasma renin activity (PRA) and in plasma aldosterone. Seven patients were classified as salt-sensitive. The GFR was significantly higher (P < 0.01) at high salt intake (125 +/- 10 ml/min) than at habitual (113 +/- 7 ml/min) and at low salt intake (97 +/- 6 ml/min). On aggregate urinary salt excretion was significantly related with the GFR (P < 0.01 by correlation analysis for repeated observations) and the slope of this relationship predicted that a 100 mmol/day increase in salt intake is associated with the 14.6 ml/min rise in the GFR. The relationship between GFR and 24 h urinary salt in salt sensitive patients did not differ from that in salt resistant patients. The GFR response to salt loading was largely independent of the renin-aldosterone system. No change in arterial pressure nor in GFR was observed in healthy subjects. At fixed protein intake, changes in salt intake in the physiological range are associated with important GFR variations in mild hypertensives. As long as hyperfiltration in mild hypertension is a predictor of renal function deterioration, high salt intake, independent of the effect of arterial pressure, could be a factor that contributes to nephronic obsolescence in patients with essential hypertension.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Electrolytes_MeSH S_blood_MeSH Electrolytes_blood_MeSH S_urine_MeSH Electrolytes_urine_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sodium__Dietary_MeSH S_administration_&_dosage_MeSH Sodium__Dietary_administration_&_dosage_MeSH S_adverse_effects_MeSH Sodium__Dietary_adverse_effects_MeSH S_metabolism_MeSH Sodium__Dietary_metabolism_MeSH 
****** 8733036
----K E
----T Effects of antihypertensive therapy on platelet cytosolic calcium responses to low density lipoprotein cholesterol.
----A This study examines the effects of antihypertensive therapy on platelet cytosolic calcium [Ca2+]i responses to low-density lipoprotein cholesterol (LDL) and vasopressin (AVP) in 15 patients (50-80 years) participating in the Hypertension Optimal Treatment International Study. All patients (diastolic blood pressure (DBP) > or = 100 mm Hg and < or = 115 mm Hg) were treated with the calcium antagonist felodipine (10 mg p.o.) with or without addition of enalapril (up to 20 mg daily as needed) to lower diastolic pressures to < 85 mm Hg. This antihypertensive therapy lowered DBP (104 +/- 0.8 to 78 +/- 1.6 mm Hg, P < 0.0001), but had no effect on basal [Ca2+]i or AVP-stimulated [Ca2+]i responses. Basal platelet [Ca2+]i following antihypertensive therapy (49 +/- 3.4 ng/ml) were not different from those prior to therapy (52 +/- 4.7 ng/ml). Additionally, [Ca2+]i responses to AVP following therapy (554 +/- 74 units) were not different from those prior to treatment (595 +/- 49 units). Following antihypertensive therapy, [Ca2+]i responses to 200 micrograms/ml of LDL were decreased fourfold (P < 0.05). These results suggest that antihypertensive therapy with a calcium channel blocker may potentially impact the atherogenic process by reducing the platelet [Ca2+]i rise, and potentially the aggregatory response, to LDL.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Blood_Platelets_MeSH S_drug_effects_MeSH Blood_Platelets_drug_effects_MeSH S_metabolism_MeSH Blood_Platelets_metabolism_MeSH M_Calcium_MeSH S_blood_MeSH Calcium_blood_MeSH M_Cytosol_MeSH S_drug_effects_MeSH Cytosol_drug_effects_MeSH S_metabolism_MeSH Cytosol_metabolism_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_pharmacology_MeSH Lipoproteins__LDL_Cholesterol_pharmacology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8733040
----K E
----T Decreased blood viscosity and serum levels of erythropoietin after anti-hypertensive treatment with amlodipine or metoprolol: results of a cross-over study.
----A The increased viscosity of blood of hypertensive patients can be assumed to be a risk factor for the development of cardiovascular diseases. The aim of the present study was to elucidate whether anti-hypertensive treatment has any impact on blood rheology. Twenty patients with previously untreated hypertension who consecutively attended our outpatient hypertension clinic were included in this prospective, open, cross-over study. The patients were randomly selected to treatment with amlodipine or metoprolol. The anti-hypertensive therapy was switched after 4 months. Haemorheological and haemodynamic variables were measured with rotational viscometry and impedance cardiography, respectively. Fifteen and 16 patients could be evaluated after amlodipine or metoprolol treatment respectively. The mean blood pressure (BP) decreased from 159 +/- 22/105 +/- 7 to 139 +/- 21/91 +/- 6 mm Hg on amlodipine and from 162 +/- 22/104 +/- 5 to 145 +/- 24/90 +/- 8 mm Hg on metoprolol therapy. After amlodipine treatment, the total peripheral resistance index decreased whereas metoprolol treatment was accompanied by a decrease in the cardiac index. Decreases in whole blood viscosity, haematocrit and serum erythropoietin were found after amlodipine as well as metoprolol treatment. After amlodipine the plasma viscosity decreased and the erythrocyte deformability increased in the majority of patients. Plasma fibrinogen decreased after metoprolol treatment. Despite the differences in haemodynamic mechanisms underlying the decrease in BP, amlodipine and metoprolol exert beneficial effects on blood viscosity. Haemodilution and a decrease in serum erythropoietin may be factors underlying this decrease in blood viscosity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Blood_Cell_Count_MeSH S_drug_effects_MeSH Blood_Cell_Count_drug_effects_MeSH M_Blood_Chemical_Analysis_MeSH M_Blood_Viscosity_MeSH S_drug_effects_MeSH Blood_Viscosity_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Erythropoietin_MeSH S_blood_MeSH Erythropoietin_blood_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 8701900
----K E
----T Effects of beta-blockade with bisoprolol on heart rate variability in advanced heart failure: analysis of scatterplots of R-R intervals at selected heart rates.
----A The effect of beta-blockade on heart-rate variability was assessed at different heart rates in 52 patients with heart failure included in the randomized, placebo-controlled, Cardiac Insufficiency Bisoprolol Study (CIBIS). Scatterplots of R-R intervals display beat-to-beat variability by plotting each R-R interval against the preceding interval. Scatterplot dispersion at different R-R intervals provides a measure of beat-to-beat heart-rate variability at different heart rates. A 24-hour Holter tape was performed at baseline and after 2 months of treatment with bisoprolol or matched placebo. Geometric measurements of scatterplots were used to determine beat-to-beat dispersion for different R-R intervals. Bisoprolol and placebo groups were well matched at base-line. After 2 months of treatment, bisoprolol significantly increased beat-to-beat variability at the longest R-R intervals (p < 0.05); however, there was no change in scatterplot dispersion at the shortest R-R intervals. This suggests that beta-blockade increases parasympathetic or decreases sympathetic tone or both in heart failure patients only at the slowest heart rates.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Parasympathetic_Nervous_System_MeSH S_physiopathology_MeSH Parasympathetic_Nervous_System_physiopathology_MeSH M_Sympathetic_Nervous_System_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Sympatholytics_MeSH S_pharmacology_MeSH Sympatholytics_pharmacology_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH 
****** 8694665
----K E
----T Mortality risk and patterns of practice in 4606 acute care patients with congestive heart failure. The relative importance of age, sex, and medical therapy. Clinical Quality Improvement Network Investigators.
----A OBJECTIVE: To define contemporary patterns of risk and management among patients with congestive heart failure (CHF). METHODS: Cross-sectional records audit of 4606 hospitalized patients with CHF in 1992 and 1993. RESULTS: Overall medication use was diuretics, 82%; angiotensin-converting enzyme inhibitors, 53%; nitrates, 49%; digoxin, 46%; potassium, 40%; acetylsalicylic acid, 36%; calcium antagonists, 20%; warfarin, 17%; beta-blockers, 15%; and magnesium, 10%. Angiotensin-converting enzyme inhibitors were used less frequently in women and patients 70 years or older (P < .01). Total in-hospital mortality was 19%. The most common single cause of death was CHF progression, but noncardiac causes accounted for 30% of all deaths. Logistic regression analysis revealed age 70 years or older and the use of magnesium and nitrates to be associated with increased relative risk of in-hospital mortality; angiotensin-converting enzyme inhibitors, acetylsalicylic acid, calcium antagonists, beta-blockers, and warfarin were associated with decreased risk. CONCLUSIONS: Hospitalized patients with CHF have high all-cause mortality risk and less than optimal use of proven efficacious therapy, particularly among women and the elderly. Increased use of proven CHF therapy would likely decrease the risk of cardiac events, but the competing non-cardiac risks in this patient population are high and may not be affected by improved use of efficacious cardiac therapies.
----P Journal_Article Multicenter_Study 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Cross-Sectional_Studies_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Medical_Records_MeSH M_Retrospective_Studies_MeSH M_Risk_MeSH M_Risk_Factors_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8724551
----K E
----T Circadian patterns and triggers of sudden cardiac death.
----A Sudden cardiac death and other acute cardiovascular events have been demonstrated to occur in certain temporal patterns. The study of these patterns may yield important clues to the pathophysiology of the disease process. Most studies of the timing of onset of sudden cardiac death have revealed a prominent midmorning peak, thought to be related to a surge in catecholamines associated with arising and assuming the upright posture, that is blunted or eliminated by beta blockers. In addition, some studies have also shown a secondary peak in late afternoon or early evening of uncertain cause. The development of third-generation implantable cardioverter defibrillators with memory capabilities offers a unique opportunity to accurately define event chronology.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Circadian_Rhythm_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH M_Heart_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Human_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 8704533
----K E
----T Double blind randomised controlled trial of effect of metoprolol on myocardial ischaemia during endoscopic cholangiopancreatography.
----A OBJECTIVE--To evaluate the effect of metoprolol, a beta adrenergic blocking drug, on the occurrence of myocardial ischaemia during endoscopic cholangiopancreatography. DESIGN--Double blind, randomised, controlled trial. SETTING--University Hospital. SUBJECTS--38 (two groups of 19) patients scheduled for endoscopic cholangiopancreatography. INTERVENTIONS--Metoprolol 100 mg or placebo as premedication two hours before endoscopy. MAIN OUTCOME MEASURES--Heart rate, arterial oxygen saturation by continuous pulse oximetry, ST segment changes during endoscopic cholangiopancreatography (an ST segment deviation > 1 mV was defined as myocardial ischaemia), electrocardiogram monitored continuously with a Holter tape recorder. RESULTS--All patients had increased heart rate during endoscopy compared with rate before endoscopy, but heart rate during endoscopy was significantly lower in the metoprolol group compared with the placebo group (P = 0.0002). Twenty one patients (16 placebo, 5 metoprolol; P = 0.0008) developed tachycardia (heart rate > 100/min) during the procedure, and 11 patients (10 placebo, 1 metoprolol; P = 0.003) developed myocardial ischaemia. One patient in the placebo group had an acute inferolateral myocardial infarction. In the 10 other patients with signs of myocardial ischaemia during endoscopy the ST deviation disappeared when the endoscope was retracted. In all patients myocardial ischaemia was related to increases in heart rate, and 10 of the 11 patients had tachycardia coherent with myocardial ischaemia. CONCLUSIONS--Metoprolol prevented myocardial ischaemia during endoscopic cholangiopancreatography, probably through lowering the heart rate. Thus, tachycardia seems to be a key pathogenic factor in the development of myocardial ischaemia during endoscopy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH P_Cholangiopancreatography__Endoscopic_Retrograde_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Oximetry_MeSH M_Oxygen_MeSH S_blood_MeSH Oxygen_blood_MeSH M_Premedication_MeSH M_Tachycardia_MeSH S_prevention_&_control_MeSH Tachycardia_prevention_&_control_MeSH 
****** 8694086
----K 3
----T A six-week dose-response study of the ocular hypotensive effect of dorzolamide with a one-year extension. Dorzolamide Dose-Response Study Group.
----A PURPOSE: To investigate the efficacy and dose-response relationship of three concentrations (0.2%, 0.7%, and 2.0%) of dorzolamide hydrochloride in lowering elevated intraocular pressure (IOP) in patients during a six-week period and to evaluate the efficacy of 0.7% and 2.0% dorzolamide administered for an additional year. METHODS: This prospective, double-masked, randomized, placebo-controlled, multinational study enrolled 333 adults with open-angle glaucoma or ocular hypertension. During the six-week dose-response phase, patients were randomized to thrice-daily dosing of four treatments: 0.2%, 0.7%, or 2.0% dorzolamide or placebo (vehicle of dorzolamide). During a one-year extension, patients received 0.7% or 2.0% dorzolamide, and, if needed, 0.5% timolol twice daily for elevated IOP. RESULTS: In the dose-response phase, mean percent reduction of IOP (peak) was 16% to 18% for 2.0% and 0.7% dorzolamide and 4% to 7% for the placebo group, for a net reduction of IOP by dorzolamide of 11% to 14%. The 0.2% concentration of dorzolamide was not sufficiently active for further consideration. During the extension, dorzolamide maintained an adequate reduction of IOP in 55% (174 of 316) of patients. Throughout the study, the reduction in IOP was numerically greater for patients receiving 2.0% vs 0.7% dorzolamide. After 12 months of receiving dorzolamide, 20% to 28% of total carbonic anhydrase activity was observed. CONCLUSIONS: Topical dorzolamide used three times daily in concentrations of 0.7% or 2.0% lowered IOP and was generally well tolerated as monotherapy or in combination with 0.5% timolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_administration_&_dosage_MeSH Carbonic_Anhydrase_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH 
****** 8694728
----K 3
----T A 90-day study of the efficacy and side effects of 0.25% and 0.5% apraclonidine vs 0.5% timolol. Apraclonidine Primary Therapy Study Group.
----A OBJECTIVE: To compare long-term intraocular pressure (IOP)-lowering efficacy of 0.25% and 0.5% apraclonidine hydrochloride with 0.5% timolol maleate. DESIGN: Multicenter, randomized, double-masked trial. Adult patients of either sex diagnosed as having open-angle glaucoma or ocular hypertension were enrolled following appropriate washout from all ocular hypotensive medications. Morning IOPs of 22 to 35 mm Hg were required for entry. Patients received 0.25% or 0.5% apraclonidine 3 times a day or 0.5% timolol twice a day for 90 days. Intraocular pressure was measured at 8 AM (before morning dosing) and at 4 PM (8 hours after dosing) on days 1, 30, and 90, and only at 8 AM on day 14. RESULTS: All 3 medications significantly reduced IOP from baseline at all observation times (P < .001): 0.5% apraclonidine reduced IOP more than 0.25% apraclonidine; no significant difference was observed between 0.5% apraclonidine and 0.5% timolol 8 hours after dosing on days 1, 30, and 90; and a significant difference (P < .05) in favour of 0.5% timolol over 0.25% apraclonidine was observed 8 hours after dosing on day 30. At all morning visits following evening dosing, 0.5% timolol significantly reduced IOP more than both concentrations of apraclonidine. CONCLUSIONS: Both 0.25% and 0.5% apraclonidine significantly reduce IOP when used as primary ocular hypotensive medication. Although 0.25% and 0.5% apraclonidine reduce IOP to a similar degree as 0.5% timolol 8 hours after morning dosing, neither concentration is as effective for reducing morning IOP after evening dosing.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Clonidine_MeSH S_administration_&_dosage_MeSH Clonidine_administration_&_dosage_MeSH S_adverse_effects_MeSH Clonidine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Clonidine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 8707127
----K E
----T Sclerotherapy versus sclerotherapy and propranolol in the prevention of rebleeding from oesophageal varices: a randomised study.
----A BACKGROUND--This trial was carried out to assess the value of propranolol in the prevention of recurrent variceal bleeding when combined with longterm endoscopic sclerotherapy. PATIENTS AND METHODS--Two hundred patients (161 male, 39 female, age range 20-68 years) with portal hypertension resulting mainly from schistosomal periportal fibrosis or posthepatitic cirrhosis presenting with their first episode of haematemesis or melena, or both were included. This was confirmed endoscopically to result from ruptured oesophageal varices. After initial control of bleeding, patients were randomised into two groups: group 1 treated with endoscopic sclerotherapy alone and group 2 treated with sclerotherapy plus propranolol. They were followed up for two years. RESULTS--Group (2) had a lower rebleeding rate (14.3% v 38.6% in group 1), lower variceal recurrence after obliteration (17% v 34% in group 1), longer period between variceal obliteration and recurrence (36 weeks v 21 weeks in group 1); but no change in mortality (12% in both groups). CONCLUSIONS--Patients treated with sclerotherapy should be given propranolol for longterm management.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH 
****** 8738729
----K E
----T Propranolol plus molsidomine vs propranolol alone in the treatment of portal hypertension in patients with cirrhosis.
----A BACKGROUND/AIMS: Effective protection from the risk of variceal bleeding is achieved when the hepatic venous pressure gradient is reduced to 12 mmHg or at least by 20% of baseline values. Such a marked decrease is rarely achieved with propranolol, and new agents or combinations of them are now being explored. The present randomized study investigated whether chronic treatment with the combination of propranolol plus molsidomine, a preferential venous dialator that reduces hepatic venous pressure gradient and does not cause pharmacological tolerance, achieves greater reduction in hepatic venous pressure gradient than propranolol alone. METHODS: A hemodynamic study was performed in 34 patients with cirrhosis with portal hypertension in baseline conditions and after 3 months of chronic oral treatment with propranolol alone (n = 19) or propranolol plus molsidomine (n = 15). RESULTS: Propranolol produced a significant reduction in hepatic venous pressure gradient (-16%, p < 0.01). Propranolol plus molsidomine also caused a slight but significant decrease in hepatic venous pressure gradient (-9%, p < 0.05). Hepatic blood flow and the hepatic and intrinsic clearance of indocyanine green were significantly reduced by propranolol. The combined administration of propranolol+molsidomine significantly reduced hepatic blood flow but not hepatic and intrinsic clearance of indocyanine green. Both treatment groups produced similar reduction in azygos blood flow, heart rate and cardiac output. However, contrary to propranolol alone, propranolol plus molsidomine did not increase cardiopulmonary pressures. CONCLUSIONS: The current study shows that although the combined administration of propranolol plus molsidomine prevents some of the adverse effects of propranolol on liver function and cardiopulmonary pressures, it does not achieve a greater reduction in hepatic venous pressure gradient than propranolol alone and therefore, does not support the use of this combined therapy for the pharmacological treatment of portal hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Liver_MeSH S_drug_effects_MeSH Liver_drug_effects_MeSH S_physiopathology_MeSH Liver_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Molsidomine_MeSH S_therapeutic_use_MeSH Molsidomine_therapeutic_use_MeSH M_Portal_System_MeSH S_drug_effects_MeSH Portal_System_drug_effects_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8726094
----K E
----T Effects of age on aortic blood velocity at rest and during exercise in patients with coronary artery disease.
----A The effect of age on aortic blood velocity has been studied in 100 patients with angiographically-documented coronary artery disease, 500 of whom were receiving beta-adrenergic blocking agents. Using continuous-wave Doppler ultrasound, the aortic blood velocity signals, both at rest and at maximal-tolerated supine exercise, were obtained. From the Doppler signals the peak velocity (Vp), stroke distance (Sd; the velocity-time integral) and minute distance (Md = Sd x heart rate) were calculated. The measurements were repeated 6 weeks after coronary artery bypass grafting (CABG), performed in 30 patients. No relationship with age (p < 0.01) was found for any of the indices, either at rest or during exercise, except for the resting Md in patients not on beta-blockers, (p < 0.02). No difference in the slope of the relationship with age was found between patients on or not on beta-blockers, except for the resting Md (p < 0.02). Following CABG, a significant age relationship with Vp, Sd and Md was restored, during both resting and exercise, suggesting improvement of systolic left ventricular function following myocardial revascularization. In conclusion, the normal age relationships of the derivatives of aortic blood velocity Doppler ultrasound signals were not seen in patients with coronary artery disease, irrespective of whether they were on or off beta-blockers. The relationship changed following myocardial revascularization, suggesting their dependence on systolic left ventricular function.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH M_Aorta_MeSH S_ultrasonography_MeSH Aorta_ultrasonography_MeSH M_Blood_Flow_Velocity_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Rest_MeSH S_physiology_MeSH Rest_physiology_MeSH M_Ultrasonography__Doppler_MeSH 
****** 8750168
----K E
----T Weakness of mucosal barrier in portal hypertensive gastropathy of alcoholic cirrhosis. Effects of propranolol and enprostil.
----A BACKGROUND/AIMS: It has been suggested that the vulnerability of gastric mucosa is increased in patients with cirrhosis as a result of a PGE2 deficiency. Therefore, we evaluated whether PGE2 mucosal generation, and gastric potential difference - a reflection of the gastric mucosal barrier - were correlated to endoscopic features and whether these alterations could be alleviated. METHODS: The potential difference was measured before (basal) and after a stimulation test by aspirin. The serum levels of gastrin and glucagon were also determined. Finally, the effects of a 1-week administration of propranolol or enprostil were tested on potential difference. The endoscopic grade of portal hypertensive gastropathy was assessed according to McCormack et al. The results are presented respectively for controls, patients with mild gastropathy, and patients with severe gastropathy. Comparisons were made using variance or covariance analysis after adjustment with age. RESULTS: Basal potential difference was significantly different between the three groups: -30.6, -28.8, -24.9 mV, p <0.05, respectively. The effects of aspirin administration on potential difference parameters were significantly different between the three groups (irritability index: 35 +/- 25, 92 +/- 98, 114 +/- 74 mV2.min, p <0.05, respectively) when non-responders to aspirin were excluded. PGE2 mucosal generation was significantly increased in both the antrum (9.8, 19.5, 19.7 ng/mg proteins, p<0.05, respectively) and in the corpus (8.1, 14.0, 20.2 ng/mg proteins, p<0.05, respectively). PGE2 generation was not related to potential difference. Glucagon serum levels were related to the grade of gastropathy. A 1-week administration of 160 mg/d long-acting propranolol, 35 micro g/d enprostil or placebo did not significantly modify basal potential difference. CONCLUSIONS: Portal hypertensive gastropathy is characterized by a decreased potential difference proportional to the endoscopic severity. The gastric mucosa of patients with cirrhosis seems to be more susceptible to aspirin than that of healthy subjects. It appears that the role of PGE2 is controversial in portal hypertensive gastropathy. Propranolol and enprostil do not improve this decreased potential difference.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Anti-Ulcer_Agents_MeSH S_pharmacology_MeSH Anti-Ulcer_Agents_pharmacology_MeSH M_Aspirin_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH M_Dinoprostone_MeSH S_physiology_MeSH Dinoprostone_physiology_MeSH M_Enprostil_MeSH S_pharmacology_MeSH Enprostil_pharmacology_MeSH M_Female_MeSH M_Gastric_Mucosa_MeSH S_drug_effects_MeSH Gastric_Mucosa_drug_effects_MeSH S_physiopathology_MeSH Gastric_Mucosa_physiopathology_MeSH M_Gastrins_MeSH S_blood_MeSH Gastrins_blood_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Liver_Cirrhosis__Alcoholic_MeSH S_physiopathology_MeSH Liver_Cirrhosis__Alcoholic_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Stomach_Diseases_MeSH S_physiopathology_MeSH Stomach_Diseases_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8750405
----K E
----T Effects of lisinopril and bisoprolol on lipoprotein metabolism in patients with mild-to-moderate essential hypertension.
----A The short- and long-term effects of the angiotensin-converting enzyme inhibitor lisinopril and the cardioselective beta-blocker bisoprolol on serum lipids, lipoproteins, apolipoproteins, and lipoprotein(a) (Lp[a]) levels were investigated in patients with mild-to-moderate essential hypertension. Fifty-two patients completed the 12-month, randomized, multicenter trial. After administration of lisinopril (10 to 20 mg/d; n = 24) and bisoprolol (2.5 to 10 mg/d; n = 28), systolic and diastolic blood pressures decreased significantly (P < 0.01) from baseline in both groups at 3, 6, and 12 months. The reduction in diastolic blood pressure was significantly (P < 0.05) greater in the lisinopril group than in the bisoprolol group only at 6 months. Heart rates dropped significantly in the bisoprolol group but not in the lisinopril group. No significant changes in lipids, lipoproteins, apolipoproteins, or Lp(a) levels were observed with either drug at 3, 6, or 12 months, and no significant differences were noted between the two drugs for these parameters. We conclude that lisinopril and bisoprolol are effective as antihypertensive drugs without adverse metabolic effects after short- and long-term treatment in patients with mild-to-moderate essential hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_blood_MeSH Angiotensin-Converting_Enzyme_Inhibitors_blood_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Bisoprolol_MeSH S_blood_MeSH Bisoprolol_blood_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Blood_Pressure_MeSH M_Body_Weight_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Lipoproteins_MeSH S_metabolism_MeSH Lipoproteins_metabolism_MeSH M_Lisinopril_MeSH S_blood_MeSH Lisinopril_blood_MeSH S_pharmacology_MeSH Lisinopril_pharmacology_MeSH M_Male_MeSH 
****** 8737100
----K E
----T The QRS score: a promising new exercise score for detecting coronary artery disease based on exercise-induced changes of Q-, R- and S-waves: a relationship with myocardial ischaemia.
----A BACKGROUND: Recently, a new exercise test criterion diagnosing coronary artery disease was proposed, based on a composite of changes in Q-, R- and S-waves: the QRS score. We compared this new criterion with conventional ST-segment depression and other compositions of Q-, R- and S-wave changes in patients and normals and related the QRS score to reversible thallium-201 scintigraphic defects and ST-segment depression as markers for ischaemia. The influence of beta-blockade on the QRS score was also studied. METHODS: The study population consisted of 155 persons with 53 normals (group I) and 102 patients with documented coronary artery disease (group II). Another 20 patients (group III) with proven coronary artery disease and a positive exercise test by ST-segment criteria were studied for the influence of beta-blockade on the QRS score. A symptom-limited exercise protocol according to the modified Bruce protocol was used. For the QRS score, Q-, R- and S-wave amplitudes which could be recovered immediately were subtracted from pretest values: delta Q, delta R, delta S respectively. The score was calculated by the formula: (delta R - delta Q - delta S)AVF + (delta R - delta Q - delta S)V5. RESULTS: Using a cut-off point of > 5 as normal, the QRS score resulted in a sensitivity of 88.2%, a specificity of 84.8% and a predictive accuracy of 87.1%. For ST-segment depression these values were 54.9%, 83% and 64.5% respectively (P < 0.001 compared to the QRS score). Predictive accuracies of changes in Q-, R- and S-waves in leads AVF and V5 separately, combinations of changes and combining the two leads, resulted-with the exception of solitary S-wave changes-in predictive accuracies higher than those of ST-segment depression, but all were lower than the QRS score. We found a significant correlation between the QRS score, the summed ST-segment depression (P < 0.004) and the extent of reversible thallium-201 defects (P < 0.001). Applying Bayes' theorem, the combination of an abnormal QRS score and ST-segment depression resulted in the highest post-test risk for coronary artery disease and a normal QRS score without ST-segment depression in the lowest post-test risk. The QRS score and the maximal ST-segment depression changed significantly under the influence of beta-blockade (P < 0.02 and P < 0.001 respectively). CONCLUSION: Our data suggest that an abnormal QRS score reflects myocardial ischaemia. Furthermore, for the interpretation of the exercise test, the combined analysis of ST-segments and the QRS score is of value for the prediction of the presence or absence of coronary artery disease and its follow-up.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH P_Electrocardiography_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_radionuclide_imaging_MeSH Myocardial_Ischemia_radionuclide_imaging_MeSH M_Predictive_Value_of_Tests_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH M_Thallium_Radioisotopes_MeSH S_diagnostic_use_MeSH Thallium_Radioisotopes_diagnostic_use_MeSH 
****** 8737105
----K I
----T Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol. Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS).
----A Two hundred and ten patients with clinical evidence of heart failure, developing after an acute myocardial infarction, were randomized to treatment with the beta 1-receptor antagonist metoprolol 50-100 mg b.i.d. (n = 106) or the beta 1-receptor partial agonist xamoterol 100-200 mg b.i.d. (n = 104). Left ventricular systolic and diastolic function were assessed with echocardiography and transmitral Doppler cardiography before and after 3 and 12 months of double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indices of systolic function. The ratio between peak early and late mitral diastolic flow (E/A ratio) and isovolumic relaxation time were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-point septal separation (P < 0.05). A difference between the treatment groups was present both at 3 months (E-point septal separation 11.4 vs 13.0 mm, P < 0.01, fractional shortening 27.1 vs 25.2%, P < 0.05) and 12 months (E-point septal separation 11.1 vs 13.2 mm. P < 0.005, fractional shortening 26.9 vs 25.0%, P < 0.05). E/A ratio increased in the metoprolol group (P < 0.05) but not in the xamoterol group. At 3 months there was a significant difference (0.85 vs 0.67, P < 0.005) between the groups but not at 12 months. In comparison with the beta 1-receptor antagonist metoprolol, the beta 1-receptor partial agonist xamoterol impaired left ventricular systolic function in patients with clinical evidence of heart failure after an acute myocardial infarction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_etiology_MeSH Cardiac_Output__Low_etiology_MeSH S_ultrasonography_MeSH Cardiac_Output__Low_ultrasonography_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Xamoterol_MeSH S_therapeutic_use_MeSH Xamoterol_therapeutic_use_MeSH 
****** 8736459
----K 3
----T Medium-term effects of betaxolol monotherapy and combination therapy with nitrendipine on lipoprotein and apolipoprotein metabolism in patients with mild to moderate essential hypertension.
----A The objective of this study was to assess the medium-term effects of betaxolol, a long-acting, lipid-soluble, cardioselective, beta-adrenergic antagonist, alone and in combination with nitrendipine on blood pressure (BP) and metabolism of lipid, lipoprotein and apolipoprotein in patients with mild to moderate hypertension. Forty-seven patients (21 men, 26 women, average age 54 years) participated in an open controlled clinical trial. After a 4-week washout period, all of the patients received betaxolol monotherapy at a dose of 5-10 mg daily for 6 months (Phase I). From month 7 through month 12 (Phase II), half of the total patients (Group B, n = 23) with diastolic blood pressure (DBP) of 95 mm Hg or more at the end of Phase I were also given nitrendipine (10-20 mg, once daily), while the remaining patients (Group A, n = 24) continued to receive only betaxolol. Systolic blood pressure (SBP), DBP, and heart rate (HR) were monitored once monthly. Serum lipid profiles were measured at study entry and after 6 and 12 months of therapy. Betaxolol significantly reduced SBP, DBP, and HR in both groups during Phase I, and the reductions in SBP and DBP were markedly less in Group B than in Group A. During Phase II, the additional reduction of SBP and DBP to levels similar to those in Group A was achieved by betaxolol in combination with nitrendipine, and HR was slightly but significantly increased. Betaxolol monotherapy reduced serum levels of high density lipoprotein cholesterol (HDL-C) and increased levels of triglyceride, apolipoprotein (apo) C-II and apo C-III. Combination therapy with betaxolol and nitrendipine increased serum apo A-I but did not affect other lipid profiles. Our results indicate that betaxolol is an effective antihypertensive drug which has a preferable effect on HR and HDL profiles when combined with nitrendipine.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Apolipoproteins_MeSH S_metabolism_MeSH Apolipoproteins_metabolism_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Lipoproteins_MeSH S_metabolism_MeSH Lipoproteins_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrendipine_MeSH S_administration_&_dosage_MeSH Nitrendipine_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8737958
----K I
----T Permutation distribution estimation applied to the comparison of the profile of the activity of two antianginal drugs.
----A The comparison of the anti-ischemic activity of trimetazidine and propranolol was evaluated by multiple end points (clinical, exercise test, and ambulatory electrocardiogram [ECG] monitoring criteria) in 149 male patients with effort angina who received either trimetazidine 20 mg tid or propranolol 40 mg tid during a period of 3 months. The distribution of the standardized differences between the two treatments for each variable was obtained by a permutation method. The medians (estimation of the actual difference between the two treatments) and the 5, 25, 75 and 95% quantiles were represented on the same diagram for all end points. The pattern of the standardized distribution of the differences showed a similar activity of both drugs on symptoms and nitrates consumption, on exercise tolerance and increase in ischemic threshold at exercise, and on ischemia recorded at ambulatory ECG monitoring. Conversely, only propranolol decreased heart rate and rate pressure product at rest as well as at exercise, underlining the difference in the mode of action of the two drugs. This descriptive technique is an attractive method to evaluate the differences between drugs considering multiple criteria favouring the estimation of these differences together with their variability.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Comparative_Study_MeSH M_Data_Interpretation__Statistical_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Tolerance_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Trimetazidine_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8762212
----K E
----T Metabolic neutrality of combined verapamil-trandolapril treatment in contrast to beta-blocker-low-dose chlortalidone treatment in hypertensive type 2 diabetes.
----A OBJECTIVE: To investigate the metabolic, antihypertensive and albuminuria-modifying effects of a heart rate-modulating calcium antagonist-angiotensin converting enzyme inhibitor combination compared with those of a beta-blocker-low-dose diuretic combination in non-insulin-dependent diabetic hypertensives. DESIGN: A prospective randomized double-blind study. SUBJECTS AND METHODS: Twenty-four diabetics with diastolic blood pressure 90-115 mmHg without azotemia (plasma creatinine level < 150 mumol/l) were evaluated after 4 weeks receiving placebo and 12 weeks receiving treatment either with combined slow-release verapamil (retard formulation) and trandolapril (mean maintenance doses, 180 and 1.6 mg daily) or with atenolol and chlortalidone (71 and 18 mg daily). Insulin sensitivity (by the minimal model method of Bergman), additional metabolic variables, clinic blood pressure, ambulatory blood pressure profile and renal indices were assessed at the end of the placebo and active treatment phases. RESULTS: Compared with placebo, the two therapies produced similar decreases in mean supine clinic blood pressure [10 +/- 3 versus 11 +/- 3% (means +/- SEM)], upright clinic blood pressure (10 +/- 4 versus 11 +/- 4%) and ambulatory daytime blood pressure (9 +/- 2 versus 12 +/- 3%). However, although the verapamil-trandolapril combination was found to be metabolically neutral, the atenolol-chlortalidone combination aggravated insulin resistance [insulin sensitivity index, from (0.8 +/- 0.2) to (0.3 +/- 0.1) x 10(-4)/min per U per ml], increased the serum triglycerides level and decreased the high-density lipoprotein cholesterol and plasma potassium levels. Although both therapies tended to reduce 24 h albuminuria, this was significant for the verapamil-trandolapril treatment only. CONCLUSIONS: Because the effect of any antihypertensive drug, including diuretics and beta-blockers, on cardiovascular morbidity and on mortality in non-insulin-dependent diabetic patients is not known, rational treatment selection can presently be based only on surrogate end-points. Therefore, the triad of metabolic neutrality with antihypertensive and antiproteinuric efficacy supports combined verapamil-trandolapril as a potentially valuable therapy for hypertension accompanying diabetes mellitus.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Carbohydrates_MeSH S_metabolism_MeSH Carbohydrates_metabolism_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_metabolism_MeSH Diabetes_Mellitus__Type_II_metabolism_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Indoles_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH 
****** 8772622
----K E
----T Relationship between sodium-lithium countertransport and insulin sensitivity in mild hypertension.
----A OBJECTIVES: To study the relationship between insulin sensitivity and sodium-lithium countertransport (Na(+)-Li+ CT) in mild, essential hypertension, and to investigate the effect of metformin and metoprolol, respectively. DESIGN: A double-blind, triple cross-over, placebo-controlled study over a total period of 18 weeks. SETTING. A hypertension out-patient clinic and research laboratory at Sahlgrenska University Hospital. SUBJECTS: Seventeen non-obese men with mild essential -hypertension and 17 weight-matched, healthy controls. INTERVENTIONS: Metformin 850 mg b.i.d., metoprolol CR 100 mg once daily and placebo were given during 18 weeks. Each treatment period was 6 weeks. A euglycaemic clamp was performed and erythrocyte Na(+)-Li+ CT measured after each 6-week treatment period. MAIN OUTCOME MEASURES: Insulin sensitivity, erythrocyte Na(+)-Li+ CT, their interrelation, and the effect of metformin and metoprolol CR on both variables, respectively. RESULTS: The hypertensive men tended to have an elevated Na(+)-Li+ CT compared with the control subjects (0.34 +/- 0.03 versus 0.26 +/- 0.02 mmol L-1 h-1, P < 0.1). Glucose disposal rate was similar, but plasma insulin levels higher (P < 0.05) among the hypertensives than the controls. Na(+)-Li+ CT exhibited a positive relationship to BMI (r = 0.53, P = 0.03) and a negative correlation to glucose disposal rate (r = -0.66, P = 0.008) in the hypertensive subjects. In multiple regression analysis, Na(+)-Li+ CT showed a significant correlation to glucose disposal rate only. In the control subjects, there was no relation between glucose metabolism and Na(+)-Li+ CT. Neither metformin nor metoprolol influenced Na(+)-Li+ CT, glucose disposal rate or plasma insulin. CONCLUSION: Erythrocyte Na(+)-Li+ CT seemed to be closely related to insulin-glucose metabolism in mild hypertension, but was not influenced by metformin or metoprolol.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antiporters_MeSH S_metabolism_MeSH Antiporters_metabolism_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Erythrocytes_MeSH S_metabolism_MeSH Erythrocytes_metabolism_MeSH M_Glucose_Clamp_Technique_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Lithium_MeSH S_metabolism_MeSH Lithium_metabolism_MeSH M_Male_MeSH M_Metformin_MeSH S_therapeutic_use_MeSH Metformin_therapeutic_use_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Sodium_MeSH S_metabolism_MeSH Sodium_metabolism_MeSH 
****** 8772669
----K I
----T Effect of carvedilol on mortality and morbidity in patients with chronic heart failure.
----A 
----P News 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Morbidity_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH 
****** 8772687
----K E
----T Changes in early and late diastolic filling patterns induced by long-term adrenergic beta-blockade in patients with idiopathic dilated cardiomyopathy.
----A BACKGROUND: beta-Blockers have been used in patients with idiopathic dilated cardiomyopathy to improve cardiac performance and theoretically would be beneficial to diastolic function. However, there are few reports on changes in diastolic function during chronic pharmacological treatment of congestive heart failure. METHODS AND RESULTS: The present study was a substudy in the international Metoprolol in Dilated Cardiomyopathy Trial. Transmitral Doppler echocardiography was used to evaluate diastolic function in 77 patients randomly assigned to placebo (n = 37) or metoprolol (n = 40). The patients were treated for 12 months. Changes in Doppler flow variables in the metoprolol group implied a less restrictive filling pattern, expressed as an increase in E-wave deceleration time (placebo, 185 +/- 126 to 181 +/- 64 ms; metoprolol, 152 +/- 63 to 216 +/- 78 ms; P = .01, placebo versus metoprolol). Maximal increase in deceleration time had occurred by 3 months, whereas systolic recovery was achieved gradually and maximal effect was seen by 12 months of treatment. Although deceleration time was correlated to heart rate at baseline, changes in deceleration time were not significantly correlated to changes in heart rate during treatment. CONCLUSIONS: During the first 3 months of treatment, maximal effects on diastolic variables were reached, whereas the most prominent effect on systolic function was seen late in the study. It is suggested that effects on diastolic filling account for subsequent later myocardial systolic recovery. The E-wave deceleration time, which in recent studies has been shown to be a powerful predictor of survival, was significantly improved in the metoprolol-treated patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Cardiomyopathy__Congestive_ultrasonography_MeSH M_Diastole_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Heart_Catheterization_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH P_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH M_Technetium_MeSH S_diagnostic_use_MeSH Technetium_diagnostic_use_MeSH 
****** 8775936
----K E
----T Applying the results of large clinical trials in the management of acute myocardial infarction.
----A Mortality from acute myocardial infarction has declined in recent years, largely due to the widespread application of new pharmacologic and mechanical interventions that have been tested in large, prospective, randomized clinical trials. For practicing generalists, we review the key data from such trials that have shaped the current management of patients with acute myocardial infarction. We discuss the roles of thrombolytic therapy, coronary angioplasty, nitrates, beta- and calcium channel blockers, angiotensin-converting-enzyme inhibitors, magnesium, and antiarrhythmic and antithrombotic agents. In addition, we highlight critical unanswered questions in the management of this disorder.
----P Journal_Article Review Review__Tutorial 
----M M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH M_Clinical_Trials_MeSH M_Coronary_Artery_Bypass_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_surgery_MeSH Myocardial_Infarction_surgery_MeSH M_Patient_Selection_MeSH M_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH 
****** 8792950
----K E
----T Angiotensin II receptor antagonists: the prototype losartan.
----A OBJECTIVE: To describe a new class of antihypertensive agents, the angiotensin II receptor antagonists, with emphasis on the prototype losartan. Pharmacokinetic data and clinical trials are reviewed, as well as adverse reactions, drug interactions, and dosing guidelines. DATA SOURCES: A MEDLINE search of English-language literature published from 1966 through 1995 was performed. In addition, Merck and Co. provided bibliographic data on file for losartan. STUDY SELECTION: Emphasis was placed on clinical and pharmacokinetic studies in humans. Controlled, double-blind studies were evaluated to assess the efficacy and adverse effect profile of losartan. DATA SYNTHESIS: Losartan is a nonpeptide, competitive antagonist of the type I angiotensin II receptor. In comparative clinical trials, losartan appears to have antihypertensive efficacy similar to that of the angiotensin-converting enzyme (ACE) inhibitors. Losartan is well tolerated, with an adverse effect profile similar to that of placebo and a reduced incidence of cough versus that with ACE inhibitors. A combination product consisting of losartan 50 mg and hydrochlorothiazide 12.5 mg has also received approval for the treatment of hypertension. The combination product is not indicated for initial therapy, but is recommended for patients who do not respond adequately to losartan monotherapy. The angiotensin II receptor antagonists are also being investigated for beneficial effects in patients with ventricular hypertrophy, renal disease, and heart failure. CONCLUSIONS: Losartan, the first angiotensin II receptor antagonist to receive approval for use in the US, appears to be an effective new antihypertensive agent with an adverse effect profile similar to that of placebo. Losartan may be an alternative for patients who cannot tolerate ACE inhibitors. However, the effect of losartan on mortality remains to be evaluated. The role of the angiotensin II receptor antagonists in areas such as ventricular hypertrophy, renal function, and heart failure has yet to be determined.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin_II_MeSH S_metabolism_MeSH Angiotensin_II_metabolism_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_pharmacokinetics_MeSH Biphenyl_Compounds_pharmacokinetics_MeSH S_pharmacology_MeSH Biphenyl_Compounds_pharmacology_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Imidazoles_MeSH S_adverse_effects_MeSH Imidazoles_adverse_effects_MeSH S_pharmacokinetics_MeSH Imidazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Imidazoles_pharmacology_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_pharmacokinetics_MeSH Tetrazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Tetrazoles_pharmacology_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 8793161
----K E
----T Age and gender differences in left ventricular function among patients with stable angina and a matched control group. A report from the Angina Prognosis Study in Stockholm.
----A To assess left ventricular systolic and diastolic function, M-mode (n = 675) and transmitral Doppler echocardiography (n = 358) were performed in patients with stable angina pectoris and compared with 50 matched healthy controls. Left ventricular fractional shortening (FS) was significantly lower in male than in female patients (32 +/- 7 vs. 35 +/- 7%, p < 0.001). A history of heart failure was as frequent in men (6%) as in women (6%), but left ventricular systolic dysfunction was more frequent in men than in women (25 vs. 12%, p < 0.005). The ratio of early/late diastolic peak flow velocity (E/A ratio) was significantly lower, indicating diastolic dysfunction, in female patients with clinical heart failure than in those without (0.79 +/- 0.25 vs. 1.02 +/- 0.3, p < 0.05). No such difference was found in male patients. Inverse relationships were found between age and E/A ratio in both controls (r = -0.45, p < 0.001) and angina patients (r = -0.44, p < 0.001). Thus, despite similar frequency of clinical heart failure, left ventricular systolic dysfunction was more common in men than in women with stable angina.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_ultrasonography_MeSH Angina_Pectoris_ultrasonography_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_ultrasonography_MeSH Ventricular_Dysfunction__Left_ultrasonography_MeSH M_Ventricular_Function__Left_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 8794822
----K E
----T Effects of losartan on insulin sensitivity in hypertensive subjects.
----A Losartan, the first specific and orally available angiotensin II receptor antagonist, is a potent antihypertensive drug with a low incidence of side effects in humans. However, the effects of losartan on insulin sensitivity and glucose metabolism have not been investigated in detail. Therefore, we carried out a randomized, double-blind study to compare the effects of losartan (50 mg QD) and metoprolol (95 mg QD) on insulin sensitivity, insulin secretion, glucose tolerance, and lipids and lipoproteins in 20 hyperinsulinemic subjects with essential hypertension. The fall in blood pressure was greater with losartan than with metoprolol. Insulin sensitivity evaluated by the euglycemic clamp technique did not change in either group after 12 weeks of treatment. Similarly, glucose oxidation (losartan: 17.0 +/- 0.9 versus 16.9 +/- 1.0 mumol/kg per minute [before versus after, P = NS]; metoprolol: 17.9 +/- 1.3 versus 16.8 +/- 1.6 [P = NS]) and nonoxidation (losartan: 22.3 +/- 4.0 versus 23.5 +/- 3.4 mumol/kg per minute [P = NS]; metoprolol: 23.3 +/- 3.2 versus 25.6 +/- 4.7 [P = NS]) remained unchanged during the last 30 minutes of the 3-hour euglycemic clamp. Losartan and metoprolol did not have any significant adverse effects on insulin secretion, glucose tolerance, or lipids and lipoproteins. In conclusion, losartan is metabolically neutral, without any significant adverse effect on glucose and lipid metabolism.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Fatty_Acids__Nonesterified_MeSH S_blood_MeSH Fatty_Acids__Nonesterified_blood_MeSH M_Female_MeSH M_Glucose_Clamp_Technique_MeSH M_Glucose_Tolerance_Test_MeSH M_Human_MeSH M_Hyperglycemia_MeSH S_blood_MeSH Hyperglycemia_blood_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Imidazoles_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH P_Insulin_Resistance_MeSH M_Lactic_Acid_MeSH S_blood_MeSH Lactic_Acid_blood_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Losartan_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 8797135
----K E
----T Effects of ramipril and enalapril on cerebral blood flow in elderly patients with asymptomatic carotid artery occlusive disease.
----A We wished to determine in asymptomatic hypertensive patients with > or = 70% stenosis of an internal carotid artery the change in regional cerebral blood flow (rCBF) produced by ramipril and enalapril and to evaluate the influence of age on drug-induced changes in rCBF. In a prospective, randomized, single-blind, placebo-controlled investigation, using the 133Xenon inhalation technique, we assessed baseline rCBF in 15 patients (9 men and 6 women aged 60-79 years) after a 24-h antihypertensive drug-free period. All patients then received a single 5-mg oral dose of ramipril, enalapril, or placebo. rCBF was reassessed 2 h postdose. There was no significant change in the median rCBF in any of the three treatment groups. Neither did we observe any lateralization of BF to any specific cerebral region in any of the three groups. There were no observed or patient-reported adverse events (AE). Single 5-mg oral doses of either ramipril or enalapril did not decrease CBF significantly in asymptomatic hypertensive patients with > or = 70% stenosis of an internal carotid artery and are probably safe starting doses in such patients. In addition, this effect was not modified by age.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carotid_Artery__Internal_MeSH M_Carotid_Stenosis_MeSH S_drug_therapy_MeSH Carotid_Stenosis_drug_therapy_MeSH S_physiopathology_MeSH Carotid_Stenosis_physiopathology_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8798100
----K E
----T Medium-term effects of beta-blockade on left ventricular mechanics: a double-blind, placebo-controlled comparison of nebivolol and atenolol in patients with ischemic left ventricular dysfunction.
----A The aim of this study was to compare the effects on left ventricular function and exercise tolerance of a selective beta-antagonist (atenolol) with those of another selective beta 1-antagonist with vasodilator properties (nebivolol) in patients with ischemic left ventricular dysfunction but no overt congestive heart failure. Beta blockers are widely used in ischemic heart disease, but their effects on left ventricular mechanics and exercise tolerance are poorly defined in the subgroup of patients with significant systolic dysfunction but without clinical evidence of ischemia or congestive heart failure. Angiographic and symptom-limited exercise data were obtained at baseline and after an 8-10-week double-blind treatment with placebo (n = 10), 50 mg atenolol daily (n = 10), or 2.5 mg (n = 10) or 5 mg (n = 10) nebivolol daily. When compared to placebo, both atenolol and nebivolol reduced resting heart rate and improved left ventricular ejection fraction (from 33.9 to 39.2% with atenolol and from 36.5 to 40.8% with nebivolol, both P < .05) while lowering mean systolic wall stress. Only nebivolol, however, produced a parallel downward shift of the pressure-volume relationship during early diastolic filling and improved the early peak filling rate when compared to placebo (+ 10%, P < .05). When compared to baseline, maximal exercise duration increased by 7 and 13 seconds with placebo and atenolol, respectively (both NS vs baseline), and increased by 44 seconds with nebivolol (P = .0077 vs baseline). Both atenolol and nebivolol decreased maximal exercise heart rate; the reduction was more pronounced with atenolol. Prolonged beta 1-adrenoceptor blockade leads to a significant increase in left ventricular ejection fraction in patients with ischemic left ventricular dysfunction. The dissociation between the changes in resting left ventricular function and the changes in exercise duration suggests that in this clinical setting, the changes in systolic function may have less impact on functional capacity than an improvement in diastolic distensibility during the rapid filling phase.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 8984131
----K E
----T ACE inhibitor ramipril is more effective than the beta-blocker atenolol in reducing left ventricular mass in hypertension. Results of the RACE (ramipril cardioprotective evaluation) study on behalf of the RACE study group.
----A OBJECTIVES: To compare the effect of the angiotensin converting enzyme (ACE) inhibitor ramipril with that of the beta-blocker atenolol on reversal of left ventricular hypertrophy, on blood pressure and on other echocardiographic parameters. DESIGN: The study was conducted in accord with the PROBE (prospective randomized open blinded endpoint) design. Randomized treatment either with ramipril or with atenolol was continued for 6 months, and echocardiograms were recorded before and after 3 and 6 months of treatment. The echo tracings were blindly evaluated in a single reading centre. METHODS: M-mode, two-dimensional guided echocardiography was used to measure left ventricular wall thicknesses and dimensions, from which left ventricular mass was calculated, according to the Penn convention. RESULTS: Of 193 patients at 16 centres, 111 had echocardiograms that could be quantitatively evaluated. The primary analysis of the study was performed using data from those patients. In addition, echocardiograms of 88 patients were analysed on an 'according to protocol' basis (patients with preset values of left ventricular mass). Systolic and diastolic blood pressures were significantly reduced both by ramipril and by atenolol without any significant difference between the two drug treatments. The heart rate was significantly reduced by atenolol only. Both the 'primary' and the 'according to protocol' analyses showed that the left ventricular mass was significantly reduced by ramipril only. Comparison between treatments according to a multivariate analysis demonstrated a significantly greater reduction in left ventricular mass during ramipril than during atenolol treatment. CONCLUSIONS: The present study is the first of suitably large size in which a direct comparison of the effects of an ACE inhibitor and a beta-blocker on echocardiographic left ventricular mass has been performed. It has demonstrated that ramipril is more effective than atenolol in reversing left ventricular hypertrophy in essential hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH P_Echocardiography_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Ramipril_MeSH S_adverse_effects_MeSH Ramipril_adverse_effects_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Systole_MeSH M_Ventricular_Function__Left_MeSH 
****** 8808164
----K E
----T Calcium antagonists during and after myocardial infarction.
----A Calcium antagonists, or calcium channel entry blockers, have been advocated as cardioprotective agents in acute myocardial infarction (AMI) on the basis of animal experiments, which show that they will reduce the harmful effects of the calcium overload which follows ischaemia, particularly during reperfusion, and also that they will reduce coronary artery spasm. Unfortunately, these promising actions have not translated into clear mortality data. An overview of the large amount of data from properly randomised controlled clinical trials shows clear differences between the dihydropyridine class of calcium antagonists such as nifedipine, and the non-dihydropyridines verapamil and diltiazem. Most of the data with the former group derive from trials with short-acting formulations of nifedipine (TRENT, HINT, SPRINT-I and -II). Overall, none of these trials showed significant benefit in either AMI or post-MI prophylaxis. There was a trend for harm, with HINT stopped early because of excess reinfarction with nifedipine, compared with metoprolol. In contrast, and when taken together, the DAVIT-I and DAVIT-II studies with verapamil show significant reductions in sudden death, reinfarction and total mortality. The greatest benefit occurred in those patients with relatively good left ventricular function. Similar but less significant trends were seen in studies with diltiazem. It is clear that calcium antagonists, unlike beta-blockers, cannot be treated as a similar class. It seems likely that the adverse effects of nifedipine are related to reflex sympathetic cardiac stimulation as a result of the predominantly vasodilator action of these dihydropyridine compounds. Data on newer dihydropyridines with fewer reflex effects are awaited. In the meantime it seems sensible to use proven agents such as beta-blockers or verapamil. These data on AMI and the months following have recently been paralleled by case control studies in hypertension, which similarly have suggested harm from the use of predominantly short acting formulations of nifedipine compared with beta-blockers and which led to a warning statement by the US National Heart, Lung, and Blood Institute on 1 September 1995.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Recurrence_MeSH 
****** 8927880
----K 1
----T [Comparative antihypertensive action of 20 mg delayed-action nifedipine with either 25 or 50 mg atenolol. A study on the treatment of patients with mild to moderately severe arterial hypertension]
----A In the present double-blind, randomized, placebo-controlled study 36 untreated patients (57.8 +/- 8.4 years) with mild to moderate hypertension were included. After a 14 days' placebo period they were treated with a combination of 20 mg retarded nifedipine and 25 or 50 mg atenolol for six weeks each. Group A started with 25 mg, group B with 50 mg atenolol. Casual sitting blood pressure was measured automatically every second week, routine laboratory parameters and side effects were evaluated at the end of placebo and the verum periods. The blood pressure of the two groups was comparable during placebo and was reduced by 31.6/14.7 mmHg in group A or 29.9/15.8 mmHg in group B (p < 0.001 vs. placebo) after six weeks. In the second treatment period with verum, blood pressure was not further reduced. Both combinations were equally efficient also in the female and the elder subgroups (> 60 years) who were characterized by higher systolic blood pressure. The response rates were 83% and 86% for the combination with 25 and 50 mg atenolol respectively. Heart rate was significantly reduced in all groups during 50 mg atenolol. Laboratory parameters were not altered by treatment. Frequency and severeness of side effects were equal in both groups. It is concluded that in patients with mild to moderate uncomplicated hypertension the combination of 20 mg retarded nifedipine with 25 mg atenolol is equally efficient to the combination with 50 mg atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH 
****** 8817135
----K E
----T Efficacy and safety of low-dose propranolol versus diltiazem in the prophylaxis of supraventricular tachyarrhythmia after coronary artery bypass grafting.
----A OBJECTIVE: Supraventricular tachyarrhythmias (SVT) complicate postoperative management after coronary bypass surgery in about 30% of all patients. Though a prophylactic treatment both with beta-adrenergic blocking agents and the calcium antagonist diltiazem has been used for the prevention of post-operative SVT, no study yet has performed a prospective comparison of the efficacy of these therapies. METHODS: To investigate the prophylactic effect of either a calcium antagonist (diltiazem, 0.1 mg/kg per h i.v.) or a beta-adrenergic blocking agent (propranolol, 10 mg every 6 h postoperatively), we randomized prospectively 103 consecutive patients into three groups, the third one serving as a control group. Anti-arrhythmic medication was started with the procedure and was continued until the 3rd postoperative day. RESULTS: Preoperative conditions were the same for the three groups concerning age, extent of coronary heart disease, ventricular function and heart-related medication. There were no differences in intraoperative parameters or postoperative enzyme patterns. Diltiazem was ineffective in preventing SVT, the incidence being exactly the same as in the control group (35%). Propranolol reduced the occurrence of SVT significantly (7%, P < 0.05). Furthermore, patients treated with diltiazem needed positive inotropic support more often in the first hours after surgery than patients of the control group (30% vs 5%, P < 0.01). CONCLUSIONS: The perioperative administration of low-dose propranolol is considered a safe and effective drug prophylaxis to avoid the occurrence of SVT after bypass surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Comparative_Study_MeSH P_Coronary_Artery_Bypass_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_surgery_MeSH Myocardial_Infarction_surgery_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Prospective_Studies_MeSH M_Tachycardia__Supraventricular_MeSH S_drug_therapy_MeSH Tachycardia__Supraventricular_drug_therapy_MeSH M_Treatment_Outcome_MeSH 
****** 8821421
----K E
----T Chronic-intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris--a pilot study.
----A Patients with coronary artery disease and severe angina pectoris refractory to conventional medical treatment (beta blockers, nitrates, calcium antagonists) and without the option for invasive revascularization procedures represent an increasing clinical problem. For these patients, chronic-intermittent urokinase therapy has been developed. Twenty patients received 500,000 IU urokinase as intravenous bolus injection 3 times a week over a period of 12 weeks. The average reduction in anginal symptoms in 19 patients was 74%, from 23.5 +/- 10.8 to 5.2 +/- 4.8 events/week (p < 0.001); 1 patient was excluded from further treatment because of an increase of > 66% in anginal events. Fibrinogen decreased by 34% from 370 +/- 57 to 244 +/- 44 mg/dl (p < 0.001), the rheological parameters plasma viscosity by 6.1% from 1.39 +/- 0.04 to 1.31 +/- 0.03 mPas (< 0.001), and red blood cell aggregation by 18% from 13.9 +/- 2.4 to 11.2 +/- 2.2 (p < 0.001). Exercise tolerance increased by 51%. Average ST-segment depression decreased from 0.16 +/- 0.10 to 0.12 +/- 0.09 (p < 0.01). After 12 weeks of follow-up, angina pectoris and fibrinogen levels were still significantly reduced compared with baseline values. Chronic-intermittent urokinase therapy represents an effective anti-ischemic and antianginal approach in patients with refractory angina pectoris and end-stage coronary artery disease. Improvement of rheological blood properties and thrombolytic effects are likely therapeutic mechanisms.
----P Journal_Article 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Blood_Viscosity_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Resistance_MeSH M_Exercise_Tolerance_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_metabolism_MeSH Fibrinogen_metabolism_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Plasminogen_Activators_MeSH S_administration_&_dosage_MeSH Plasminogen_Activators_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Urinary_Plasminogen_Activator_MeSH S_administration_&_dosage_MeSH Urinary_Plasminogen_Activator_administration_&_dosage_MeSH 
****** 8826572
----K E
----T Valproic acid: a migraine prophylaxis alternative.
----A While studies have noted possible benefits of valproate for migraine prophylaxis, most have small study samples (range 22-34 patients). The more recent, larger clinical trial confirms the effectiveness of valproate in the prevention of migraines. The available evidence suggests that valproic acid should provide another alternative to conventional migraine prophylaxis. However, it would still be beneficial to see other large studies conducted to determine valproate's place among the migraine prophylactic therapies currently available. The Food and Drug Administration recently approved divalproex sodium for the prevention of migraine headaches. The usual starting dosage is 250 mg bid, titrating to 1000 mg/d if necessary.
----P Journal_Article Review Review__Tutorial 
----M M_Anticonvulsants_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Treatment_Outcome_MeSH M_Valproic_Acid_MeSH S_adverse_effects_MeSH Valproic_Acid_adverse_effects_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH 
****** 8831060
----K E
----T Effects on salivary flow rate and composition of withdrawal of and re-exposure to the beta 1-selective antagonist metoprolol in a hypertensive patient population.
----A Secretion rates and composition of unstimulated and chewing-stimulated whole saliva and 3% citric acid stimulated parotid and submandibular-sublingual secretions were studied in 12 hypertensive patients during withdrawal of and re-exposure to antihypertensive pharmacotherapy. All the patients' blood pressures were well controlled by monotherapy with metoprolol, a beta 1-selective adrenoceptor antagonist. Blood pressure measurements and saliva sampling were performed at about 9:30 a.m., 2 h after intake of breakfast, on days 0 (medicated baseline), 7, 14, 28 (nonmedicated experimental values and nonmedicated baseline) and 35 (medicated experimental values). A significant increase in unstimulated whole saliva secretion rate was observed when metoprolol was withdrawn and a corresponding decrease when the drug was reintroduced. A positive correlation was found between diastolic blood pressure levels and chewing-stimulated whole saliva secretion rates. In unstimulated whole saliva and 3% citric acid stimulated submandibular-sublingual secretion, the output of total protein, amylase, potassium, calcium and phosphate was significantly increased during the withdrawal period and decreased when metoprolol was reintroduced. For chewing-stimulated whole saliva, the corresponding changes were restricted to output of total protein and amylase, while for citric acid stimulated parotid secretion, no changes in salivary composition were observed. Finally, in all secretions one or both of the ratios hexosamine/total protein and sialic acid/total protein were affected, indicating a possible effect of beta-adrenoceptor antagonists on salivary protein synthesis.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amylases_MeSH S_analysis_MeSH Amylases_analysis_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_MeSH S_analysis_MeSH Calcium_analysis_MeSH M_Citric_Acid_MeSH S_pharmacology_MeSH Citric_Acid_pharmacology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hexosamines_MeSH S_analysis_MeSH Hexosamines_analysis_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Mastication_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_N-Acetylneuraminic_Acid_MeSH S_analysis_MeSH N-Acetylneuraminic_Acid_analysis_MeSH M_Parotid_Gland_MeSH S_drug_effects_MeSH Parotid_Gland_drug_effects_MeSH S_secretion_MeSH Parotid_Gland_secretion_MeSH M_Phosphates_MeSH S_analysis_MeSH Phosphates_analysis_MeSH M_Potassium_MeSH S_analysis_MeSH Potassium_analysis_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__beta-1_antagonists_&_inhibitors_MeSH M_Saliva_MeSH S_chemistry_MeSH Saliva_chemistry_MeSH S_drug_effects_MeSH Saliva_drug_effects_MeSH S_secretion_MeSH Saliva_secretion_MeSH M_Salivary_Proteins_MeSH S_analysis_MeSH Salivary_Proteins_analysis_MeSH M_Secretory_Rate_MeSH S_drug_effects_MeSH Secretory_Rate_drug_effects_MeSH M_Sublingual_Gland_MeSH S_drug_effects_MeSH Sublingual_Gland_drug_effects_MeSH S_secretion_MeSH Sublingual_Gland_secretion_MeSH M_Submandibular_Gland_MeSH S_drug_effects_MeSH Submandibular_Gland_drug_effects_MeSH S_secretion_MeSH Submandibular_Gland_secretion_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8831181
----K I
----T Treatment of hypertension associated with stable angina pectoris: favourable interaction between new metoprolol formulation (OROS) and nifedipine.
----A This was a double-blind, within-patient, crossover study to evaluate the effects of a new formulation of metoprolol on blood pressure (BP) and myocardial ischemia. Twenty outpatients with mild to moderate essential arterial hypertension, chronic stable angina pectoris and positive exercise test, after a 2-week baseline placebo period, were randomized to receive long-acting metoprolol (OROS) 14/190 mg o.d., nifedipine SR 20 mg b.i.d. or their combination in a sequence of a 3 x 3 Latin square design. Two patients withdrew from the study (1 for adverse event during metoprolol and 1 for rise of BP during nifedipine). Nifedipine, metoprolol and their combination significantly reduced the weekly number of angina attacks and nitroglycerin consumption with respect to baseline. The total number of ischemic events (at 24-hour ECG monitoring) significantly decreased after each treatment with respect to baseline. Twenty-four hours mean systolic and diastolic BP were reduced by both nifedipine alone and metoprolol alone; the combination of the two drugs led to a further decrease in both systolic and diastolic BP. The duration of silent ischemic episodes was significantly reduced by nifedipine and combination but not by metoprolol. On the other hand 24 hours symptomatic attacks/patient were significantly reduced by beta-blocker and combination, but not by nifedipine. Metoprolol alone and administered with nifedipine caused a decrease, with respect to placebo baseline, in 24-hour mean heart rate (HR) and reduced the increase of HR and systolic BP at the onset of ST depression during symptomatic ischemic episodes. The effort time and time to ST = -1 mm at treadmill were significantly increased by treatment with nifedipine alone, with metoprolol alone and with their combination, but the combination was more effective than the individual therapies. ST depression at peak exercise was significantly reduced by each treatment. The slopes of correlations between the ST-segment variation and systolic BP, HR and rate-pressure product during exercise, significantly decreased after all treatments with respect to placebo baseline, more with the combination therapy than with nifedipine alone and metoprolol alone. In conclusion, based on our results the favourable interaction of metoprolol OROS and nifedipine given concomitantly, is likely to be due to a better control, respect to each individual therapy, of the pathogenetic mechanism of myocardia ischemia: BP and HR increases during exercise and during symptomatic ischemic episodes are controlled by the beta-blocker and coronary vasoconstriction during silent ischemia is prevented by the calcium-antagonist.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Synergism_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Regression_Analysis_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8834027
----K E
----T Measurement of variceal pressure with an endoscopic pressure sensitive gauge: validation and effect of propranolol therapy in chronic conditions.
----A AIM/METHODS: Variceal pressure was measured at endoscopy in 98 patients with a non-invasive, pressure-sensitive gauge technique. RESULTS: In nine patients undergoing sclerotherapy, the values obtained correlated closely with those determined by fine-needle puncture of the varices (r = 0.95, p < 0.001). In 15 patients receiving placebo as part of a double-blind, placebo-controlled prospective evaluation of prophylactic treatment with propranolol, variceal pressure did not change significantly over a 1-year period: 16.5 +/- 3.2 mmHg at onset: 16.7 +/- 3.4 after 3 months and 15.9 +/- 3.5 after 12 months. In contrast, propranolol therapy given to 15 patients decreased the pressure from 16.2 +/- 3.0 mmHg before therapy to 13.5 +/- 2.0 after 3 months (p < 0.001) and to 13.1 +/- 4.1 after 12 months (p < 0.05). Patients with a recent bleeding episode had higher pressures than those who had not yet experienced any haemorrhage (19.3 +/- 3.5 mmHg, n = 17 vs 13.9 +/- 3.3, n = 62) (p < 0.001). This was confirmed in a prospective study: the last variceal pressure in bleeders and non-bleeders was respectively 17.2 +/- 1.7 mmHg (n = 4) and 14.8 +/- 4.1 mmHg (n = 26) (p < 0.01). Overall, variceal pressure measurements correlated with the size of varices, the presence of red colour signs and with the North Italian Endoscopic Club score. CONCLUSIONS: This study has shown that the non-invasive pressure gauge Varipress represents a reproducible method to regularly assess variceal pressure, an important parameter related to the risk of bleeding, and to assess the effects of pharmacological therapy with propranolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH M_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pressure_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 8840055
----K E
----T Esmolol blunts the haemodynamic responses to tracheal intubation in treated hypertensive patients.
----A PURPOSE: To compare the ability of different bolus doses of esmolol to blunt the haemodynamic effects of laryngoscopy and tracheal intubation in treated hypertensive patients. METHODS: In this randomised, double-blind placebo controlled study, 45 ASA II patients, treated for essential hypertension with drugs other than beta blockers, were divided into three groups of 15 patients each. Patients in different groups either received 20 ml normal saline (Group P), or 100 mg esmolol (Group E100) or 200 mg esmolol (Group E200) as a single bolus intravenous dose before laryngoscopy and intubation. Systolic, diastolic and mean arterial pressure and heart rate were monitored for up to 10 min following intubation and were compared with respective basal readings as well as across groups. RESULTS: Esmolol alone reduced systolic arterial pressure (P < 0.01 in Group E100 and P < 0.001 in Group E200) and heart rate (P < 0.001). Though there was an increase in arterial pressure and heart rate in the control group, esmolol 100 mg maintained arterial pressure and heart rate at levels comparable to basal values throughout the study (P > 0.05). Patients receiving esmolol 200 mg had lower values (P < 0.001) than their basal readings during most of the post-intubation study period. CONCLUSION: Esmolol 100 mg given as bolus, is effective as well as safe in blunting the haemodynamic responses to laryngoscopy and tracheal intubation in treated hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Intubation__Intratracheal_MeSH M_Laryngoscopy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH 
****** 8840367
----K E
----T Pharmacologic prophylaxis of supraventricular tachyarrhythmias after coronary artery bypass.
----A Coronary artery bypass surgery is an accepted treatment for patients with coronary artery disease. Perioperative morbidity includes development of supraventricular arrhythmias. To prevent this, prophylactic administration of drugs such as calcium channel blockers, digoxin, and beta-blockers have been advised.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Coronary_Disease_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Human_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Tachycardia__Supraventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Supraventricular_prevention_&_control_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 8842136
----K E
----T Resistant hypertension: an overview.
----A OBJECTIVE: To review the factors contributing to treatment resistance in hypertensive patients and assess the evidence from therapeutic trials in these patients. DESIGN: A MEDLINE search using the words 'resistant hypertension', 'refractory hypertension' and 'treatment resistance, hypertension' was carried out to identify relevant articles. The bibliographies of articles were used to screen for other relevant articles. All available English-language articles on the epidemiology, prognosis and management of hypertension resistant to standard treatment were reviewed. RESULTS: Resistant hypertension is an important public health problem and a common reason for referral of patients to specialized hypertension clinics. Patients with uncontrolled hypertension are at increased risk of stroke, myocardial infarction, congestive heart failure and renal failure. Many factors may play a role in the development of resistant hypertension, including misdiagnosis (pseudoresistance), noncompliance, occult secondary causes for hypertension, volume overload, obesity, cigarette smoking, excess alcohol intake, sleep apnea, interfering medications and suboptimal combinations of antihypertensives. Only beta-blockers and thiazide diuretics have been demonstrated to reduce cardiovascular morbidity and mortality in hypertension. The trials evaluating third-line agents in patients with resistant hypertension have demonstrated additional blood pressure lowering with all classes of agents, and the randomized controlled trials have not demonstrated any statistically significant differences between the agents in either efficacy or tolerability. CONCLUSIONS: Evaluation of the patient with resistant hypertension should include 24 h ambulatory blood pressure monitoring and an extensive search for hypertensive end organ damage. Contributing factors should be sought and stepped care should still form the basis for treatment decisions. The choice of third-line agent should be dictated by the patient's renin profile, current medication and any concomitant diseases.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chlorothiazide_MeSH S_therapeutic_use_MeSH Chlorothiazide_therapeutic_use_MeSH M_Drug_Resistance_MeSH M_Female_MeSH M_Human_MeSH P_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertension__Malignant_MeSH S_prevention_&_control_MeSH Hypertension__Malignant_prevention_&_control_MeSH M_Male_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Ontario_MeSH S_epidemiology_MeSH Ontario_epidemiology_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8842782
----K E
----T The effect of trimetazidine on reperfusion arrhythmias in acute myocardial infarction.
----A The study aims to evaluate the effect of trimetazidine in reducing reperfusion arrhythmias in patients with acute myocardial infarction after successful thrombolysis. A total of 169 patients were included in the study, 83 of whom received trimetazidine orally at an initial dose of 60 mg followed by 20 mg tid for 5 days. These patients formed the study group (group T) while the remaining 86, the control group (group C). Successful thrombolysis by clinical and electrocardiographic criteria was observed in 53 patients of group T and in 55 patients of group C. Reperfusion arrhythmias were observed in 16 patients in group T (30.1%) and in 31 in group C (56.3%). This difference was statistically significant. Serious ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation) were observed in 1 patient of group T (1.8%) and in 6 patients of group C (10.9%). This difference was also statistically significant. It is concluded that trimetazidine administration can reduce the rate of reperfusion arrhythmias. This conclusion should be confirmed by larger clinical trials in order to give to the clinical results a stronger statistical power.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Chi-Square_Distribution_MeSH M_Confidence_Intervals_MeSH M_Female_MeSH M_Free_Radical_Scavengers_MeSH S_therapeutic_use_MeSH Free_Radical_Scavengers_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Myocardial_Reperfusion_MeSH S_adverse_effects_MeSH Myocardial_Reperfusion_adverse_effects_MeSH M_Odds_Ratio_MeSH M_Severity_of_Illness_Index_MeSH M_Thrombolytic_Therapy_MeSH S_adverse_effects_MeSH Thrombolytic_Therapy_adverse_effects_MeSH M_Trimetazidine_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH 
****** 8843892
----K E
----T Beneficial effects of pravastatin on fasting hyperinsulinemia in elderly hypertensive hypercholesterolemic subjects.
----A We undertook this prospective double-blind, placebo-controlled study to evaluate the efficacy and safety of low-dose (15 mg) pravastatin in elderly hypercholesterolemic hypertensive subjects with concurrent antihypertensive treatment and to determine whether fasting hyperinsulinemia could also be improved. At three hypertension and lipid clinics of two medical centers, 96 elderly (49 women, 47 men) ambulatory subjects were randomized to active treatment or placebo for 12 months after a 3-month single-blind lead-in period. Hypertensive subjects with plasma total cholesterol levels of at least 6.47 mmol/L (250 mg/dL) and triglyceride levels less than 3.39 mmol/L (300 mg/dL) were treated with 15 mg pravastatin for 12 months after receiving 3 months of the American Heart Association step I diet. Lipid, glucose, and fasting insulin levels were measured; clinical laboratory tests included liver function and creatine kinase determinations. After 12 months of pravastatin therapy, plasma total cholesterol concentration decreased by 25.1% (from a mean of 7.29 to 5.47 mmol/L, P < .05), low-density lipoprotein cholesterol decreased by 30.2% (from 5.27 to 3.68 mmol/L, P < .05), and triglycerides decreased by 10.7% (from 1.68 to 1.50 mmol/L, P < .05). High-density lipoprotein cholesterol increased by 9.2% (from 1.20 to 1.31 mmol/L, P < .05). Fasting insulin levels decreased from 89.0 to 61.5 pmol/L (P < .05). All of these changes were greater (P < .05) than any tendency toward change in the placebo group. Adverse events and clinical laboratory abnormalities were generally mild and transient in both placebo and pravastatin groups. Study drugs were withdrawn from one subject in each group with asymptomatic creatine kinase elevations. We conclude that low-dose pravastatin was effective and safe in the treatment of hypercholesterolemic hypertensive subjects on concurrent antihypertensive therapy. It also improved fasting hyperinsulinemia despite the use of beta-blockers and diuretics in these hypertensive subjects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Hyperinsulinism_MeSH S_drug_therapy_MeSH Hyperinsulinism_drug_therapy_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Male_MeSH M_Patient_Compliance_MeSH M_Pravastatin_MeSH S_adverse_effects_MeSH Pravastatin_adverse_effects_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 8855996
----K E
----T Antihypertensive medication use among recruits for the Trial of Nonpharmacologic Interventions in the Elderly (TONE).
----A OBJECTIVES: To examine the distribution and correlates of the classes of antihypertensive medications taken by persons aged 60 to 80. DESIGN: Cross-sectional screening. SETTING: Four academic medical centers in the southern and eastern United States. PARTICIPANTS: Volunteers (N = 2601) entering a clinical trial testing the value of nonpharmacologic approaches to control blood pressure who were either taking one or two (single or combined) medications for the treatment of hypertension and expressed willingness to be withdrawn from these medications according to a standardized protocol. MEASUREMENTS: Medication use, blood pressure, and data from self-administered questionnaires collected during standardized clinic visits. RESULTS: Calcium channel blockers (23.9%) were the most frequent single agent antihypertensive medications used by cohort members, followed by diuretics (17.9%) and angiotension-converting enzyme (ACE) inhibitors (17.5%). The most common combination agents were composed of diuretics with either calcium channel blockers (5.4%), ACE inhibitors (4.0%), or beta-blockers (3.7%). Women were twice as likely to be taking diuretics, and less likely to be taking ACE inhibitors and beta-blockers, than men. Blacks were more likely to be taking diuretics and calcium channel blockers, and less likely to be taking beta-blockers and ACE inhibitors, than others. These relationships could not be attributed to differences in geographical area, other demographic factors, age, or medical history. CONCLUSIONS: These usage patterns appear to mirror those in the population of the United States as a whole, which has trended toward greater usage of calcium channel blockers and ACE inhibitors with declining use of diuretics. The distribution of antihypertensive medications among older hypertensives is markedly different between women and men and between black Americans and others.
----P Journal_Article Multicenter_Study 
----M M_Academic_Medical_Centers_MeSH M_African_Americans_MeSH M_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Cross-Sectional_Studies_MeSH M_European_Continental_Ancestry_Group_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Questionnaires_MeSH M_Socioeconomic_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH 
****** 8857071
----K E
----T Lisinopril reduces postexercise albuminuria more effectively than atenolol in primary hypertension.
----A Physical exercise causes transient albuminuria. The mechanisms of postexercise albuminuria are not fully clarified but stimulation of the reninangiotensin system (RAS) probably plays a major role through intrarenal haemodynamic changes causing an elevated filtration pressure. In a randomised, double-blind, crossover study we compared the effects on urinary albumin excretion (UAE) of lisinopril (L) and atenolol (A) therapy, i.e. we aimed to investigate whether inhibition of the RAS or inhibition of beta1-adrenoceptor-mediated effects of the sympathetic nervous system differed with regard to changes in UAE. Sixteen patients with uncomplicated primary hypertension were studied. Four standardised bicycle ergometer exercise tests were performed, before and after each active treatment period. UAE 30 min postexercise, determined by radioimmunoassay, was significantly lowered by both treatments: -278 mu g center dot min-1 (L) and -199 mu g center dot min-1 (A). The reduction of postexercise UAE achieved by treatment with the angiotensin-converting enzyme (ACE) inhibitor (L) was significantly greater than that achieved by the beta1-selective adrenoceptor blocker treatment. Blood pressure (BP) at rest and during exercise were equally reduced by both drugs. In conclusion, this study showed that antihypertensive treatment with an ACE inhibitor was more effective in reducing exercise-induced albuminuria than a beta1-selective adrenoceptor-blocking agent with a similar degree of BP reduction in patients with uncomplicated primary hypertension. This suggests that the RAS plays a major role in postexercise albuminuria in hypertensive subjects. The clinical significance of this finding, however, remains to be clarified.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Albuminuria_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH S_prevention_&_control_MeSH Albuminuria_prevention_&_control_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH P_Exercise_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 8857482
----K E
----T Effects of carvedilol on systolic and diastolic left ventricular performance in idiopathic dilated cardiomyopathy or ischemic cardiomyopathy.
----A Recent evidence has shown that improvement in left ventricular (LV) systolic function in patients with New York Heart Association class II to III heart failure occurs with beta-adrenergic blocking agents. However the specific effects on LV diastolic function have been subjected to only limited examination. This study investigated the effects of the combined beta blocker/vasodilator, carvedilol, on systolic and diastolic LV performance in dilated cardiomyopathy. Thirty-six patients with New York Heart Association II to III heart failure and LV ejection fraction < or = 0.35 were entered into either arm of this placebo-controlled, double-blind 4-month trial. Twenty-one subjects were entered into the carvedilol treatment arm and 15 patients were entered into the placebo arm in a 3:2 ratio. Carvedilol therapy resulted in a significant improvement in LV ejection fraction, from 0.22 +/- 0.02 to 0.30 +/- 0.02 when compared with the placebo group (0.19 +/- 0.02 to 0.21 +/- 0.02 at baseline and after 4 months of therapy, respectively; p = 0.0001). However, no significant change in radionuclide parameters of LV diastolic function, including peak filling rate or time to peak filling rate, was observed. LV end-diastolic volume index did not change with carvedilol therapy, whereas end-diastolic volume index increased in the placebo group, although the difference between groups at 4 months was significant (p = 0.02). In conjunction with these changes, end-systolic volume index was smaller at 4 months after carvedilol treatment compared with that of the placebo group (p = 0.04). Thus, these results demonstrate that in moderate chronic heart failure, systolic LV performance improves but diastolic LV function does not improve when compared with placebo after treatment with carvedilol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Volume_MeSH S_drug_effects_MeSH Cardiac_Volume_drug_effects_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8862216
----K E
----T Assessing medication adherence by pill count and electronic monitoring in the African American Study of Kidney Disease and Hypertension (AASK) Pilot Study.
----A The Medication Event Monitoring System (MEMS), an electronic monitor which records the date and time of bottle cap openings, and pill counts were used to assess patterns of adherence for the primary antihypertensive drug in the African American Study of Kidney Disease and Hypertension Pilot Study (AASK). Blacks with hypertension and moderately reduced renal function were randomized to one of two levels of blood pressure control and to one of three antihypertensive drug regimens: primary therapy with a calcium channel blocker, an angiotension converting enzyme inhibitor, or a beta-blocker. Of the 94 participants in AASK, 91 had MEMS recordings and pill counts for 313 regularly scheduled monthly follow-up visits. The average length of follow-up was 4.6 months. An acceptable level of adherence by pill count was achieved if 80% to 100% of the prescribed pills were not returned to the clinic. Adherence by MEMS to a once-a-day drug dosing schedule was acceptable if 80% of the time intervals between MEMS openings were within 24 +/- 6 h. Acceptable adherence by pill count was observed at 68% of the follow-up visits; MEMS indicated nonadherence at 47% of those visits. Blood pressure was within goal in 50% of the participants who were adherent by both pill count and MEMS throughout their follow-up visits, and only 14% of the participants who were identified nonadherent by one or both methods. These findings suggest that electronic monitoring is a useful adjunct to pill counts in assessing adherence to antihypertensive drugs. Feedback of electronically collected information on dosing intervals to participants and staff may enhance adherence.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_African_Americans_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Diseases_MeSH S_drug_therapy_MeSH Kidney_Diseases_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Patient_Compliance_MeSH M_Pilot_Projects_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH 
****** 8869768
----K I
----T Post-marketing cohort study comparing the safety and efficacy of flunarizine and propranolol in the prophylaxis of migraine.
----A A comparative post-marketing surveillance study of the safety and efficacy of flunarizine and propranolol in the treatment of migraine was carried out. General practitioners in Belgium and the Netherlands each recruited patients for whom they would prescribe one of the study medications in the normal course of their treatment and recorded all medical events on follow-up forms for up to 8 months. A total of 1601 migraine patients were enrolled; 838 in the flunarizine cohort and 763 in the propranolol cohort. Propranolol was somewhat better than flunarizine in reducing the severity of migraine attacks, although this may have been due to a selection bias. Discontinuations of therapy due to events considered likely to be treatment-related were mostly due to the recognized side effects of the two drugs. As regards the occurrence of depressions, a total of 58 patients had depressive events, 34 in the flunarizine cohort and 24 in the propranolol cohort. Whereas migraine itself appears to be associated with an increased risk of depression, the number of previous migraine treatments was shown to be an additional risk factor for the development of depression in patients receiving flunarizine as was a history of depression. Overall, there was no appreciable difference in the risk/benefit ratio between flunarizine and propranolol.
----P Clinical_Trial Clinical_Trial__Phase_IV Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Basal_Ganglia_Diseases_MeSH S_chemically_induced_MeSH Basal_Ganglia_Diseases_chemically_induced_MeSH S_epidemiology_MeSH Basal_Ganglia_Diseases_epidemiology_MeSH M_Belgium_MeSH M_Child_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH S_epidemiology_MeSH Depression_epidemiology_MeSH M_Fatigue_MeSH S_chemically_induced_MeSH Fatigue_chemically_induced_MeSH M_Female_MeSH M_Flunarizine_MeSH S_adverse_effects_MeSH Flunarizine_adverse_effects_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Netherlands_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Safety_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Weight_Gain_MeSH S_drug_effects_MeSH Weight_Gain_drug_effects_MeSH 
****** 8877595
----K E
----T Effects of antihypertensive drugs on the circadian blood pressure profile.
----A We compared the effect of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium antagonists on the circadian blood pressure (BP) profile in essential hypertension. We reviewed all studies published between 1980 and August 1993 reporting the circadian efficacy of antihypertensive drugs and using ambulatory BP monitoring. In all, 815 patients with essential hypertension were assessed in 51 studies of eight different beta-blockers, six ACE inhibitors, and eight calcium antagonists. As main outcome measures, relative (percentage) BP reductions during the day and at night were compared between the three classes of antihypertensive drugs. Results were also separated for different dosing schemes (once and more than once daily). With all three classes of antihypertensive agents, the percentage night BP reduction was approximately 1-3% less as compared with percentage reductions during the day. Only for systolic BP (SBP) of the calcium antagonists administered once daily was this difference significant [2.2%, confidence interval (CI) 0.3-4.0%, p < 0.05], due to a higher statistical power in this group of agents. Our results show that beta-blockers, ACE inhibitors, and calcium antagonists are comparably effective during the day and at night, and no evidence indicates that either of the three agents is preferable to obtain the best possible antihypertensive effect at night.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8879339
----K E
----T Effect of 14 years of antihypertensive treatment on renal function and urinary albumin excretion in primary hypertension.
----A The effects on blood pressure (BP), renal function, and urinary albumin excretion (UAE) of 14 years of antihypertensive treatment were studied and compared to the changes seen with normal aging. The studied groups included randomly selected men with newly diagnosed primary hypertension at baseline (n = 23) and normotensive (NT) men of the same age (n = 11). The hypertensives (HT) were treated with beta-blockers either as monotherapy or combined with diuretics or hydralazine. Glomerular filtration rate (GFR; inulin clearance), renal blood flow (RBF, para-aminohippurate clearance), renal vascular resistance (RVR), and 24-h UAE were determined. The two groups were investigated at baseline (before treatment) and after 7 and 14 years. At baseline, BP and RVR were significantly increased and RBF was significantly decreased in the HT over that in the NT. The BP in the HT was significantly reduced after 7 years of treatment and a further but nonsignificant reduction to 139 +/- 14/88 +/- 6 mm Hg (mean +/- SD) was seen after 14 years. GFR in the HT was significantly reduced from 103 +/- 15 mL/min to 84 +/- 19 mL/min (mean +/- SD) after 7 years, but no further reduction was seen after 14 years. During the 14 years RBF decreased and RVR increased in the HT but these changes were of the same magnitude as in the NT. The UAE did not change significantly during the study. In conclusion, good blood pressure control with conventional antihypertensive treatment in mild to moderate primary hypertension seems to protect the kidney from progressive decline in GFR and increase in UAE. The increase in RVR and the decrease in RBF seen during 14 years of antihypertensive treatment was of the same magnitude as that seen with normal aging.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Albuminuria_MeSH S_urine_MeSH Albuminuria_urine_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diuretics__Thiazide_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hydralazine_MeSH S_pharmacology_MeSH Hydralazine_pharmacology_MeSH S_therapeutic_use_MeSH Hydralazine_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Kidney_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 8879340
----K E
----T Long-term renal preservation in essential hypertension. Angiotensin converting enzyme inhibition is superior to beta-blockade.
----A Antihypertensive treatment is known to slow down the decline in glomerular filtration rate (GFR) with time. Angiotensin converting enzyme (ACE) inhibition has been shown to be more effective in this regard than conventional antihypertensive therapy. In a recent prospective, randomized, double blind trial in 257 patients with essential hypertension, the loss of GFR, determined with 51Cr-EDTA clearance, was significantly less with an ACE inhibitor (cilazapril) than with a beta-adrenoceptor blocker (atenolol) during the first year of treatment. However, after 2 years, the two therapies were equally effective in this regard, thereby creating doubts about the long-term superiority of ACE inhibition in this regard. In order to elucidate whether the superior renal preservation with the ACE inhibitor was a transient effect, GFR was measured after 1 more year of treatment, i.e., after 36 months. At that time, the decline in GFR was significantly smaller in the ACE inhibitor group as compared to the beta-adrenoceptor blocker group (-3.0 [-5.5, -1.0; 95% CI] v -7.0 [-9.0, -4.5; 95% CI] mL/min x 1.73 m2; P = .026). This demonstrates that in the treatment of essential hypertension ACE inhibition preserves GFR significantly better than beta-adrenoceptor blockade during long-term therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH 
****** 8879341
----K I
----T Antihypertensive therapy and quality of life. Influence of blood pressure reduction, adverse events, and prior antihypertensive therapy.
----A Quality of life is an important attribute of antihypertensive therapy. Previous studies have not addressed the importance of a patient's prior pharmacotherapy on quality of life, which may serve as the basis of reference for a new therapy. Nor have previous studies compared commonly used quality of life instruments for consistency, or investigated whether improvement or worsening of quality of life correlates with adverse events or blood pressure reduction. Two hundred eighteen hypertensive patients with diastolic blood pressure (95 to 114 mm Hg) after a 4- to 5-week placebo washout period were enrolled in a randomized double-blind, parallel group dose-escalation trial to compare the effects of amlodipine (2.5 to 10 mg), bisoprolol (2.5 to 10 mg)/hydrochlorothiazide (HCTZ) 6.25, and enalapril (5 to 20 mg) on blood pressure, adverse events, and quality of life. Three quality of life instruments (General Well-Being Index, Vital Signs Quality of Life, Zung Self-Rating Depression Scale) were administered during original therapy, after placebo washout, and after 12 weeks of optimally titrated clinical trial pharmacotherapy. Our results demonstrated that removal from prior therapy had no detectable influence on subsequent evaluation of quality of life. The three quality of life instruments were consistent with the changes observed with the three therapies: a trend toward better quality of life with amlodipine and bisoprolol/HCTZ. Adverse events, but not systolic or diastolic blood pressure reduction correlated directly with changes in quality of life.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH 
****** 8879603
----K E
----T The Swedish Trial in old patients with hypertension-2 (STOP-hypertension-2): a progress report.
----A OBJECTIVE: The Swedish Trial in Old Patients with Hypertension-2 (STOP-Hypertension-2) was designed by a project group of the Swedish Hypertension Society to test whether the "newer" treatment alternatives (ACE inhibitors and calcium antagonists) are as good as, better or less good than, the "older" ones (beta-blockers and diuretics) in terms of preventing cardiovascular morbidity and mortality in elderly hypertensives. The aim of the present paper is to report on the progress of the study. DESIGN: Prospective, open trial with blinded end-point committee and centralized randomization (PROBE design). STOP-Hypertension-2 may be regarded as a scientific follow-up of the previously published Swedish Trial in Old Patients with Hypertension (STOP-Hypertensioon-1) (6) using the same study organization. SUBJECTS: By the end of 1994 when recruitment was stopped, 6628 hypertensive men (34%) and women (66%) aged 70-84 (mean age 76) had been included at 312 Swedish health centres (out of approximately 850). In the whole cohort 11% are diabetics and 9% smokers. The mean total cholesterol value is 6.5 mmol/L. RESULTS: In the whole study cohort, blood pressure was lowered from 194/98 mmHg to 167/85 mmHg after one year. At the end of 1995, 319 fatal events (all-cause mortality) had been reported, corresponding to a mortality rate of 21.3 per 1000 person-years. CONCLUSION: In STOP-Hypertension-2, 6628 elderly hypertensive have been randomized to three different treatment regimes: beta-blocker+diuretics (the active treatment arm in STOP-Hypertension-1), ACE inhibitors, or calcium antagonists. Their average lowering of blood pressure was 27/13 mmHg and end-points have occurred at the expected rate. Thus, it should be possible to terminate STOP-Hypertension-2 within two to three years.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8879897
----K E
----T Efficacy and tolerability of subcutaneous sumatriptan administered using the IMITREX STATdose System.
----A The efficacy and tolerability of subcutaneous (SC) sumatriptan administered with the IMITREX (sumatriptan succinate) STATdose System, which circumvents the need for patients or health care professionals to handle a syringe, were evaluated in two randomized, double-masked, parallel-group, placebo-controlled, multicenter studies. In the clinic, 158 adults with migraine diagnosed according to International Headache Society criteria received SC sumatriptan (6 mg) or placebo delivered with the IMITREX STATdose System for treatment of a migraine attack. By 120 minutes after SC dosing, 73% and 79% of sumatriptan-treated patients, compared with 28% and 37% of placebo-treated patients in studies 1 and 2, respectively, experienced headache relief (a statistically significant difference). Clinical disability scores 120 minutes after dosing showed that 75% and 85% of sumatriptan-treated patients, compared with 30% and 42% of placebo-treated patients, were normal or only mildly impaired (a statistically significant difference). Similar efficacy rates were observed for nausea, phonophobia, and photophobia. No serious or unusual adverse events occurred, and no clinically relevant abnormalities in laboratory test values were reported. Based on these results, we concluded that SC sumatriptan (6 mg) administered using the IMITREX STATdose System is effective for the treatment of migraine. The efficacy and tolerability profiles of SC sumatriptan administered with this device are similar to those reported for SC sumatriptan administered with a conventional syringe.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Double-Blind_Method_MeSH M_Drug_Tolerance_MeSH M_Female_MeSH M_Human_MeSH M_Injections__Subcutaneous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Sumatriptan_MeSH S_administration_&_dosage_MeSH Sumatriptan_administration_&_dosage_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8880046
----K I
----T Postmarketing study of the use of flunarizine in vestibular vertigo and in migraine.
----A OBJECTIVE: This international postmarketing observational study of flunarizine was designed to evaluate, in routine clinical practice, the risk/benefit ratio of flunarizine in its approved indications, namely prophylaxis of migraine and treatment of vertigo. Comparator drugs were propranolol in migraine and betahistine in vertigo. The study was carried out by 498 general practitioners in Belgium, The Netherlands and Germany, whose participation had been requested by mail. In total 3186 patients were entered: 1601 in the two migraine cohorts and 1585 in the two vertigo cohorts. RESULTS: In the migraine study, treatment results with propranolol tended to be somewhat better than those with flunarizine, but a selection bias cannot be excluded. There was no clear difference regarding efficacy between flunarizine and betahistine in the vertigo study. The safety evaluation focused on extrapyramidal symptoms (EPS) and depression. Overall, EPS were noted in only four patients, two in the vertigo-betahistine and two in the migraine-flunarizine cohort. A total of 70 patients developed depressive symptoms (34 in the flunarizine and 24 in the propranolol migraine cohorts, but only 7 in the flunarizine and 5 in the betahistine vertigo cohorts). Patients with migraine were clearly more prone to depression than patients with vertigo, regardless of their treatment. Additional risk factors for depression were a history of depression, and, in the migraine flunarizine cohort, a high number of previous migraine treatments.
----P Journal_Article Multicenter_Study 
----M M_Basal_Ganglia_Diseases_MeSH S_chemically_induced_MeSH Basal_Ganglia_Diseases_chemically_induced_MeSH M_Betahistine_MeSH S_adverse_effects_MeSH Betahistine_adverse_effects_MeSH S_therapeutic_use_MeSH Betahistine_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Depression_MeSH S_chemically_induced_MeSH Depression_chemically_induced_MeSH M_Female_MeSH M_Flunarizine_MeSH S_adverse_effects_MeSH Flunarizine_adverse_effects_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Histamine_H1_Antagonists_MeSH S_adverse_effects_MeSH Histamine_H1_Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Histamine_H1_Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH P_Product_Surveillance__Postmarketing_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Vertigo_MeSH S_drug_therapy_MeSH Vertigo_drug_therapy_MeSH 
****** 8880057
----K E
----T Effect of the lipase inhibitor orlistat on the pharmacokinetics of four different antihypertensive drugs in healthy volunteers.
----A OBJECTIVE: To study the influence of the lipase inhibitor orlistat on the pharmacokinetics of the antihypertensive drugs atenolol, furosemide, captopril and nifedipine. METHODS: Four open-label, crossover studies were performed on six to eight healthy male volunteers. Orlistat was given in doses of 50 mg 3 times daily mid-meal for 7 (nifedipine and captopril) or 8 days (atenolol and furosemide). The four antihypertensive drugs (atenolol 100-mg tablet, furosemide 40-mg tablet, captopril 50-mg tablet and nifedipine 20-mg slow-release tablet) were administered in single doses twice, once before and once together, with orlistat at the end of the orlistat treatment period. RESULTS: The plasma concentration time profiles and the pharmacokinetic parameters estimated for these drugs were in the expected range, except for furosemide, whose bioavailability was lower than reported in the literature. This was probably due to the fact that furosemide was given during a meal. There were minor, but statistically significant, differences in one of the pharmacokinetic parameters of furosemide and nifedipine (no difference for captopril and atenolol) when these drugs were given alone and in combination with orlistat: the half-life of furosemide was slightly longer, the time to peak plasma concentrations of nifedipine was slightly longer. None of these are considered to be clinically significant changes. CONCLUSIONS: The lipase inhibitor orlistat given 50 mg 3 times daily does not alter the pharmacokinetics of atenolol, furosemide, nifedipine and captopril to a clinically significant extent.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_blood_MeSH Adrenergic_beta-Antagonists_blood_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_blood_MeSH Angiotensin-Converting_Enzyme_Inhibitors_blood_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH M_Atenolol_MeSH S_blood_MeSH Atenolol_blood_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH M_Calcium_Channel_Blockers_MeSH S_blood_MeSH Calcium_Channel_Blockers_blood_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH M_Captopril_MeSH S_blood_MeSH Captopril_blood_MeSH S_pharmacokinetics_MeSH Captopril_pharmacokinetics_MeSH M_Chromatography__High_Pressure_Liquid_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Sulfamyl_MeSH S_blood_MeSH Diuretics__Sulfamyl_blood_MeSH S_pharmacokinetics_MeSH Diuretics__Sulfamyl_pharmacokinetics_MeSH M_Drug_Therapy__Combination_MeSH M_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Enzyme_Inhibitors_pharmacology_MeSH M_Female_MeSH M_Furosemide_MeSH S_blood_MeSH Furosemide_blood_MeSH S_pharmacokinetics_MeSH Furosemide_pharmacokinetics_MeSH M_Human_MeSH M_Hypertension_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Lactones_MeSH S_pharmacology_MeSH Lactones_pharmacology_MeSH M_Male_MeSH M_Nifedipine_MeSH S_blood_MeSH Nifedipine_blood_MeSH S_pharmacokinetics_MeSH Nifedipine_pharmacokinetics_MeSH 
****** 8889897
----K E
----T Chronopharmacologic considerations when treating the patient with hypertension: a review.
----A Recognition of the existence of circadian variation in exacerbation of cardiovascular disease may have relevance to clinical use of cardioactive agents. Physiologic rational for the chronobiology of cardiac disease exists and can provide a basis on which to examine the efficacy of agents to manage cardiac disease. The use of 24-hour ambulatory blood pressure monitoring (ABPM) devices have advanced our ability to describe the interplay of chronobiologic rhythms and pharmacodynamic response to antihypertensive medications. This review summarizes the studies evaluating the use of various antihypertensive medications in the context of using 24-hour blood pressure monitoring devices. The studies are described in an attempt to increase awareness of chronobiology and potential implications of designing chronotherapeutic regimens.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_Antagonists_administration_&_dosage_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH P_Chronotherapy_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 8892775
----K E
----T Treatment and post-treatment effects of alpha- versus beta-receptor blockers on left ventricular structure and function in essential hypertension.
----A This study was undertaken to compare the effects of alpha-receptor blockade and beta-receptor blockade on left ventricular structure and function in essential hypertension. The increase in left ventricular mass in patients with essential hypertension is at least partly induced by the sympathetic nervous system. We conducted a double-blind, randomized, controlled clinical trial to compare the effects of alpha-blockers and beta-blockers on left ventricular structure and function. Forty-three patients with mild to moderate essential hypertension were randomly allocated to receive antihypertensive therapy with either the alpha-blocker bunazosin (n = 23) or the beta-blocker metoprolol (n = 20). Twenty-four-hour blood pressure measurements and echocardiographic measurements of left ventricular structure and function were performed before therapy, after 6 months of therapy, and 4 weeks after discontinuation of therapy. Bunazosin and metoprolol led to similar reductions in systolic/diastolic blood pressure (-11 +/- 11/-9 +/- 8 mm Hg vs -11 +/- 12/-8 +/- 9 mm Hg, respectively) and left ventricular mass (-25 +/- 42 gm vs -28 +/- 44 gm, respectively) (p = no significant difference, bunazosin vs metoprolol). Neither metoprolol nor bunazosin significantly affected left ventricular systolic function. Diastolic left ventricular filling, however, was increased with beta-blocker medication, as indicated by a decrease in atrial filling fraction (39% +/- 5% to 34% +/- 5%; p < 0.05), but not with the alpha-blocker. The effect of metoprolol resulted from its bradycardiac effect. Four weeks after discontinuation of therapy, blood pressure and left ventricular mass increased to pretreatment levels in both groups similarly. Furthermore, the increase in diastolic filling was lost shortly after withdrawal of metoprolol concomitant with the increase in heart rate. We conclude that alpha-blockers and beta-blockers are equally capable of reducing left ventricular mass in hypertensive patients. beta-Blockers lead to an increase in diastolic left ventricular filling. This effect may be of therapeutic value because diastolic dysfunction may precede systolic dysfunction in hypertensive heart disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Quinazolines_MeSH S_pharmacology_MeSH Quinazolines_pharmacology_MeSH S_therapeutic_use_MeSH Quinazolines_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8894261
----K E
----T Evaluation of the sympathetic nervous system using heart rate variability and plasma hormones in hypertensive patients treated with cilazapril and atenolol.
----A In a double-blind placebo-controlled parallel study, we assessed basal and post-therapeutic sympathetic activity both in supine and standing positions in mildly to moderately hypertensive patients by two different methods: frequency domain indices of heart rate variability (HRV) and plasma levels of both noradrenaline (NA) and its metabolite, 3,4-dihydroxyphenylglycol (DOPEG). Patients were evaluated on placebo and after 8 weeks of treatment with either cilazapril, 2.5-5 mg/day (13 patients) or atenolol, 50-100 mg/day (14 patients). Twenty-four-hour blood pressure was similarly reduced (p < 0.01) by both cilazapril and atenolol. Heart rate decreased with atenolol by 14 beats per min (p < 0.001) but did not change with cilazapril. When compared to the placebo, cilazapril did not modify sympathetic activity indices of HRV but did significantly reduce NA and DOPEG levels in both the supine and standing (p < 0.05) positions. As expected, atenolol reduced (p < 0.05) sympathetic activity indices of HRV but did not modify NA levels in either position. Moreover, while on placebo, patients showed no significant correlations between values of NA or DOPEG, nor in any of the HRV indices. We conclude that: (1) the antihypertensive effects of cilazapril and atenolol are similar, but in these patients, sympathetic activity indices showed divergent results both before and after therapy; (2) this may be due to different aspects of sympathetic activators, assessed independently by different methods, and (3) these discrepancies must be taken into account when evaluating autonomous nervous system parameters.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Methoxyhydroxyphenylglycol_MeSH S_analogs_&_derivatives_MeSH Methoxyhydroxyphenylglycol_analogs_&_derivatives_MeSH S_blood_MeSH Methoxyhydroxyphenylglycol_blood_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH 
****** 8894262
----K I
----T Analysis of adverse effects among patients with essential hypertension receiving an ACE inhibitor or a beta-blocker.
----A Evaluation of safety and efficacy of new drugs is based largely on data from clinical trials involving a limited number of patients. This approach does not necessarily detect the rare adverse events that may only be observed when very large numbers of patients are studied. Consequently, we designed a double-blind 12-week trial comparing the new angiotensin-converting enzyme (ACE) inhibitor, quinapril (n = 5,053), with a well-established beta-adrenergic receptor blocker, metoprolol (n = 506). Essentially hypertensive patients (diastolic blood pressure 95-114 mm Hg) received either 10 mg quinapril or 50 mg metoprolol once daily, and the doses were doubled at 4-week intervals to a maximum of 40 and 200 mg, respectively, in nonresponders. Responder rates were similar under both regimens. Adverse events were assessed by interview as well as by a standard questionnaire. The overall prevalence of adverse events reported by standard questionnaire was higher than that reported spontaneously during interviews. With respect to typical ACE inhibitor adverse reactions (e.g. cough and taste disturbances), there was no difference between quinapril and metoprolol independent of the mode of reporting. In summary, both drugs showed comparable overall tolerance and safety. The discrepancy between spontaneously reported and questionnaire-reported adverse events was noteworthy, and this finding prevailed in a volunteer group of 327 patients who were treated with quinapril for 52 weeks. Thus, a questionnaire is of great significance in addition to the patient history/interview in a large-scale, double-blind study designed to learn about details of drug safety.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Tolerance_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Interviews_MeSH M_Isoquinolines_MeSH S_adverse_effects_MeSH Isoquinolines_adverse_effects_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Questionnaires_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 8901656
----K E
----T A prospective study of anger and coronary heart disease. The Normative Aging Study.
----A BACKGROUND: Recent laboratory and epidemiological studies have suggested that high levels of anger may increase the risk of coronary heart disease (CHD). METHODS AND RESULTS: We examined prospectively the relationship of anger to CHD incidence in the Veterans Administration Normative Aging Study, an ongoing cohort of older (mean age, 61 years) community-dwelling men. A total of 1305 men who were free of diagnosed CHD completed the revised Minnesota Multiphasic Personality Inventory (MMPI-2) in 1986. Subjects were categorized according to their responses to the MMPI-2 Anger Content Scale, which measures the degree to which individuals have problems controlling their anger. During an average of 7 years of follow-up, 110 cases of incident CHD occurred, including 30 cases of nonfatal myocardial infarction hostility. (MI), 20 cases of fatal CHD, and 60 cases of angina pectoris. Compared with men reporting the lowest levels of anger, the multivariate-adjusted relative risks among men reporting the highest levels of anger were 3.15 (95% confidence interval) [CI]: 0.94 to 10.5) for total CHD (nonfatal MI plus fatal CHD) and 2.66 (95% CI: 1.26 to 5.61) for combined incident coronary events including angina pectoris. A dose-response relation was found between level of anger and overall CHD risk (P for trend, .008). CONCLUSIONS: These data suggest that high levels of expressed anger may be a risk factor for CHD among older men.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH M_Anger_MeSH S_physiology_MeSH Anger_physiology_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_epidemiology_MeSH Angina_Pectoris_epidemiology_MeSH S_psychology_MeSH Angina_Pectoris_psychology_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_administration_&_dosage_MeSH Anti-Inflammatory_Agents__Non-Steroidal_administration_&_dosage_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_psychology_MeSH Coronary_Disease_psychology_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Longitudinal_Studies_MeSH M_MMPI_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Stress__Psychological_MeSH S_epidemiology_MeSH Stress__Psychological_epidemiology_MeSH S_physiopathology_MeSH Stress__Psychological_physiopathology_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH M_United_States_Department_of_Veterans_Affairs_MeSH 
****** 8902255
----K I
----T Cyclandelate in the prophylaxis of migraine: a randomized, parallel, double-blind study in comparison with placebo and propranolol. The Study group.
----A Cyclandelate inhibits calcium-induced contraction of vascular smooth muscle cells, platelet aggregation induced by thrombin, platelet-activating-factor and adenosine, and also suppresses a provoked 5HT release from platelets. This pharmacological profile suggests that cyclandelate may have a potential prophylactic effect in migraine. To test this hypothesis, a double-blind multicentre study was performed in 214 patients to investigate the efficacy and tolerability of cyclandelate compared to placebo and propranolol. After a 4-week baseline period, eligible patients (randomization 3:2:3) were treated for 12 weeks with daily doses of 1.200 mg cyclandelate (n = 81), placebo (n = 55) or 120 mg propranolol (n = 78). The number of migraine attacks (> or = 50% responders) and the migraine duration/month were compared based on the difference between baseline and the last 4 weeks of prophylactic treatment. The percentage of patients with a reduction in migraine attacks of > or = 50% treated with cyclandelate (37.0%) or propranolol (42.3%) was not significantly superior to placebo (30.9%; p > 0.025). The mean duration of migraine in hours (h) per month decreased in both active treatment groups (cyclandelate: 36.8 h, p = 0.046; propranolol: 34.4 h, p = 0.039) compared to placebo (13.7 h) without reaching statistical significance (alpha/2 = 0.025). The clinical efficacy of cyclandelate and propranolol was comparable. Adverse experiences were reported by 13 patients (16.0%) treated with cyclandelate, by 5 patients (9.1%) treated with placebo and by 19 patients (24.4%) treated with propranolol. These were drug-related in 7.1% (n = 6) of patients treated with cyclandelate and in 9% (n = 7) of patients treated with propranolol. In summary, cyclandelate has a comparable efficacy to that of propranolol, an established drug of first choice in the prophylaxis of migraine. Both drugs were better than placebo, but not significantly so. Both active treatments were well tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Comparative_Study_MeSH M_Cyclandelate_MeSH S_administration_&_dosage_MeSH Cyclandelate_administration_&_dosage_MeSH S_adverse_effects_MeSH Cyclandelate_adverse_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Pain_Measurement_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 8904256
----K E
----T Haemodynamic effects of high-dose vecuronium compared with pancuronium in beta-blocked patients with coronary artery disease during fentanyl-diazepam-nitrous oxide anaesthesia.
----A BACKGROUND: Different combinations of neuromuscular blockers and opioids have been used in patients with angina pectoris to provide cardiovascular stability and reduce risk of myocardial ischaemia during anaesthesia. METHODS: We have compared the haemodynamic effects of high-dose vecuronium (0.3 mg kg-1) with those of a standard dose of pancuronium (0.1 mg kg-1) in patients scheduled for coronary artery bypass grafting during fentanyl-diazepam-nitrous oxide anaesthesia. All patients were receiving beta-adrenergic blocking agents. The given doses of vecuronium and pancuronium are equieffective with respect to duration of neuromuscular blockade. RESULTS: During a 25-min experimental period following the administration of the randomly selected drug, no significant changes in the haemodynamic parameters were observed in the vecuronium group. The administration of pancuronium, however, resulted in a significant mean increase in heart rate (20%), rate-pressure product (23%) and cardiac index (21%). Following endotracheal intubation in the pancuronium group, we observed an additional significant increase in mean arterial pressure and rate-pressure product. CONCLUSION: High-dose administration of vecuronium has minimal haemodynamic effects and may thus offer a better alternative than pancuronium for long-lasting neuromuscular blockade in patients with coronary artery disease during fentanyl-diazepam-nitrous oxide anaesthesia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH P_Anesthesia_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Diazepam_MeSH S_administration_&_dosage_MeSH Diazepam_administration_&_dosage_MeSH M_Female_MeSH M_Fentanyl_MeSH S_administration_&_dosage_MeSH Fentanyl_administration_&_dosage_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neuromuscular_Nondepolarizing_Agents_MeSH S_pharmacology_MeSH Neuromuscular_Nondepolarizing_Agents_pharmacology_MeSH M_Nitrous_Oxide_MeSH S_administration_&_dosage_MeSH Nitrous_Oxide_administration_&_dosage_MeSH M_Pancuronium_MeSH S_pharmacology_MeSH Pancuronium_pharmacology_MeSH M_Vecuronium_Bromide_MeSH S_pharmacology_MeSH Vecuronium_Bromide_pharmacology_MeSH 
****** 8913546
----K E
----T Global efficacy and tolerability of losartan, an angiotensin II subtype 1-receptor antagonist, in the treatment of hypertension.
----A Losartan is the first drug of a new therapeutic class, the angiotensin II (A II)-receptor antagonists, to be clinically studied and become available for the management of hypertension. Clinical experience with losartan from worldwide, double-blind, controlled studies has been obtained in more than 2900 hypertensive patients treated with losartan alone or in combination with hydrochlorothiazide, with 1700 patients receiving treatment for more than a year. The efficacy of losartan was evaluated in the young and old, in different degrees of hypertension, in blacks and nonblacks, and in patients with renal impairment. Tolerability parameters were assessed by subgroup as well. In dose-ranging studies, 50 mg once daily has generally been shown to produce near maximum effects and a dose of 100 mg does not produce additional effects. The efficacy of losartan (50 to 100 mg once daily) has been compared to atenolol (50 to 100 mg once daily), felodipine ER (5 to 10 mg once daily), and enalapril (20 mg once daily). The blood pressure-lowering effect of losartan was comparable to felodipine, enalapril, and atenolol. The efficacy of losartan was demonstrated using ambulatory blood pressure monitoring, which showed that losartan 50 mg once daily produced gradual reduction in blood pressure, providing 24-h control without affecting the body's circadian rhythm. In subgroups of study populations, no differences in efficacy were noted with respect to age, gender and the severity of hypertension. No initial dosage adjustment is necessary in the elderly and patients with renal impairment (even those on dialysis). Among blacks, the mean response of losartan was lower, which is not surprising given the lesser activation of the renin-angiotensin system in this population. A subgroup safety and tolerability analysis confirmed that there were no important differences in adverse events when assessed by age, race, or gender. The data obtained from controlled clinical trials conducted with losartan, the first A II-receptor antagonist, has shown that a single daily 50-mg dose provides adequate 24-h control of blood pressure in most patients with comparable efficacy to other classes and is well tolerated.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Imidazoles_MeSH S_adverse_effects_MeSH Imidazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 8914031
----K E
----T Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy.
----A Treatment of hypertension with ACE inhibitors in diabetic patients reduces proteinuria and slows progression of nephropathy compared with agents that do not maintain declines in proteinuria. Calcium channel blockers (CCBs) have variable effects on proteinuria; their long-term effects on progression of diabetic nephropathy are not known. The current study examines the hypothesis that CCBs that maintain reductions in proteinuria slow progression of nephropathy associated with non-insulin dependent diabetes mellitus (NIDDM) by a degree comparable to ACE inhibitors, given similar levels of blood pressure control. To test this hypothesis we randomized 52 patients with NIDDM associated nephropathy and hypertension, mean age of 63 +/- 8 years, to either the ACE inhibitor, lisinopril (N = 18), nondihydropyridine CCBs (NDCCBs), verapamil SR (N = 8) or diltiazem SR (N = 10), or the beta blocker, atenolol (N = 16). Goal blood pressure was < or = 140/90 mm Hg. Patients were followed for a mean period of 63 +/- 7 months. The primary end point was change in creatinine clearance (CCr) slope in each group. There was no significant difference in mean arterial pressure reduction among the groups over the study period (P = 0.14). The mean rate of decline in CCr was greatest in the atenolol group (-3.48 ml/min/year/1.73 m2; P < 0.0001). There was no difference in the CCr slopes between lisinopril and NDCCBs groups (P = 0.36). Proteinuria was reduced to a similar extent in the lisinopril and NDCCBs groups (P > 0.99). Therefore, in persons with renal insufficiency secondary to NIDDM, similar levels of blood pressure control with either lisinopril or NDCCBs slowed progression of renal disease to a greater extent than atenolol. Moreover, this enhanced slowing of renal disease progression correlated with sustained and significant reductions in proteinuria, findings not observed in the atenolol group.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH S_metabolism_MeSH Creatinine_metabolism_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Nephropathies_MeSH S_blood_MeSH Diabetic_Nephropathies_blood_MeSH S_physiopathology_MeSH Diabetic_Nephropathies_physiopathology_MeSH S_prevention_&_control_MeSH Diabetic_Nephropathies_prevention_&_control_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8929262
----K E
----T Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research Group.
----A BACKGROUND: Perioperative myocardial ischemia is the single most important potentially reversible risk factor for mortality and cardiovascular complications after noncardiac surgery. Although more than 1 million patients have such complications annually, there is no effective preventive therapy. METHODS: We performed a randomized, double-blind, placebo-controlled trial to compare the effect of atenolol with that of a placebo on overall survival and cardiovascular morbidity in patients with or at risk for coronary artery disease who were undergoing noncardiac surgery. Atenolol was given intravenously before and immediately after surgery and orally thereafter for the duration of hospitalization. Patients were followed over the subsequent two years. RESULTS: A total of 200 patients were enrolled. Ninety-nine were assigned to the atenolol group, and 101 to the placebo group. One hundred ninety-four patients survived to be discharged from the hospital, and 192 of these were followed for two years. Overall mortality after discharge from the hospital was significantly lower among the atenolol-treated patients than among those who were given placebo over the six months following hospital discharge (0 vs. 8 percent, P<0.001), over the first year (3 percent vs. 14 percent, P=0.005), and over two years (10 percent vs. 21 percent, P=0.019). The principal effect was a reduction in deaths from cardiac causes during the first six to eight months. Combined cardiovascular outcomes were similarly reduced among the atenolol-treated patients; event-free survival throughout the two-year study period was 68 percent in the placebo group and 83 percent in the atenolol group (P=0.008). CONCLUSIONS: In patients who have or are at risk for coronary artery disease who must undergo noncardiac surgery, treatment with atenolol during hospitalization can reduce mortality and the incidence of cardiovascular complications for as long as two years after surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Disease-Free_Survival_MeSH M_Double-Blind_Method_MeSH M_Heart_Diseases_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH S_prevention_&_control_MeSH Heart_Diseases_prevention_&_control_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Premedication_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Surgical_Procedures__Operative_MeSH M_Survival_Analysis_MeSH 
****** 8915229
----K E
----T Dipyridamole and dobutamine-atropine stress echocardiography in the diagnosis of coronary artery disease. Comparison with exercise stress test, analysis of agreement, and impact of antianginal treatment.
----A STUDY OBJECTIVES: To compare the usefulness of dipyridamole echocardiography, dobutamine-atropine echocardiography, and exercise stress testing in the diagnosis of coronary artery disease and to analyze the agreement among the tests. DESIGN: Performance of these three tests in random order on a consecutive cohort of patients. SETTING: A tertiary care and university center. PATIENTS: One hundred two consecutive patients with chest pain and no history of coronary artery disease. INTERVENTIONS: Dipyridamole echocardiography, dobutamine-atropine echocardiography, exercise stress testing, and coronary angiography. MEASUREMENTS AND RESULTS: Dobutamine-atropine test was positive in 49 (77%) of 63 patients with coronary artery disease, dipyridamole test in 49 (77%), and exercise stress test in 44 (68%; p = NS). Both echocardiographic tests showed an overall specificity (dipyridamole, 97%; dobutamine, 95%) higher than exercise stress test (79%; p < 0.05). Sensitivity of dipyridamole testing decreased from 93 to 61% (p = 0.002) if patients were receiving antianginal treatment but sensitivity of dobutamine-atropine testing was not affected (77% in patients receiving and not receiving treatment). When results were considered as positive-negative, agreement between dipyridamole and dobutamine-atropine echocardiography was 85% (kappa = 0.70). With regards to regional analysis, concordance was good (93% for segments, kappa = 0.76; and 95% for coronary arteries, kappa = 0.92). Major complications were more frequent during dobutamine-atropine (n = 7) than during dipyridamole infusion (n = 2) (p = 0.06). CONCLUSIONS: Dobutamine-atropine and dipyridamole echocardiography have a similar sensitivity and a higher specificity than that obtained by exercise ECG for the diagnosis of coronary artery disease. Similar information is obtained with dipyridamole and dobutamine-atropine echocardiography. It is our thought that pharmacologic stress echocardiography should be used as a first-step test to rule out coronary artery disease in patients not capable of exercising.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_diagnostic_use_MeSH Anti-Arrhythmia_Agents_diagnostic_use_MeSH M_Atropine_MeSH S_adverse_effects_MeSH Atropine_adverse_effects_MeSH S_diagnostic_use_MeSH Atropine_diagnostic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Coronary_Vessels_MeSH S_physiopathology_MeSH Coronary_Vessels_physiopathology_MeSH S_ultrasonography_MeSH Coronary_Vessels_ultrasonography_MeSH M_Dipyridamole_MeSH S_adverse_effects_MeSH Dipyridamole_adverse_effects_MeSH S_diagnostic_use_MeSH Dipyridamole_diagnostic_use_MeSH M_Dobutamine_MeSH S_adverse_effects_MeSH Dobutamine_adverse_effects_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH P_Echocardiography_MeSH M_Electrocardiography_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sensitivity_and_Specificity_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 8916473
----K E
----T Efficacy and safety of procainamide in preventing arrhythmias after coronary artery bypass surgery.
----A Arrhythmias are common after cardiac surgery and are associated with hemodynamic compromise, stroke, and prolonged hospitalization. Beta blockers prevent atrial fibrillation postoperatively, but there are few data regarding the prophylactic use of type 1 antiarrhythmic agents or the prevention of ventricular arrhythmias. Accordingly, we performed a randomized, double-blind, placebo-controlled study of the effects of oral procainamide on 100 patients undergoing elective coronary artery bypass surgery. Procainamide was received for 4 days; the dosage was adjusted for body weight. Patients receiving procainamide had a significant reduction in atrial fibrillation (16 vs 29 patient-days, p < 0.05) and ventricular tachycardia (2% vs 20%, p < 0.01). However, the incidence of atrial fibrillation was not significantly reduced (38% vas 26%). In the group achieving therapeutic serum procainamide levels, there was reduction in all measured postoperative arrhythmias. No serious cardiac or noncardiac adverse events were noted during procainamide therapy, although there was a significant increase in the incidence of nausea. We conclude that procainamide reduces arrhythmias in the early postoperative period after coronary artery bypass surgery, most prominently in patients who achieve therapeutic serum levels. This was associated with no serious cardiac adverse reactions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nausea_MeSH S_chemically_induced_MeSH Nausea_chemically_induced_MeSH M_Postoperative_Complications_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Procainamide_MeSH S_adverse_effects_MeSH Procainamide_adverse_effects_MeSH S_therapeutic_use_MeSH Procainamide_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Ventricular_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Treatment_Outcome_MeSH 
****** 8916563
----K E
----T Divalproex sodium in headache: literature review and clinical guidelines.
----A Divalproex sodium is an anticonvulsant agent approved for use either alone or in combination with other antiepileptic drugs for simple and complex absences seizures and mania. Four double-blind placebo-controlled studies have confirmed that divalproex sodium/valproate is an effective migraine treatment. In all of the clinical studies, whether open, retrospective, or placebo-controlled and double-blind, valproate was an effective preventive treatment for migraine. There was a reduction in the number of migraine attacks, and migraine duration and intensity were also reduced in some instances. It is equally as effective in patients with severe frequent migraines as in those with less severe migraines. In clinical trials, the most frequent adverse events reported by patients treated with divalproex sodium were nausea, asthenia, dyspepsia, dizziness, somnolence, and diarrhea, with most adverse events being mild to moderate in severity.
----P Journal_Article Review Review_Literature 
----M M_Chronic_Disease_MeSH M_Clinical_Trials_MeSH M_Double-Blind_Method_MeSH M_Headache_MeSH S_drug_therapy_MeSH Headache_drug_therapy_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Risk_Factors_MeSH M_Valproic_Acid_MeSH S_adverse_effects_MeSH Valproic_Acid_adverse_effects_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH 
****** 9019639
----K 1
----T [Combination antihypertensive therapy in patients with an increased risk profile]
----A BACKGROUND: Antihypertensive drug combinations have two major advantages: First, dosage of the single components can be reduced, and second, putative side effects can be minimized. Therefore, we analysed in a cohort of patients with multiple cardiovascular risk factors the metabolic effects of two fixed antihypertensive drug combinations. PATIENTS AND METHODS: 225 patients with essential hypertension (dBP > or = 95 < or = 115 mm Hg) and adipositas (BMI 30.6 +/- 2.5) were randomly treated during 6 months with either quinapril and hydrochlorothiazide (HCTZ) or with metoprolol and hydrochlorothiazide. Compared with healthy controls, patients exhibited significant elevated concentrations of triglycerides (226 +/- 86 vs. 146 +/- 73 mg/dl) and fasting insulin (22.2 +/- 1.8 vs. 9.8 +/- 4.6 microU/ml). RESULTS: The antihypertensive effects and the tolerance of both substances were good and comparable after 3 and 6 months. Serum triglycerides increased during metoprolol/hydrochlorothiazide treatment (230 +/- 81 vs. 244 +/- 185 mg/dl; median 174 vs. 204; + 17%), as well as during treatment with quinapril/hydrochlorothiazide (222 +/- 155 vs. 235 +/- 162 mg/dl; median 166 vs. 174; + 5%). Fasting blood glucose levels, insulin, fructosamine, HbA1c and free fatty acids remained unchanged. In a subgroup of 88 postmenopausal women with upper body obesity (WHR > 0.85) treatment with quinapril/hydrochlorothiazide normalized the VLDL-triglyceride/VLDL-cholesterol ratio (3.8 vs. 5.9, p < 0.05), whereas the ratio only increased from 3.6 to 4.2 in the metoprolol/hydrochlorothiazide group. These changes in the ACE-inhibitor group were due to a decrease in VLDL-cholesterol (41.4 +/- 4.2 vs. 33.9 +/- 9.6). CONCLUSION: These data demonstrate that quinapril or metoprolol in combination with hydrochlorothiazide do not differ significantly with regard to their effects on blood-pressure lowering, lipoprotein profile, and glucose metabolism. Only in the subgroup of adipose postmenopausal women, the modulated VLDL-composition might suggest the elimination of atherogenic VLDL-remnants/IDL during quinapril/hydrochlorothiazide treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isoquinolines_MeSH S_adverse_effects_MeSH Isoquinolines_adverse_effects_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH P_Tetrahydroisoquinolines_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 8933239
----K I
----T Comparison of the therapeutic effects of the beta-blocking agent bisoprolol and the calcium-blocking agent diltiazem in patients with heart failure due to dilated cardiomyopathy.
----A Beta-blocking agents reduce mortality and improve symptoms in patients with dilated cardiomyopathy (DCM). There have been reports that diltiazem, a calcium-blocking agent, is also effective in such patients. We prospectively compared the effects of the beta-blocking agent bisoprolol with those of the calcium-blocking agent diltiazem in 18 patients (11 males and 7 females, age 14 to 68) with DCM. The 18 patients, (10 in New York Heart Association functional class III and 8 in class IV) were randomly assigned to 2 groups. Bisoprolol was administered as the first drug in 10 patients and diltiazem was administered in 8. Cross-over to bisoprolol was also performed in 3 patients. At the end of the study, among the 13 patients who had been given bisoprolol, 9 showed a good response (efficacy rate: 69%). In contrast, only 3 of the 8 patients who received diltiazem showed a good response (efficacy rate: 37.5%). Among the patients in NYHA class III, all 7 (100%) who were treated with bisoprolol responded but only 2 of the 4 (50%) treated with diltiazem responded (p < 0.05). Among the patients in class IV, 2 of 6 (33%) responded to bisoprolol and 1 of 4 (25%) responded to diltiazem (not significant). These results suggest that diltiazem, like bisoprolol, has a beneficial effect in patients with DCM, with a greater effect in class III patients. However, we conclude that diltiazem should usually be used as a second choice to improve heart failure in DCM, and as the first medication only in those with contraindications to beta-blocking agents.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Prospective_Studies_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8935302
----K E
----T Ambulatory blood pressure monitoring for evaluation of long-acting beta-blockers in Taiwan.
----A This study attempted to evaluate the efficacy of several "long-acting" antihypertensive agents. One-hundred consecutive hypertensive subjects with normal casual blood pressure after once-daily antihypertensive monotherapy treatment were studied. They were divided into three groups: group A, metoprolol (100 mg, daily); group B, atenolol (100 mg, daily); and group C, nadolol (80 mg, daily). Ambulatory blood pressure monitoring (ABPM) was used to evaluate the efficacy of the antihypertensive agents. The overall average ambulatory blood pressures were within the normal limits for all three groups. However, there were some abnormally high blood pressure (BP) readings shown on ABPM. Patients with an abnormally high systolic blood pressure (SBP) average > 140 mmHg accounted for 16.7% of group A, 19.4% of group B and 20% of group C. Those with an abnormally high diastolic blood pressure (DBP) average > 90 mmHg accounted for 16.7%, 19.4% and 10%, respectively, of the corresponding groups. There were no significant differences in the frequency of abnormally high SBP and DBP among the three groups. These "long-acting" antihypertensive drugs did not effectively control BP throughout the entire day. The duration of antihypertensive effect is not necessarily reflected by the blood half-life of the drug. ABPM is an effective way to ascertain the efficacy of "long-acting" hypertensive agents.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Delayed-Action_Preparations_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Taiwan_MeSH 
****** 8937059
----K E
----T Perioperative myocardial infarction in coronary artery disease patients and 'at-risk' for coronary artery disease patients undergoing non-cardiac surgery.
----A BACKGROUND: Perioperative myocardial infarction (POMI) carries a high mortality and occurs more commonly in patients with a history of coronary artery disease (CAD). However, there are also other patients undergoing surgery who are 'at risk' for CAD but who do not have a history of infarction or angina. We compared the incidence of POMI in these two groups. METHODS: In a prospective study of 69 men and 39 women over 30 years of age undergoing non-cardiac surgery under general or regional anaesthesia, 56 had definite CAD and 52 were 'at-risk' for CAD. All these patients were followed up with serial postoperative electrocardiography and CK-MB isoenzyme analysis for the diagnosis of POMI. RESULTS: The POMI rate was 32% in definite CAD patients and 15% in patients 'at-risk' for CAD. Mortality in patients with POMI was 17% in those with CAD and 13% in those 'at-risk' for CAD. Perioperative myocardial infarction was maximal in the first 24 hours following surgery (77%). All the POMIs were painless. Anaesthesia techniques--whether regional or general--did not influence the incidence of POMI (Chi-square, p > 0.05). The type of drugs used in the treatment of CAD such as beta-blockers, calcium channel blockers and antiplatelet agents did not cause any difference in the incidence of POMI (Chi-square, p > 0.05). Patients who had either an intraoperative hypertensive episode, tachycardia, arrhythmias or ST-segment changes had a higher incidence of POMI (Chi-square, p > 0.05). The incidence of POMI was not lower in patients undergoing transurethral resection of the prostate compared to patients undergoing other types of non-cardiac surgery (Chi-square, p > 0.05). CONCLUSION: POMI occurs in one-third of patients with a history of CAD and one-sixth of those 'at-risk'. It carries a mortality of 17% and 13% respectively. Decisions to operate on such patients should be taken with caution.
----P Journal_Article 
----M M_Aged_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Female_MeSH M_Human_MeSH P_Intraoperative_Complications_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH P_Postoperative_Complications_MeSH M_Prospective_Studies_MeSH P_Surgical_Procedures__Operative_MeSH 
****** 8941104
----K I
----T Double-blind, placebo-controlled study of the effects of carvedilol in patients with moderate to severe heart failure. The PRECISE Trial. Prospective Randomized Evaluation of Carvedilol on Symptoms and Exercise.
----A BACKGROUND: Carvedilol has improved the symptomatic status of patients with moderate to severe heart failure in single-center studies, but its clinical effects have not been evaluated in large, multicenter trials. METHODS AND RESULTS: We enrolled 278 patients with moderate to severe heart failure (6-minute walk distance, 150 to 450 m) and a left ventricular ejection fraction < or = 0.35 at 31 centers. After an open-label, run-in period, each patient was randomly assigned (double-blind) to either placebo (n = 145) or carvedilol (n = 133; target dose, 25 to 50 mg BID) for 6 months, while background therapy with digoxin, diuretics, and an ACE inhibitor remained constant. Compared with placebo, patients in the carvedilol group had a greater frequency of symptomatic improvement and lower risk of clinical deterioration, as evaluated by changes in the NYHA functional class (P = .014) or by a global assessment of progress judged either by the patient (P = .002) or by the physician (P < .001). In addition, treatment with carvedilol was associated with a significant increase in ejection fraction (P < .001) and a significant decrease in the combined risk of morbidity and mortality (P = .029). In contrast, carvedilol therapy had little effect on indirect measures of patient benefit, including changes in exercise tolerance or quality-of-life scores. The effects of the drug were similar in patients with ischemic heart disease or idiopathic dilated cardiomyopathy as the cause of heart failure. CONCLUSIONS: These findings indicate that, in addition to its favorable effects on survival, carvedilol produces important clinical benefits in patients with moderate to severe heart failure treated with digoxin, diuretics, and an ACE inhibitor.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_mortality_MeSH Cardiac_Output__Low_mortality_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Morbidity_MeSH M_Placebos_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 8941105
----K I
----T Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. US Carvedilol Heart Failure Study Group.
----A BACKGROUND: We tested the hypothesis that carvedilol inhibits clinical progression in patients with mildly symptomatic heart failure due to left ventricular (LV) systolic dysfunction. METHODS AND RESULTS: Patients (n = 366) who had mildly symptomatic heart failure with an LV ejection fraction (LVEF) < or = 0.35, had minimal functional impairment (defined as the ability to walk 450 to 550 m on a 6-minute walk test), and were receiving optimal standard therapy, including ACE inhibitors, were randomized double-blind to carvedilol (n = 232) or placebo (n = 134) and followed up for 12 months. The primary end point was clinical progression, defined as death due to heart failure, hospitalization for heart failure, or a sustained increase in heart failure medications. Clinical progression of heart failure occurred in 21% of placebo patients and 11% of carvedilol patients, reflecting a 48% (P = .008) reduction in the primary end point of heart failure progression (relative risk, 0.52; CI, 0.32 to 0.85). This effect of carvedilol was not influenced by sex, age, race, cause of heart failure, or baseline LVEF. Carvedilol also significantly improved several secondary end points, including LVEF, heart failure score, NYHA functional class, and the physician and patient global assessments. Carvedilol reduced all-cause mortality but had no effects on the Minnesota Living With Heart Failure scale, the distance walked in 9 minutes on a self-powered treadmill, or cardiothoracic index. The drug was well tolerated. CONCLUSIONS: Carvedilol, when added to standard therapy, including an ACE inhibitor, reduces clinical progression in patients who are only mildly symptomatic with well-compensated heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_mortality_MeSH Cardiac_Output__Low_mortality_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8941106
----K I
----T Carvedilol produces dose-related improvements in left ventricular function and survival in subjects with chronic heart failure. MOCHA Investigators.
----A BACKGROUND: We conducted a multicenter, placebo-controlled trial designed to establish the efficacy and safety of carvedilol, a "third-generation" beta -blocking agent with vasodilator properties, in chronic heart failure. METHODS AND RESULTS: Three hundred forty-five subjects with mild to moderate, stable chronic heart failure were randomized to receive treatment with placebo, 6.25 mg BID carvedilol (low-dose group), 12.5 mg BID carvedilol (medium-dose group), or 25 mg BID carvedilol (high-dose group). After a 2- to 4-week up-titration period, subjects remained on study medication for a period of 6 months. The primary efficacy parameter was submaximal exercise measured by two different techniques, the 6-minute corridor walk test and the 9-minute self-powered treadmill test. Carvedilol had no detectable effect on submaximal exercise as measured by either technique. However, carvedilol was associated with dose-related improvements in LV function (by 5, 6, and 8 ejection fraction [EF] units in the low-, medium-, and high-dose carvedilol groups, respectively, compared with 2 EF units with placebo, P < .001 for linear dose response) and survival (respective crude mortality rates of 6.0%, 6.7%, and 1.1% with increasing doses of carvedilol compared with 15.5% in the placebo group, P < .001). When the three carvedilol groups were combined, the all-cause actuarial mortality risk was lowered by 73% in carvedilol-treated subjects (P < .001). Carvedilol also lowered the hospitalization rate (by 58% to 64%, P = .01) and was generally well tolerated. CONCLUSIONS: In subjects with mild to moderate heart failure from systolic dysfunction, carvedilol produced dose-related improvements in LV function and dose-related reductions in mortality and hospitalization rate.
----P Clinical_Trial Comment Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_mortality_MeSH Cardiac_Output__Low_mortality_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH M_Chronic_Disease_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 8948517
----K E
----T The benefits of ACE inhibitors and calcium antagonists in slowing progressive renal failure: focus on fixed-dose combination antihypertensive therapy.
----A During the past two decades, major investigative interest has been focused on the determinants of chronic renal disease and interventions to retard the inexorable progression to end-stage renal disease. Recent studies have provided a theoretic framework for anticipating that angiotensin-converting enzyme (ACE) inhibitors, and possibly calcium antagonists, may preferentially retard the progression of renal disease. Whereas the majority of available clinical trials have assessed the effects of ACE inhibitors in patients with insulin-dependent diabetes mellitus (IDDM), there are relatively few long-term studies that have evaluated the renal protective effects of ACE inhibitors and calcium antagonists in patients with nondiabetic renal disease. Although clinical trials have been initiated using both of these drug classes as monotherapy, theoretical considerations suggest that fixed-dose combinations of an ACE inhibitor and a calcium antagonist might be appealing as renal protective agents. Several lines of evidence suggest that the renal microcirculatory effects of coadministration of both agents should be complementary. Similarly, recent observations suggest that the two classes may act in a complementary manner to countervail pathogenetic mechanisms at the level of the mesangium. A recent study in type II diabetic patients demonstrated that combination therapy with an ACE inhibitor and a calcium antagonist induced the greatest reduction in proteinuria, and reduced the rate of decline in glomerular filtration rate (GFR) more than did either agent alone at the same level of blood pressure reduction. Based on such considerations, recent randomized prospective studies have been initiated to compare the renal protective effects of combination calcium antagonist-ACE inhibitor therapy versus monotherapy with agents of either of these two antihypertensive classes.
----P Journal_Article Review Review__Academic 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_I_MeSH S_complications_MeSH Diabetes_Mellitus__Type_I_complications_MeSH M_Disease_Progression_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Prognosis_MeSH 
****** 8960472
----K E
----T Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators.
----A BACKGROUND: Unsustained ventricular tachycardia in patients with previous myocardial infarction and left ventricular dysfunction is associated with a two-year mortality rate of about 30 percent. We studied whether prophylactic therapy with an implanted cardioverter-defibrillator, as compared with conventional medical therapy, would improve survival in this high-risk group of patients. METHODS: Over the course of five years, 196 patients in New York Heart Association functional class I, II, or III with prior myocardial infarction; a left ventricular ejection fraction < or = 0.35; a documented episode of asymptomatic unsustained ventricular tachycardia; and inducible, nonsuppressible ventricular tachyarrhythmia on electrophysiologic study were randomly assigned to receive an implanted defibrillator (n = 95) or conventional medical therapy (n=101). We used a two-sided sequential design with death from any cause as the end point. RESULTS: The base-line characteristics of the two treatment groups were similar. During an average follow-up of 27 months, there were 15 deaths in the defibrillator group (11 from cardiac causes) and 39 deaths in the conventional-therapy group (27 from cardiac causes) (hazard ratio for overall mortality, 0.46; 95 percent confidence interval, 0.26 to 0.82; P=0.009). There was no evidence that amiodarone, beta-blockers, or any other antiarrhythmic therapy had a significant influence on the observed hazard ratio. CONCLUSIONS: In patients with a prior myocardial infarction who are at high risk for ventricular tachyarrhythmia, prophylactic therapy with an implanted defibrillator leads to improved survival as compared with conventional medical therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH P_Defibrillators__Implantable_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH 
****** 8960842
----K E
----T Hypertension in Diabetes Study IV. Therapeutic requirements to maintain tight blood pressure control.
----A We report the efficacy of therapy over 5 years follow-up in 758 non-insulin-dependent diabetic patients in a prospective, randomised controlled study of therapy of mild hypertension. Patients were recruited who on antihypertensive therapy had systolic blood pressure over 150 mmHg or diastolic over 85 mmHg, or if not on therapy had systolic blood pressure over 160 mmHg or diastolic over 90 mmHg. Their mean blood pressure at entry to the study was 160/94 mmHg at a mean age of 57 years. They were allocated to tight control (aiming for systolic < 150/diastolic < 85 mmHg) or to less tight control (aiming for systolic < 180/diastolic < 105 mmHg). The tight control group were allocated to primary therapy either with a beta blocker (atenolol) or with an antiotensin converting enzyme inhibitor (captopril), with addition of other agents as required. Over 5 years, the mean blood pressure in the tight control group was significantly lower (143/82 vs 154/88 mmHg, p < 0.001). No difference was seen between those allocated to atenolol or captopril. The proportion of patients requiring three or more antihypertensive therapies to maintain tight control in those allocated to atenolol or captopril increased from 16 and 15%, respectively at 2 years to 25 and 26%, respectively at 5 years, whereas in the less tight control group at 2 and 5 years only 5 and 7%, respectively required three or more therapies. There was no difference in the incidence of side effects or hypoglycaemic episodes between those allocated to atenolol or captopril, but those allocated to atenolol increased their body weight by a mean of 2.3 kg compared with 0.5 kg in those allocated to captopril (p < 0.01). Allocation to atenolol was also associated with small increases in triglyceride, and decreases in LDL and HDL cholesterol, which are of uncertain clinical relevance. The study is continuing to determine whether the improved blood pressure control, which was obtained, will be beneficial in maintaining the health of patients by decreasing the incidence of major clinical complications, principally myocardial infarction and strokes, and microvascular complications, such as severe retinopathy requiring photocoagulation and deterioration of renal function.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Electrolytes_MeSH S_blood_MeSH Electrolytes_blood_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypoglycemia_MeSH S_epidemiology_MeSH Hypoglycemia_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH 
****** 8960851
----K E
----T Renal and metabolic effects of 1-year treatment with ramipril or atenolol in NIDDM patients with microalbuminuria.
----A The clinical importance of selection of different antihypertensive drugs for the treatment of diabetic patients is still unclear. Thus we performed a randomised, controlled study in 105 hypertensive non-insulin-dependent diabetic (NIDDM) patients with microalbuminuria over 1 year. Patients received either the angiotensin converting enzyme (ACE) inhibitor ramipril (2.5-5.0 mg/day; in addition 24% of patients also received felodipine) or the beta blocking agent atenolol (50-100 mg/day; in addition 24% of patients also received hydrochlorothiazide). Blood pressure, metabolic control, lipid levels and albumin excretion rate were studied during the follow-up. After 1 year an almost identical fall (p < 0.001) in blood pressure was observed with ramipril (170/100 vs 150/ 85 mmHg, median) and atenolol (180/100 vs 150/ 80 mmHg, median). With ramipril a reduction of total cholesterol (6.3 vs 5.9 mmol/l), of LDL cholesterol (3.8 vs 3.6 mmol/l) and HDL cholesterol (1.3 vs 1.2 mmol/l) was found, whereas triglycerides slightly increased (1.8 vs 2.0 mmol/l). With atenolol a similar reduction of total cholesterol (6.3 vs 5.9 mmol/l), LDL cholesterol (3.8 vs 3.7 mmol/l) and HDL cholesterol (1.4 vs 1.2 mmol/l) and an increase of triglycerides (1.4 vs 1.7 mmol/l) was noted. Metabolic control of the patients was maintained with both ramipril and atenolol treatment. With ramipril treatment urinary albumin creatinine ratio (14.4 vs 13.8 mg/mmol) and creatinine clearance (82 vs 84 ml/min) were constant, but with atenolol an increase of albumin creatinine ratio (13.9 vs 19 mg/mmol, p < 0.001) and a slight decrease of creatinine clearance (80 vs 66 ml/min, p < 0.05, not significant after Bonferroni correction) was observed. In conclusion: 1-year treatment of NIDDM patients with ramipril or atenolol does not influence metabolic control, the changes in serum lipids were similar. Despite almost identical blood pressure reduction in both groups the albumin creatinine ratio was constant under ramipril, but increased under atenolol treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Albuminuria_MeSH S_drug_therapy_MeSH Albuminuria_drug_therapy_MeSH S_metabolism_MeSH Albuminuria_metabolism_MeSH S_physiopathology_MeSH Albuminuria_physiopathology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_metabolism_MeSH Creatinine_metabolism_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_metabolism_MeSH Diabetes_Mellitus__Type_II_metabolism_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Nephropathies_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH S_metabolism_MeSH Diabetic_Nephropathies_metabolism_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_pharmacology_MeSH Felodipine_pharmacology_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_metabolism_MeSH Kidney_metabolism_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9005172
----K 1
----T [Hypertension secondary to multiple malignant paragangliomas]
----A We describe a case of severe hypertension, due to multiple malignant norepinephrine secreting paragangliomas. Neuroendocrine system tumours are responsible for 0.1-0.5% cases of hypertension. Their extra-adrenal localisation is about 10%. Only 20% of paragangliomas are catecholamine secreting, and causing a syndrome similar to that of pheochromocytoma. In our patient the diagnosis of retroperitoneal multiple paragangliomas was made two years after the beginning of the typical symptoms. At surgery 6 paragangliomas were removed; some vascular and muscular structures (inferior vena cava, ileopsoas) were infiltrated. A radiotherapy treatment was conducted for a total dose of 55.8 Gy. Immediately after the operation blood pressure decreased, but the administration of alpha and beta blockers was required to reach normotension. This treatment was confirmed at six months follow-up, in consideration of the persistently high norepinephrine plasma levels.
----P Case_Reports Journal_Article 
----M M_Adult_MeSH M_Combined_Modality_Therapy_MeSH M_English_Abstract_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Male_MeSH P_Neoplasms__Multiple_Primary_MeSH S_radiotherapy_MeSH Neoplasms__Multiple_Primary_radiotherapy_MeSH S_surgery_MeSH Neoplasms__Multiple_Primary_surgery_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH S_secretion_MeSH Norepinephrine_secretion_MeSH M_Paraganglioma__Extra-Adrenal_MeSH S_complications_MeSH Paraganglioma__Extra-Adrenal_complications_MeSH S_radiotherapy_MeSH Paraganglioma__Extra-Adrenal_radiotherapy_MeSH S_surgery_MeSH Paraganglioma__Extra-Adrenal_surgery_MeSH M_Radiotherapy_Dosage_MeSH M_Retroperitoneal_Neoplasms_MeSH S_complications_MeSH Retroperitoneal_Neoplasms_complications_MeSH S_radiotherapy_MeSH Retroperitoneal_Neoplasms_radiotherapy_MeSH S_surgery_MeSH Retroperitoneal_Neoplasms_surgery_MeSH M_Time_Factors_MeSH 
****** 9082680
----K E
----T [Value of beta-blocker therapy in treatment of coronary heart disease and sudden cardiac death with special reference to carvedilol]
----A Beta-blocking agents are well established in the treatment of patients with coronary artery disease. Synergistic effects on mortality, myocardial ischemia, the risk for myocardial (re-)infarction and, as most recently shown, on sudden cardiac death form the basis for the convincing prognostic impact of these agents. The present paper is directed to summarize the clinical evidence for the therapeutic benefit of beta-blocking agents in post-infarction patients, to characterize subgroups of patients who will benefit most from such a therapeutic intervention and to discuss the present impact of newer beta-blocking agents, such as carvedilol which beside its effects on beta-1 and beta-2 receptors exerts potent vasodilating properties via an alpha-1 receptor blockade.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_English_Abstract_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Survival_Rate_MeSH 
****** 8968014
----K I
----T Effect of diuretic-based antihypertensive treatment on cardiovascular disease risk in older diabetic patients with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group.
----A OBJECTIVE: To assess the effect of low-dose, diuretic-based antihypertensive treatment on major cardiovascular disease (CVD) event rates in older, non-insulin-treated diabetic patients with isolated systolic hypertension (ISH), compared with nondiabetic patients. DESIGN: Double-blind, randomized, placebo-controlled trial: the Systolic Hypertension in the Elderly Program (SHEP). SETTING: Multiple clinical and support centers in the United States. PARTICIPANTS: A total of 4736 men and women aged 60 years and older at baseline with ISH (systolic blood pressure [BP], > or = 160 mm Hg; diastolic BP, <90 mm Hg) at baseline, 583 non-insulin-dependent diabetic patients and 4149 nondiabetic patients (4 additional patients not so classifiable were randomized but not included in these analyses). Diabetes mellitus defined as physician diagnosis, taking oral hypoglycemic drugs, fasting glucose level of 7.8 mmol/L or more (> or = 140 mg/dL), or any combination of these characteristics. INTERVENTION: The active treatment group received a low dose of chlorthalidone (12.5-25.0 mg/d) with a step-up to atenolol (25.0-50.0 mg/d) or reserpine (0.05-0.10 mg/d) if needed. The placebo group received placebo and any active antihypertensive drugs prescribed by patient's private physician for persistently high BP. MAIN OUTCOME MEASURES: The 5-year rates of major CVD events, nonfatal plus fatal stroke, nonfatal myocardial infarction (MI) and fatal coronary heart disease (CHD), major CHD events, and all-cause mortality. RESULTS: The SHEP antihypertensive drug regimen lowered BP of both diabetic and nondiabetic patients, with few adverse effects. For both diabetic and nondiabetic patients, all outcome rates were lower for participants randomized to the active treatment group than for those randomized to the placebo group. Thus, 5-year major CVD rate was lower by 34% for active treatment compared with placebo, both for diabetic patients (95% confidence interval [CI], 6%-54%) and nondiabetic patients (95% CI, 21%-45%). Absolute risk reduction with active treatment compared with placebo was twice as great for diabetic vs nondiabetic patients (101/1000 vs 51/1000 randomized participants at the 5-year follow-up), reflecting the higher risk of diabetic patients. CONCLUSION: Low-dose diuretic-based (chlorthalidone) treatment is effective in preventing major CVD events, cerebral and cardiac, in both non-insulin-treated diabetic and nondiabetic older patients with ISH.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Dementia_MeSH M_Depression_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 8970416
----K E
----T Hemodynamic effects of the class III antiarrhythmic drug, d-sotalol, in patients with congestive heart failure.
----A In contrast to Vaughan Williams class I drugs, class III drugs, such as d-sotalol, may not be negative inotropic. These drugs block potassium ion channels and prolong repolarization, theoretically leading to improved contractility. We investigated the hemodynamic actions of acute intravenous administration of 1.5 mg/kg of d-sotalol in 28 patients with congestive heart failure randomized to receive placebo (n = 10) or active drug (n = 18) in a double-blind study. A Swan-Ganz catheter was placed in all patients > or = 16 hours before drug administration. All hemodynamic variables were assessed at baseline and 30 minutes and 1, 2, 4, 8, and 12 hours after administration of the drug. Electrocardiograms were obtained before and 1, 2, 4, and 12 hours after drug administration. The QT interval increased from 370 +/- 9 to 426 +/- 14 ms at 1 hour, whereas the QTc increased from 433 +/- 5 to 470 +/- 12 ms (both p < 0.001). The increase was still statistically significant at 12 hours. There was no change in the placebo group. Although heart rate decreased in the d-sotalol group (84 +/- 2 to 76 +/- 2 at 1 hour, p < 0.001), there were no changes in blood pressure or right atrial pressure. Cardiac index decreased slightly (2.0 +/- 0.2 to 1.9 +/- 0.1 mm Hg), consistent with the lower heart rate. Pulmonary capillary wedge pressure decreased from 18.9 +/- 2.4 to 17.9 +/- 1.9 mm Hg at 1 hour despite reduced cardiac index. We conclude that in contrast to class I, II, and IV antiarrhythmic drugs, d-sotalol exerts no clinically important acute hemodynamic actions at doses that produce electrophysiologic effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_blood_MeSH Anti-Arrhythmia_Agents_blood_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sotalol_MeSH S_blood_MeSH Sotalol_blood_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 8972892
----K I
----T The effects of replacing beta-blockers with an angiotensin converting enzyme inhibitor on the quality of life of hypertensive patients.
----A The aim was to evaluate the effects of a change of treatment from beta-blocker to captopril on the quality of life of hypertensive patients. One hundred forty-nine mild to moderate hypertensive patients who were being treated with beta-blockers were randomly assigned to receive captopril (12.5 to 50 mg twice daily), or to continue on beta-blocker treatment (atenolol: 25 to 100 mg once daily [n = 121], or propranolol, 10 to 80 mg twice daily [n = 12]). When required, 25 mg hydrochlorothiazide was added in each group. The patients were followed over periods ranging from 6 to 12 months. Blood pressure, treatment side effects, and quality of life were monitored. Blood pressure was equally well managed in both groups, though a lower level of treatment was required in the captopril group. The captopril treated patients exhibited favorable changes in several aspects of quality of life: sleep-related, gastrointestinal, and physical activity-related symptoms improved from baseline to end of follow-up. Drowsiness and the ability to concentrate significantly improved in the captopril group only (P <.01). Change in treatment from beta-blocker to captopril resulted in equally well controlled blood pressure on a lower drug dose. Moreover, the change to captopril had a positive impact on the quality of life.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH 
****** 8973428
----K 3
----T Randomised trial of nadolol alone or with isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis. Gruppo-Triveneto per L'ipertensione portale (GTIP)
----A BACKGROUND: The risk of having a first cirrhosis-associated variceal bleed is lowered by about 50% by beta-blockers. Use of beta-blockers is currently recommended for patients with cirrhosis and oesophageal varices that are at risk of bleeding. We aimed to test the effectiveness of isosorbide mononitrate as an adjunct to the beta-blocker nadolol in the prophylaxis of first variceal bleeding in these patients. METHODS: We did a randomised multicentre study to compare the non-selective beta-blocker, nadolol, with nadolol plus isosorbide mononitrate in 146 relatively well (Child-Pugh score < or = 11) patients who had oesophageal varices at risk of bleeding. Patients on nadolol alone received a single oral 40 mg daily dose. Every second day the dose was titrated to achieve 20-25% decrease in resting heart rate (maximum dose 160 mg daily). Patients receiving both drugs received nadolol as above then isosorbide mononitrate was added starting with 10 mg orally twice daily, which was increased to 20 mg unless hypotension or severe headache occurred. The main endpoint was the occurrence of variceal bleeding of any severity. Patients were followed up for up to 40 months. FINDINGS: During the study period 11 of 74 patients from the nadolol alone group and four of 72 from the nadolol plus isosorbide mononitrate group had variceal bleeding (log-rank test p = 0.03). Cumulative risk of variceal bleeding was 18% in the nadolol group and 7.5% in the combined treatment group (95% CI for difference 1-25%). Two patients in each group had a non-variceal bleed related to portal hypertension. 14 patients from the nadolol only group and eight from the combined treatment group died during the study period (log-rank test p = 0.09). Four and eight patients, respectively, had to discontinue one of the drugs because of side-effects. INTERPRETATION: Nadolol plus isosorbide mononitrate is significantly more effective than nadolol alone in the primary prophylaxis of variceal bleeding in relatively well patients with cirrhosis, and has few side-effects.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_administration_&_dosage_MeSH Nadolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Nadolol_adverse_effects_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Regression_Analysis_MeSH M_Risk_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 8973753
----K E
----T Effects of bunazosin and atenolol on serum lipids and apolipoproteins in a randomised trial.
----A The effects of bunazosin and atenolol on serum lipids and lipoproteins after 6 months of treatment were compared in this multicentric, double-blind, randomised trial. A total of 174 patients with mild to moderate essential hypertension from 15 hospitals in Germany and Poland was included in the study. Eighty-seven were treated with the alpha-receptor blocker bunazosin and the same number with the beta-blocker atenolol. Systolic and diastolic blood pressure decreased significantly in both groups, whereas only atenolol decreased pulse rate. In the bunazosin group HDL-cholesterol was significantly increased after 6 months of treatment, whereas all other analysed parameters remained unchanged. In the atenolol group total cholesterol, LDL-cholesterol, total triglycerides, apolipoprotein E, VLDL-cholesterol and VLDL-triglycerides were significantly increased after 6 months of therapy. There was a significant difference between bunazosin and atenolol for total cholesterol, HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides, VLDL-triglycerides and apolipoprotein B levels. As a consequence, there was a significant difference in the atherogenic index of both groups. We conclude that bunazosin is favorable in the treatment of high blood pressure, because the coronary risk is not negatively influenced as shown for atenolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Apolipoproteins_MeSH S_blood_MeSH Apolipoproteins_blood_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Quinazolines_MeSH S_administration_&_dosage_MeSH Quinazolines_administration_&_dosage_MeSH M_Treatment_Outcome_MeSH 
****** 8973780
----K E
----T Prevalence of carotid atherosclerosis in hypertension: preliminary baseline data from the European Lacidipine Study on Atheroscelerosis (ELSA).
----A In the ELSA trial, the effects of lacidipine-based treatment and beta-blocker (atenolol)-based treatment on the development and progression of carotid wall alterations are assessed in hypertensive patients. The primary endpoint of this study is the rate of change in the intima-media thickness of the carotid artery wall, measured with B-mode ultrasound. About 2300 hypertensive patients have been recruited and randomized to either of the antihypertensive agents. Baseline data for 1965 patients are available, showing a high prevalence of carotid wall lesions: about 82% of the subjects have an intima-media thickness > or = 1.3 mm, defined as plaque in the ELSA protocol; 16% of the subjects have intima-media thickening (> or = 1.0 mm, < 1.3 mm) and only about 1% have normal carotid artery walls. Analysis of demographic data and risk factor prevalence in ELSA patients, and comparison of these preliminary observations with data from other intervention or observational studies indicate that high blood pressure is a very important risk factor for carotid atherosclerosis.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteriosclerosis_MeSH S_etiology_MeSH Arteriosclerosis_etiology_MeSH M_Carotid_Artery_Diseases_MeSH S_etiology_MeSH Carotid_Artery_Diseases_etiology_MeSH M_Dihydropyridines_MeSH S_adverse_effects_MeSH Dihydropyridines_adverse_effects_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Europe_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH 
****** 8973986
----K E
----T A cardiologist's perspective on evolving concepts in the management of congestive heart failure.
----A The conceptual framework for treatment of congestive heart failure has changed dramatically in the past 30 years. The 1950s and 1960s were characterized by manipulation of the left ventricular function curve by digitalis and diuretics. The 1970s focused on relief of symptoms by afterload reduction with vasodilators. Then stimulation of cardiac output with inotropes was shown to relieve symptoms, but patients died sooner. Now the focus is on the neurohumeral milieu and methods to counteract excess renin-angiotensin and sympathetic nervous system stimulation. Angiotensin-converting enzyme inhibitors are the drugs of choice because they also improve survival, but beta-blockers are becoming popular. The effect of molecular cardiology on practice guidelines for congestive heart failure is yet to be seen.
----P Journal_Article Review Review__Tutorial 
----M M_Clinical_Trials_MeSH M_Drug_Therapy_MeSH S_trends_MeSH Drug_Therapy_trends_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH 
****** 8973991
----K E
----T No effect of high-protein food on the stereoselective bioavailability and pharmacokinetics of verapamil.
----A The effects of high-protein food on the bioavailability of both the racemate and individual enantiomers of verapamil were investigated in 12 healthy volunteers using a randomized crossover design. Food had no effect on any parameter of bioavailability for both the racemate and the individual enantiomers of verapamil except time to maximum concentration (tmax), which was significantly prolonged after food intake. The pharmacokinetics of the enantiomers of norverapamil were not significantly changed by food intake. These results suggest that high-protein food does not alter the pharmacokinetics and bioavailability of either the racemate or the individual enantiomers of verapamil. Therefore, the clinical efficacy of verapamil is not related to food intake, except for a slight prolongation in the time to onset of the pharmacologic effects. The present data can be applied to the high-protein content meal intake.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adult_MeSH M_Biological_Availability_MeSH M_Calcium_Channel_Blockers_MeSH S_blood_MeSH Calcium_Channel_Blockers_blood_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH M_Chromatography_MeSH S_methods_MeSH Chromatography_methods_MeSH M_Cross-Over_Studies_MeSH M_Dietary_Proteins_MeSH S_pharmacology_MeSH Dietary_Proteins_pharmacology_MeSH M_Drug_Interactions_MeSH M_Female_MeSH M_Food_MeSH M_Human_MeSH M_Male_MeSH M_Stereoisomerism_MeSH M_Verapamil_MeSH S_analogs_&_derivatives_MeSH Verapamil_analogs_&_derivatives_MeSH S_blood_MeSH Verapamil_blood_MeSH S_pharmacokinetics_MeSH Verapamil_pharmacokinetics_MeSH 
****** 8985266
----K E
----T Beta-adrenergic antagonists in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis.
----A A meta-analysis of 12 selected randomized trials was performed to assess the efficacy of beta-blockers in the prevention of rebleeding and the effect on long-term survival in patients with cirrhosis. Five end points were assessed: rebleeding, variceal rebleeding, death, death from bleeding, and adverse events. Analyses were performed according to the intention-to-treat method. For each end point, heterogeneity and treatment efficacy were assessed by the Der Simonian and Peto methods. When a significant difference was observed, sensitivity analyses were performed by successive stratifications according to treatment duration, cause of initial bleeding, use of placebo, type of beta-blocker, type of publication, certainty of randomization, severity of cirrhosis, interval between index bleed and randomization, and methodological quality. Beta-blockers significantly increased the mean percentage of patients free of rebleeding (21% mean improvement rate, CI 95%: 10%-32%, P < .001, relative risk 1.42), the mean percentage of patients free of variceal rebleeding (20% mean improvement rate, CI 95%: 11%-28%, P < .001), the mean survival rate (5.4% mean improvement rate, CI 95%: 0%-11%, P = .05, relative risk 1.27), the mean percentage of patients free of bleeding death (7.4%, CI 95%: 2%-13%, P < .01, relative risk 1.50). Five patients would need to be treated with beta-blockers to prevent one rebleeding episode, 14 treated to prevent one death, and 13 treated to prevent one death from bleeding. There was no significant heterogeneity among studies by both methods of analysis. In patients with esophageal varices, beta-blockers significantly increase the mean percentage of patients free of rebleeding and the mean survival rate at 2 years.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Survival_Rate_MeSH 
****** 8986932
----K E
----T Insulin sensitivity following treatment with the alpha 1-blocker bunazosin retard and the beta 1-blocker atenolol in hypertensive non-insulin-dependent diabetes mellitus patients.
----A OBJECTIVE: To compare the effects of the alpha 1-blocker bunazosin retard and the beta 1-blocker atenolol (Uniloc) on insulin sensitivity and glucose and lipid homeostasis in patients with type-2 diabetes and hypertension. METHODS: Patients with controlled type-2 diabetes (non-insulin-dependent diabetes mellitus), treated by diet or oral sulphonylurea derivatives, and with mild-to-moderate hypertension were include in a randomized, parallel group, double-blind, multicentre study. After a single-blind placebo run-in period lasting 4-6 weeks, the patients were treated either with bunazosin retard or with atenolol for a further 16 weeks including an initial dose titration period to achieve blood pressure control. Treatment involved 3, 6 or 12 mg bunazosin retard tablets or 25, 50 or 100 mg atenolol tablets, administered orally once a day and prescribed according to blood pressure response. The euglycaemic hyper-insulinaemic clamp technique was used to assess insulin sensitivity both after the placebo period and after the active treatment. A total of 95 patients was enrolled in the study (placebo phase). Forty-eight patients were withdrawn from the placebo phase, mainly due to their blood pressures being outside the required range (seated diastolic blood pressure 90-114 mmHg) and 47 patients were allocated randomly to active treatment. Of these, 23 were administered bunazosin retard and 24 atenolol. All evaluations were on an intention-to-treat basis. RESULTS: Insulin sensitivity assessed as glucose utilization during the clamp was significantly higher following bunazosin retard compared with following atenolol administration (3.52 +/- 0.27 versus 2.86 +/- 0.19 units of metabolic clearance rate of glucose index, P < 0.05). The insulin level attained during clamps (infusion rate 56 mU/m2 per min) was higher (P < 0.05) following atenolol (117 +/- 5 mU/l) than it was following bunazosin retard administration (102 +/- 5) or placebo (108 +/- 3), possibly due to an impaired insulin clearance. Compared with placebo, atenolol treatment resulted in significantly increased glucosylated haemoglobin whereas bunazosin retard had no significant effect. The two drugs did not show any consistent differences in lipid profile or fibrinogen and plasminogen activator inhibitor 1 levels. During the study seven serious adverse events were reported and one was reported shortly after completion of the study. All except one were classified as not related to the study drug and five of them occurred during placebo treatment. The non-serious side effects were in general considered to be either unrelated to the test drugs or expected effects of the two respective drug classes. Both bunazosin retard and atenolol displayed acceptable safety profiles. CONCLUSION: Bunazosin retard treatment in hypertensive non-insulin-dependent diabetes mellitus patients appears to be associated with a slightly higher insulin sensitivity than is atenolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Insulin_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Quinazolines_MeSH S_adverse_effects_MeSH Quinazolines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinazolines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 8988452
----K E
----T Efficacy of treatment with trazodone in combination with pindolol or fluoxetine in major depression.
----A Fluoxetine, a selective serotonin (5-HT) reuptake inhibitor (SSRI), and trazodone, a heterocyclic antidepressant, are effective in the treatment of major depression and treatment resistant depression (TRD). Chronic treatment with both drugs causes increases in extracellular 5-HT through 5-HT reuptake inhibition and desensitization of inhibitory 5-HT1A autoreceptors. It has been shown that pindolol, a serotonin (5-HT)1A-receptor antagonist, may shorten the latency of onset of SSRIs in depression. The aim of the present study was to examine whether pindolol may increase the efficacy of a subtherapeutical dosage of trazodone in the treatment of major depression and TRD, defined according to the Thase and Rush criteria (1995). Thirty-three major depressed inpatients of whom 26 with TRD participated in this study. Ten days after hospitalization, treatment with trazodone 100 mg/day was started. After 1 week trazodone treatment, patients were randomized-using a double blind placebo controlled design-to receive trazodone 100 mg/day+placebo; trazodone 100 mg/day+pindolol 7.5 mg/day: or trazodone 100 mg/day+fluoxetine 20 mg/day and treated during 4 weeks. The 17-item Hamilton Depression Rating Scale (HDRS) was used as outcome measure. It was found that trazodone+pindolol was as effective as trazodone+fluoxetine in the treatment of major depression and TRD and significantly more effective than trazodone+placebo. Using an outcome measure of 50% reduction in the HDRS, we found that 72.5% of the depressed patients treated with trazodone+pindolol and 75% of depressed patients treated with trazodone+fluoxetine showed a clinically significant response compared with 20.0% of trazodone+placebo-treated patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antidepressive_Agents__Second-Generation_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents__Second-Generation_administration_&_dosage_MeSH S_adverse_effects_MeSH Antidepressive_Agents__Second-Generation_adverse_effects_MeSH M_Comparative_Study_MeSH M_Depressive_Disorder_MeSH S_diagnosis_MeSH Depressive_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH S_psychology_MeSH Depressive_Disorder_psychology_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_administration_&_dosage_MeSH Fluoxetine_administration_&_dosage_MeSH S_adverse_effects_MeSH Fluoxetine_adverse_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Personality_Inventory_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH M_Serotonin_Antagonists_MeSH S_administration_&_dosage_MeSH Serotonin_Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Antagonists_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Trazodone_MeSH S_administration_&_dosage_MeSH Trazodone_administration_&_dosage_MeSH S_adverse_effects_MeSH Trazodone_adverse_effects_MeSH 
****** 8994285
----K I
----T Prevention of recurrent esophageal bleeding and survival in patients with alcoholic cirrhosis: a randomized study.
----A OBJECTIVES: To compare endoscopic sclerotherapy, propranolol and distal splenorenal shunt in the prevention of rebleeding esophageal varices and mortality in alcoholic cirrhotics. METHODS: Forty-three alcoholic cirrhotics that had bled from esophageal varices were randomized to sclerotherapy (13), shunt (15) or propranolol(15). Outcomes measured were rebleeding from varices and death. RESULTS: There was no significant difference between the three treatment groups in relation to rebleeding rate or death. Continued alcohol consumption did not influence outcome. CONCLUSIONS: All three therapies were equally effective in preventing rebleeding from varices.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Liver_Cirrhosis__Alcoholic_MeSH S_complications_MeSH Liver_Cirrhosis__Alcoholic_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH P_Splenorenal_Shunt__Surgical_MeSH M_Survival_Analysis_MeSH 
****** 9004102
----K E
----T Long-term effects of losartan on blood pressure and left ventricular structure in essential hypertension.
----A In a 12-week, randomized, double-blind study, 24 patients with essential hypertension were given the angiotensin II antagonist losartan, or the beta-adrenoceptor blocker atenolol. Both drugs reduced blood pressure (BP) well, but losartan tended to reduce left ventricular mass (LVM) in contrast to atenolol. Following the double-blind phase 19 patients entered an open treatment period with losartan and additional treatment if BP was uncontrolled. LV structures were measured by echocardiography. The mean follow-up period was 29 +/- 2.6 (range 26-32) months. BP was reduced from 155.6 +/- 15.6/103.4 +/- 5.2 mm Hg to 131.3 +/- 10.5/82.7 +/- 3.3 mm Hg (P < 0.001). LV internal diameter was reduced (50.7 +/- 4.5 to 49.1 +/- 4.0 mm; P = 0.006), while there was an increase in interventricular septal thickness (10.2 +/- 1.1 to 11.2 +/- 1.3 mm; P = 0.001) and posterior wall thickness (10.0 +/- 0.9 to 10.6 +/- 1.1 mm; P = 0.023). Calculated LVM was not significantly altered during the follow-up period. In conclusion, losartan is effective in reducing BP during long-term treatment. No significant effect on LVM was observed, but there was an increase in LV wall thickness.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Imidazoles_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 9008243
----K E
----T Reduction in drug requirements for hypertension by means of a cognitive-behavioral intervention.
----A The purpose of the present study was to test the effectiveness of a cognitive-behavioral intervention as an adjunctive treatment of hypertension. To qualify for the study, subjects had to have an unmedicated clinic diastolic blood pressure > or = 95 mm Hg. After qualification, minimal drug requirements were established using a diuretic and a beta-blocker to control blood pressure at < or = 90 mm Hg. Subjects were then randomized into a 6-week cognitive-behavioral intervention or a measurements-only control group. After the treatment phase, medication levels were reduced in all subjects by means of a systematic stepdown procedure. Subjects were followed for 1 year after the stepdown was completed. Addition of the cognitive-behavioral intervention was twice as effective as the control procedure in reducing drug requirements. At 12-months follow-up, 73% of the treatment group were at lower levels of medication than at the time of randomization, compared to 35% in the control group. Moreover, 55% of the treatment group remained completely free of medication, compared to 30% of the control group, at the 12-month follow-up. The reductions in medication were associated with maintained controlled levels of clinic, ambulatory, and home blood pressure. The addition of a standardized and inexpensive group-administered cognitive-behavioral intervention to the drug treatment of hypertension is beneficial as an adjunctive treatment in reducing drug requirements for patients with hypertension, thereby reducing the costs and potential side effects of antihypertensive medications.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH P_Cognitive_Therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_psychology_MeSH Hypertension_psychology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Quality_of_Life_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9008249
----K E
----T A randomized study comparing a patient-directed hypertension management strategy with usual office-based care.
----A This study aimed to compare the efficacy of a patient-directed management strategy with office-based management in maintaining blood pressure control in patients with chronic stable hypertension using a randomized trial of two months duration. The subjects had chronic stable essential hypertension without secondary causes or unstable cardiovascular disease and were selected through the offices of 11 family physicians and a tertiary care hypertension research unit. Patients were randomly assigned (2:1 ratio) to either a patient-directed management strategy using home blood pressure monitoring to adjust drug therapy if readings consistently exceeded defined limits, or office-based management through physician visits. The primary endpoint was the change from baseline in mean arterial pressure as determined by automatic ambulatory blood pressure monitoring. Secondary endpoints were changes in compliance, quality of life, and health care resource use. Ninety-one potential subjects were screened and 31 were randomized. Subjects in the patient-directed management group employed the drug adjustment protocols appropriately without complications. A significant difference in change in mean blood pressure was observed, favoring the patient-directed management (-0.95 mm Hg and +1.90 mm Hg, respectively, for patient-directed management and office-based management, P = .039). Compliance rates and quality of life scores were not significantly different between groups. Physician visits were more frequent in the patient-directed management group (1.05 v 0.20 visits/8 weeks, respectively, for patient-directed management and office-based management groups, P = .045). A patient-directed hypertensive management strategy may be feasible for patients with chronic stable hypertension. Such a strategy may improve blood pressure control compared with usual office-based care. However, physician visits may be increased using this strategy, at least in the short term.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Middle_Aged_MeSH P_Self_Care_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9010695
----K E
----T Haemodynamic effects and pharmacokinetics of oral d- and l-nebivolol in hypertensive patients.
----A OBJECTIVE: Nebivolol is a selective beta 1-adrenergic receptor blocker possessing an ancillary vasodilating effect. The objective of the present study was to study the haemodynamic and pharmacokinetic properties of nebivolol 5 mg once daily in a double-blind, placebo-controlled cross-over study. METHODS: Fifteen patients, 12 men and 3 women, with essential hypertension were investigated. Blood pressure and peripheral circulation were determined after acute oral nebivolol administration, 5 mg daily, and after 4 weeks treatment. RESULTS: The acute effect on blood pressure upon single-dosing was weak and non-significant. After 4 weeks both systolic blood pressure (152 vs 163 mmHg) and diastolic blood pressure (89 vs 97 mmHg) were significantly reduced after nebivolol treatment as compared to placebo. Following the first dose the venous volume was higher on placebo (5.88 ml.100 ml-1 tissue) as compared to active nebivolol treatment (5.17 ml.100 ml-1 tissue), while there were no statistically significant differences with regard to venous plethysmographic findings after 1 month on placebo (5.53 ml.100 ml-1 tissue) or on active treatment (5.97 ml.100 ml-1 tissue). Calculated peripheral resistance did not differ between active treatment (617 units) or placebo (548 units) after the first dose, whereas it was significantly lowered after 4 weeks of nebivolol treatment (483 units) as compared to placebo (593 units). CONCLUSIONS: Oral nebivolol 5 mg once daily lowered blood pressure and heart rate during steady state compared to placebo. Moreover, venous volume was reduced during acute but not steady-state dosing, while peripheral resistance was unaffected in the acute phase but reduced during steady state. Plasma concentrations of the separate enantiomers plus hydroxylated metabolites after the first and last dose in hypertensive patients were similar to those in healthy subjects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzopyrans_MeSH S_pharmacokinetics_MeSH Benzopyrans_pharmacokinetics_MeSH S_pharmacology_MeSH Benzopyrans_pharmacology_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_pharmacokinetics_MeSH Ethanolamines_pharmacokinetics_MeSH S_pharmacology_MeSH Ethanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Stereoisomerism_MeSH 
****** 9013266
----K I
----T Nifedipine gastrointestinal therapeutic system versus atenolol in stable angina pectoris. The Netherlands Working Group on Cardiovascular Research (WCN).
----A The gastrointestinal therapeutic system formulation of nifedipine enables a once-daily dosing resulting in predictable, relatively constant plasma concentrations. To evaluate the efficacy and safety of this formulation and to compare this with the beta-blocker atenolol, we conducted a double-blind, randomised, multi-centre study in 129 male patients with documented exercise induced angina pectoris. After 4 weeks' treatment, nifedipine (60 mg), improved time to onset of 0.1 mV ST-segment depression from 536 s by 72 +/- 117s, time to onset of pain from 619 s by 56 +/- 120 s, and total exercise time from 685 s by 40 +/- 88 s. Atenolol 100 mg, had a comparable effect, time to onset of 0.1 mV ST-segment depression improved from 496 s by 53 +/- 129 s, time to onset of pain from 572 s by 57 +/- 118 s, and total exercise time from 653 s by 33 +/- 99 s. Between group analysis revealed no statistically significant differences for these exercise parameters. Atenolol, but not nifedipine, significantly reduced heart rate and systolic blood pressure at rest and during exercise (P < 0.001 between groups), indicating different modes of action of the drugs. With regard to safety, both drugs were generally well tolerated. There were significantly (P = 0.01) more vasodilation related side effects with nifedipine. These data demonstrate that gastrointestinal therapeutic system formulation of nifedipine and atenolol as once-daily monotherapy are equally effective and safe, but with different effects on exercise parameters.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 9015908
----K E
----T A study to investigate the comparative efficacy and tolerability of nisoldipine coat-core and atenolol in the treatment of mild to moderate hypertension.
----A The efficacy and tolerability of nisoldipine coat-core (nisoldipine CC 10, 20, 40 mg) and atenolol (50, 100 mg) were compared in 230 patients with mild to moderate essential hypertension. Treatment was titrated at two-weekly intervals as necessary to control blood pressure. After eight weeks of active therapy, the two treatments proved to be equally effective in reducing sitting diastolic blood pressure (13.7 +/- 8.3 mmHg and 14.2 +/- 9.1 mmHg for nisoldipine CC and atenolol, respectively), and provided equivalent reduction in systolic blood pressure and identical response rates (69%). Heart rate was reduced from baseline in the atenolol group but remained unchanged in the nisoldipine CC group (p < 0.001 difference between the two groups). Both nisoldipine CC and atenolol were well tolerated and had no detectable metabolic effects. Adverse events were minor and of the type commonly associated with drugs of these classes.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nisoldipine_MeSH S_therapeutic_use_MeSH Nisoldipine_therapeutic_use_MeSH 
****** 9031766
----K I
----T Asystole during dipyridamole infusion in patients without coronary artery disease or beta-blocker therapy.
----A The authors report two patients without coronary artery disease who experienced asystole during the IV infusion of dipyridamole on routine TI-201 myocardial perfusion imaging and review the literature for possible explanations of this rare side effect. Until now, this side effect was only reported in patients with coronary artery disease or beta-blocker therapy. Yet, the cases lacked both concomitant factors and autonomic dysregulation is suggested as a cause for asystole.
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH M_Autonomic_Nervous_System_Diseases_MeSH S_complications_MeSH Autonomic_Nervous_System_Diseases_complications_MeSH M_Bradycardia_MeSH S_chemically_induced_MeSH Bradycardia_chemically_induced_MeSH M_Coronary_Circulation_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Dipyridamole_MeSH S_administration_&_dosage_MeSH Dipyridamole_administration_&_dosage_MeSH S_adverse_effects_MeSH Dipyridamole_adverse_effects_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH M_Follow-Up_Studies_MeSH M_Heart_MeSH S_radionuclide_imaging_MeSH Heart_radionuclide_imaging_MeSH M_Heart_Arrest_MeSH S_chemically_induced_MeSH Heart_Arrest_chemically_induced_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Thallium_Radioisotopes_MeSH S_diagnostic_use_MeSH Thallium_Radioisotopes_diagnostic_use_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 9033462
----K E
----T Randomised, placebo-controlled trial of carvedilol in patients with congestive heart failure due to ischaemic heart disease. Australia/New Zealand Heart Failure Research Collaborative Group.
----A BACKGROUND: In patients with heart failure, beta-blocker therapy improves left-ventricular function after 3-6 months of treatment, but effects of such treatment on symptoms and exercise performance are inconsistent, and the longer-term effects on death and other serious clinical events remain uncertain. We have investigated these issues in a double-blind, placebo-controlled, randomised trial of the beta-adrenergic blocker carvedilol (which also has alpha 1-blocking properties). METHODS: 415 patients with chronic stable heart failure were randomly assigned treatment with carvedilol (207) or matching placebo (208). At baseline, 6 months, and 12 months, we measured left-ventricular ejection fraction, left-ventricular dimensions, treadmill exercise duration, 6 min walk distance, New York Heart Association (NYHA) class, and specific activity scale (SAS) score. Double-blind follow-up continued for an average of 19 months, during which all deaths, hospital admissions, and episodes of worsening heart failure were documented. FINDINGS: After 12 months, left-ventricular ejection fraction had increased by 5.3% (2p < 0.0001) and end-diastolic and end-systolic dimensions had decreased by 1.7 mm (2p = 0.06) and 3.2 mm (2p = 0.001), respectively, in the carvedilol group compared with the placebo group. During the same period that were no clear changes in treadmill exercise duration, 6 min walk distance, NYHA class, or SAS score. After 19 months, the frequency of episodes of worsening heart failure was similar in the carvedilol and placebo groups (82 vs 75; relative risk 1.12 [95% Cl 0.82-1.53]) but the rate of death or hospital admission was lower in the carvedilol group than in the placebo group (104 vs 131; relative risk 0.74 [0.57-0.95]). INTERPRETATION: The beneficial effects of carvedilol on left-ventricular function and size were maintained for at least a year after the start of treatment, but carvedilol had no effect on exercise performance, symptoms, or episodes of worsening heart failure. There was an overall reduction in events resulting in death or hospital admission, and a year of treatment with carvedilol resulted in the avoidance of one such serious event among every 12-13 (SE 5) of these patients with chronic stable heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Australia_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Function_Tests_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH M_New_Zealand_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9053382
----K E
----T Super hype for super hormones.
----A 
----P Editorial 
----M M_Aged_MeSH M_Aging_MeSH S_drug_effects_MeSH Aging_drug_effects_MeSH M_Dehydroepiandrosterone_MeSH S_adverse_effects_MeSH Dehydroepiandrosterone_adverse_effects_MeSH P_Health_Food_MeSH M_Human_MeSH M_Human_Growth_Hormone_MeSH S_adverse_effects_MeSH Human_Growth_Hormone_adverse_effects_MeSH M_Melatonin_MeSH S_adverse_effects_MeSH Melatonin_adverse_effects_MeSH M_Testosterone_MeSH S_adverse_effects_MeSH Testosterone_adverse_effects_MeSH M_United_States_MeSH M_United_States_Food_and_Drug_Administration_MeSH 
****** 9038037
----K E
----T Calcium antagonists, a useful additional therapy in treatment resistant hypertension: comparison of felodipine ER and nifedipine Retard by 24-h ambulatory blood pressure monitoring.
----A OBJECTIVE: To compare the efficacy and tolerability of felodipine extended release (ER) 2.5 mg (F2.5) and 5 mg (F5) once daily with nifedipine Retard 10 mg (N20) and 20 mg (N40) twice daily as additional therapy in patients who remained hypertensive despite treatment with an ACE-inhibitor, beta-blocker or diuretic. DESIGN AND METHODS: In a multicentre, double-blind parallel study, 61 men and 54 women, aged 35-75, with a supine diastolic blood pressure between 95 and 115 mmHg were randomised to treatment with F2.5, F5, N20 or N40 for 8 weeks, with optional doubling of the dose after 4 weeks. Blood pressure was measured at the office after 0, 4 and 8 weeks and by 24-h ambulatory monitoring (ABPM) after 0 and 4 weeks. Spontaneously reported adverse events and a subjective symptom assessment questionnaire were used for side-effect profiling. RESULTS: Mean office systolic/diastolic blood pressure was clinically relevantly reduced in all treatment groups after 4 weeks by 8/7, 12/9, 11/9 and 18/11 mmHg for F2.5, F5, N20 and N40, respectively, and after 8 weeks (F2.5-5: 17/11 mmHg: F5-10: 18/14 mmHg; N20-40: 19/14 mmHg; N40-80: 25/14 mmHg) with no statistically significant differences between these groups. The lowest dose of felodipine (F2.5) was the least effective. After 4 weeks the ABPM showed consistent 24-h reductions in blood pressure (4/2; 8/5; 7/5; 10/6 mmHg, respectively) over 24 h for the felodipine ER 5 mg group only and for both nifedipine groups. No statistically significant difference between these groups was found. An office responder does not appear to be identical to an ambulatory one and vice versa. The adverse events, mostly oedema, flushing and headache, were dose-related. CONCLUSIONS: Both felodipine ER and nifedipine Retard are effective "add-on' drugs in patients with monotherapy-resistant hypertension. The blood-pressure-lowering effect is dose-dependent and tolerability is inversely related to efficacy. The results emphasize the benefits of combining two agents with low doses.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH S_methods_MeSH Blood_Pressure_Monitoring__Ambulatory_methods_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Tolerance_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9038691
----K E
----T Impaired left ventricular filling dynamics in patients with angina and angiographically normal coronary arteries: effect of beta adrenergic blockade.
----A OBJECTIVE: To assess exercise performance and resting left ventricular filling dynamics in patients with syndrome X (SX) in basal conditions and after 10 days treatment with oral atenolol. DESIGN AND PATIENTS: Exercise performance was studied and left ventricular filling assessed by Doppler-derived transmitral flow pattern analysis in 22 patients (16 female, mean (SD) age 53 (4) years) with angina, a positive exercise test, and angiographically smooth coronary arteries. Patients were studied after two 10 day treatment periods with either atenolol or placebo in a single-blind, randomised, crossover trial. The same protocol was followed in 10 patients with documented coronary artery disease (CAD) and in 13 controls (C). RESULTS: Unlike the controls, patients with SX and those with CAD consistently showed exercise-induced ST segment abnormalities and impaired resting left ventricular filling while on placebo. Atenolol significantly reduced episodes of angina, completely prevented exercise-induced ST segment changes in 18 SX patients, and delayed their onset in all patients with CAD: in both groups the agent significantly improved Doppler-derived indices (mean (SD)) of ventricular filling (E/A 0.97 (0.27) v 1.22 (0.32) and 0.84 (0.21) v 1.19 (0.37), respectively). CONCLUSIONS: The objective documentation of left ventricular filling abnormalities may be useful in confirming the clinical diagnosis of SX and in providing objective evidence of therapeutic benefit. The similarity of the symptoms and electrocardiographic and ventricular filling abnormalities found in patients with SX and in those with CAD suggests that ischaemia is involved in both groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH M_Coronary_Angiography_MeSH M_Cross-Over_Studies_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Syndrome_X_MeSH S_drug_therapy_MeSH Syndrome_X_drug_therapy_MeSH S_physiopathology_MeSH Syndrome_X_physiopathology_MeSH S_radiography_MeSH Syndrome_X_radiography_MeSH 
****** 9039073
----K I
----T Long-term effects on sexual function of five antihypertensive drugs and nutritional hygienic treatment in hypertensive men and women. Treatment of Mild Hypertension Study (TOMHS)
----A Problems with sexual function have been a long-standing concern in the treatment of hypertension and may influence the choice of treatment regimens and decisions to discontinue drugs. The Treatment of Mild Hypertension Study (TOMHS) provides an excellent opportunity for examination of sexual function and effects of treatment on sexual function in men and women with stage I diastolic hypertension because of the number of drug classes studied, the double-blind study design, and the long-term follow-up. TOMHS was a double-blind, randomized controlled trial of 902 hypertensive individuals (557 men, 345 women), aged 45 to 69 years, treated with placebo or one of five active drugs (acebutolol, amlodipine maleate, chlorthalidone, doxazosin maleate, or enalapril maleate). All participants received intensive lifestyle counseling regarding weight loss, dietary sodium reduction, alcohol reduction (for current drinkers), and increased physical activity. Sexual function was ascertained by physician interviews at baseline and annually during follow-up. At baseline, 14.4% of men and 4.9% of women reported a problems with sexual function. In men, 12.2% had problems obtaining and/or maintaining an erection; 2.0% of women reported a problem having an orgasm. Erection problems in men at baseline were positively related to age, systolic pressure, and previous antihypertensive drug use. The incidences of erection dysfunction during follow-up in men were 9.5% and 14.7% through 24 and 48 months, respectively, and were related to type of antihypertensive therapy. Participants randomized to chlorthalidone reported a significantly higher incidence of erection problems through 24 months than participants randomized to placebo (17.1% versus 8.1%, P = .025). Incidence rates through 48 months were more similar among treatment groups than at 24 months, with nonsignificant differences between the chlorthalidone and placebo groups. Incidence was lowest in the doxazosin group but was not significantly different from the placebo group. Incidence for acebutolol, amlodipine, and enalapril groups was similar to that in the placebo group. In many cases, erection dysfunction did not require withdrawal of medication. Disappearance of erection problems among men with problems at baseline was common in all groups but greatest in the doxazosin group. Incidence of reported sexual problems in women was low in all treatment groups. In conclusion, long-term incidence of erection problems in treated hypertensive men is relatively low but is higher with chlorthalidone treatment. Effects of erection dysfunction with chlorthalidone appear relatively early and are often tolerable, and new occurrences after 2 years are unlikely. The rate of reported sexual problems in hypertensive women is low and does not appear to differ by type of drug. Similar incidence rates of erection dysfunction in placebo and most active drug groups caution against routine attribution of erection problems to antihypertensive medication.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_adverse_effects_MeSH Acebutolol_adverse_effects_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_adverse_effects_MeSH Doxazosin_adverse_effects_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Libido_MeSH S_drug_effects_MeSH Libido_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Orgasm_MeSH S_drug_effects_MeSH Orgasm_drug_effects_MeSH M_Penile_Erection_MeSH S_drug_effects_MeSH Penile_Erection_drug_effects_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9041374
----K E
----T The effect of metoprolol treatment on insulin sensitivity and diurnal plasma hormone levels in hypertensive subjects.
----A To evaluate the effect of metoprolol on insulin sensitivity and diurnal plasma hormone levels, seven mildly hypertensive subjects were investigated (four men and three women, age 52 +/- 8, body mass index 25.4 +.- 1.9, mean +/- SD). The study had a placebo-controlled, double-blind, crossover design with 6 weeks' metoprolol treatment (100 mg b.i.d) vs. placebo. At the end of each treatment period 24-h blood samples were collected continuously for diurnal analysis of hormone levels and a hyperinsulinaemic euglycaemic clamp combined with [3-3H]-D-glucose infusion was performed. Insulin sensitivity was evaluated by means of three different methods: diurnal plasma insulin and glucose levels; glucose consumption; and insulin sensitivity index during euglycaemic clamp conditions. Fasting blood glucose and insulin concentrations as well as mean plasma diurnal levels of insulin, growth hormone, testosterone and cortisol were similar after placebo and metoprolol treatment, whereas noradrenaline and adrenaline levels were significantly increased after metoprolol. During the clamp, plasma insulin was significantly higher after metoprolol treatment than after placebo treatment (56 +/- 3 vs. 64 +/- 2 mU L(-1), P < 0.05). Consequently, the insulin sensitivity index [glucose infusion rate (GIR)/ plasma insulin] was lower after metoprolol treatment (16.1 +/- 2.6 vs. 10.2 +/- 1.2, P < 0.05), although GIR was not significantly changed. We suggest that the insulin sensitivity index may not accurately reflect the insulin effect as the plasma level of insulin was significantly increased during insulin infusion but not at 24 h, possibly because of alteration of distribution and/or degradation rate of exogenous insulin. Thus, the likelihood of metoprolol inducing insulin resistance in hypertensive subjects may be less than previously proposed.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Blood_Glucose_MeSH S_chemistry_MeSH Blood_Glucose_chemistry_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_Clamp_Technique_MeSH M_Hormones_MeSH S_blood_MeSH Hormones_blood_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH S_physiology_MeSH Insulin_physiology_MeSH P_Insulin_Resistance_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9042095
----K E
----T Haemostatic markers, inflammatory parameters and lipids in male and female patients in the Angina Prognosis Study in Stockholm (APSIS). A comparison with healthy controls.
----A OBJECTIVES: To investigate haemostatic markers (especially fibrinolysis), inflammatory parameters and lipids in patients with stable angina pectoris. Special attention was paid to differences between male and female patients, and to the reactivity to exercise or the diurnal variation of certain parameters. SUBJECTS: Eight hundred and nine patients (31% females) and a matched healthy control group (n = 50). RESULTS: The patients had signs of disturbed fibrinolysis, with elevated plasma levels of tissue plasminogen activator (tPA) antigen and plasminogen activator inhibitor (PAI-1) activity at rest, and attenuated responses of tPA antigen and activity to exercise. Elevated levels of fibrinogen, white blood cell counts and orosomucoid were found, suggesting increased inflammatory activity, as well as a more disturbed lipid profile (higher triglycerides and lower HDL cholesterol levels) than among controls. Female patients had higher HDL cholesterol and lower triglyceride levels than male patients, but higher platelet counts and signs of enhanced platelet activity (beta-thromboglobulin excretion). In addition, female patients had lower white blood cell counts, suggesting lesser inflammatory activity. CONCLUSIONS: Patients with stable angina pectoris have signs of markedly disturbed fibrinolysis both at rest and in response to exercise, as well as signs of enhanced inflammatory activity and dyslipidemia. The observed sex differences suggest that male patients with stable angina pectoris may have a more lipid-related disease, whereas it may be more dependent on platelet function in females.
----P Journal_Article 
----M M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_enzymology_MeSH Angina_Pectoris_enzymology_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Case-Control_Studies_MeSH M_Circadian_Rhythm_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_metabolism_MeSH Fibrinogen_metabolism_MeSH M_Fibrinolysis_MeSH M_Hemostasis_MeSH M_Human_MeSH M_Inflammation_MeSH M_Leukocyte_Count_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Orosomucoid_MeSH S_metabolism_MeSH Orosomucoid_metabolism_MeSH M_Plasminogen_Activator_Inhibitor_1_MeSH S_blood_MeSH Plasminogen_Activator_Inhibitor_1_blood_MeSH M_Platelet_Count_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Tissue_Plasminogen_Activator_MeSH S_blood_MeSH Tissue_Plasminogen_Activator_blood_MeSH 
****** 9042847
----K I
----T Health outcomes associated with antihypertensive therapies used as first-line agents. A systematic review and meta-analysis.
----A OBJECTIVE: To review the scientific evidence concerning the safety and efficacy of various antihypertensive therapies used as first-line agents and evaluated in terms of major disease end points. DATA SOURCES: MEDLINE searches and previous meta-analyses for 1980 to 1995. DATA SELECTION: We selected long-term studies that assessed major disease end points as an outcome. For the meta-analysis, we chose placebo-controlled randomized trials. For randomized trials using surrogate end points such as blood pressure, we selected the largest studies that evaluated multiple drugs. Where clinical trial evidence was lacking, we relied on information from observational studies. DATA SYNTHESIS: Diuretics and beta-blockers have been evaluated in 18 long-term randomized trials. Compared with placebo, beta-blocker therapy was effective in preventing stroke (relative risk [RR], 0.71; 95% confidence interval [CI], 0.59-0.86) and congestive heart failure (RR, 0.58; 95% CI, 0.40-0.84). The findings were similar for high-dose diuretic therapy (for stroke, RR, 0.49; 95% CI, 0.39-0.62; and for congestive heart failure, RR, 0.17; 95% CI, 0.07-0.41). Low-dose diuretic therapy prevented not only stroke (RR, 0.66; 95% CI, 0.55-0.78) and congestive heart failure (RR, 0.58; 95% CI, 0.44-0.76) but also coronary disease (RR, 0.72; 95% CI, 0.61-0.85) and total mortality (RR, 0.90; 95% CI, 0.81-0.99). Although calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure in hypertensive patients, the clinical trial evidence in terms of health outcomes is meager. For several short-acting dihydropyridine calcium channel blockers, the available evidence suggests the possibility of harm. Whether the long-acting formulations and the nondihydropyridine calcium channel blockers are safe and prevent major cardiovascular events in patients with hypertension remains untested and therefore unknown. CONCLUSION: Until the results of large long-term clinical trials evaluating the effects of calcium channel blockers and ACE inhibitors on cardiovascular disease incidence are completed, the available scientific evidence provides strong support for the current national guidelines, which recommend diuretics and beta-blockers as firstline agents and low-dose therapy for all antihypertensive agents.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Likelihood_Functions_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 9043840
----K E
----T Effects of antianginal therapy with a calcium antagonist and nitrates on dobutamine-atropine stress echocardiography. Comparison with exercise electrocardiography.
----A BACKGROUND: Anti-ischaemic therapy with nitrates and/or calcium channel blockers profoundly affects the results of pharmacological stress echocardiography with coronary vasodilators but the influence on catecholamine stress testing remains unsettled. AIMS: The present study aimed to assess the effects of non-beta-blocker antianginal therapy on dobutamine (up to 40 micrograms.kg-1.min-1)-atropine (up to 1 mg) stress. echo-cardiography and to evaluate whether drug-induced changes in the dobutamine atropine stress echocardiography response may predict variations in exercise tolerance. METHODS: Twenty six patients with angiographically assessed coronary artery disease (seven patients with single-, 10 with double-, and nine with triple-vessel disease) performed a dobutamine atropine stress echocardiography and an exercise electrocardiography test in random order both off and on antianginal drugs (nitrates and calcium antagonists). In doubtamine-atropine stress echocardiography, we evaluated: dobutamine time (i.e. the time from initiation of the dobutamine infusion to obvious dyssynergy), wall motion score index (in a 16-segment model of the left ventricle, each segment ranging from 1 = normal, to 4 = dyskinetic), and rate-pressure product at peak stress. RESULTS: Dobutamine-atropine stress echocardiography positivity occurred in 26 out of 26 patients off and in 23 patients on therapy (100 vs 88%, P = ns). Atropine coadministration was needed to evoke echo positivity in no patient off and in five out of 26 on therapy (0 vs 19% P < 0.01). The achieved rate pressure product during dobutamine-atropine stress echocardiography was comparable on and off therapy (17 +/- 4 vs 19 +/- 5 x 10(3) mmHg x heart rate. min-1, P = ns). Therapy induced an increase in dobutamine time (on = 16 +/- 3 vs of = 13 +/- 3 min, P < 0.01) and a decrease in peak wall motion score index (on = 1.3 +/- 0.2 vs off = 1.5 +/- 0.3, P < 0.01). The therapy induced changes in exercise time during the exercise electrocardiography test were not significantly correlated to dobutamine-atropine stress echocardiography variations in either dobutamine time (r = 0.07, P = ns), or peak rate pressure product (r = 0.24, P = ns), or peak wall motion score index (r = 0.02, P = ns). CONCLUSIONS: (1) non-beta-blocker antianginal therapy only modestly reduces dobutamine-atropine stress echocardiography sensitivity, although atropine coadministration is more often required to reach stress echo positivity under therapy; (2) therapy reduces the severity of dobutamine atropine stress echocardiography ischaemia stratified in the time and space domain, but these changes are only poorly correlated to variations in exercise tolerance.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Atropine_MeSH S_administration_&_dosage_MeSH Atropine_administration_&_dosage_MeSH S_diagnostic_use_MeSH Atropine_diagnostic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Dobutamine_MeSH S_administration_&_dosage_MeSH Dobutamine_administration_&_dosage_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Female_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Nitrates_MeSH S_administration_&_dosage_MeSH Nitrates_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Parasympatholytics_MeSH S_administration_&_dosage_MeSH Parasympatholytics_administration_&_dosage_MeSH S_diagnostic_use_MeSH Parasympatholytics_diagnostic_use_MeSH M_Prospective_Studies_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9046949
----K I
----T Beta-adrenergic blocking agents in the treatment of congestive heart failure: mechanisms and clinical results.
----A Congestive heart failure is a major public health problem in Western countries. Despite current treatment including angiotensin converting enzyme inhibitors, mortality and morbidity remain high. The sympathetic nervous system is markedly activated in heart failure, and inhibition of this system with the beta-adrenergic blocking agents may provide further benefit. Several clinical trials involving over 3,000 patients have shown that beta-blocker therapy improves left ventricular function in patients with heart failure. However, the effects of such therapy on symptoms and exercise tolerance have been variable. Recent reports have suggested that survival is improved with the beta-blocker carvedilol. Large-scale, long-term clinical trials are required to confirm these findings and to clearly define the role of this promising therapy for patients with heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 9048267
----K I
----T Beta-blocker use in systolic heart failure and dilated cardiomyopathy.
----A Statistics regarding long-term survival for patients with heart failure are discouraging today. Converting enzyme inhibitors have produced a modest effect on mortality. beta-Blockers may be the next addition to standard therapy for heart failure because they generate consistent improvements in hemodynamic factors, symptom scores, and submaximal exercise tolerance in randomized, controlled clinical trials. They augment ejection fraction, reduce heart volume, and consistently lower neurohormonal activation as reflected by plasma norepinephrine levels. Trials with carvedilol and bisoprolol suggest an effect on mortality similar to that with converting enzyme inhibitor trials. Future studies, especially the beta-blocker Evaluation Survival Trial (BEST), with mortality as the main end point should elucidate the degree of effect on mortality further.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_mortality_MeSH Cardiomyopathy__Congestive_mortality_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 9048789
----K E
----T Calcium-channel blockers and risk of cancer.
----A BACKGROUND: Previous studies have been interpreted as suggesting an increase in risk of cancer among users of calcium-channel blockers compared with users of beta-blockers. To explore this issue further, we studied a large group of hypertensive patients to investigate the relation of calcium-channel blockers and cancer. METHODS: In cohorts of users of calcium-channel blockers, angiotensin-converting-enzyme (ACE) inhibitors, and beta-blockers, we identified all cases of cancer diagnosed in 1995. We used a nested case-control analysis to estimate the risk of cancer among users of calcium-channel blockers and ACE inhibitors, with users of beta-blockers as a reference group. The study was based on information taken from the General Practice Research Database, and the study population was restricted to patients with at least 4 years of medical history recorded on computer. FINDINGS: The study was based on 446 cases of cancer and 1750 controls. The relative risk estimates for all cancers combined were 1.27 (95% CI 0.98-1.63) and 0.79 (0.58-1.06) for users of calcium-channel blockers and ACE inhibitors, respectively, relative to users of beta-blockers. There was little difference in risk estimates with duration of use of calcium-channel blockers of less than 1.0 year (relative risk 1.46), 1.0-3.9 years (1.26), and 4.0 years or more (1.23). INTERPRETATION: The small positive association between calcium-channel blockers and risk of cancer is unlikely to be causal since there is no increase in risk with increasing duration of calcium-channel blocker use.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Neoplasms_MeSH S_chemically_induced_MeSH Neoplasms_chemically_induced_MeSH M_Questionnaires_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9049571
----K E
----T Control of bias in dietary trial to prevent coronary recurrences: The Lyon Diet Heart Study.
----A BACKGROUND AND OBJECTIVES: A major limitation of dietary trials is that double blind design is not feasible. These trials are therefore prone to biases. The Lyon diet heart study is a single-blind secondary prevention trial to test the hypothesis that a Mediterranean-type of diet may prevent recurrences after a first myocardial infarction. A surprising 73% reduction of the risk of new major cardiac events was observed in the experimental group. For this reason, it is important to describe the methods used in the trial. We now report our techniques to randomize the patients, to change their diet and to control for possible bias, in particular any investigator or attending physician bias. DESIGN: In this dietary trial, a specific design was used to recruit and randomize the patients without informing them and their physicians that they were participating in a comparative trial. The attending physician bias was evaluated by studying drug usage and the investigator bias by constructing a questionnaire from which specific scores were used to evaluate (1) how the patients appreciated their participation in the study and (2) whether this participation resulted in significant changes in their way of living. SUBJECTS: 605 survivors of a first myocardial infarction were randomized into either a control or a Mediterranean group. RESULTS: The two randomized groups were similar for all the variables of prognosis. Drug usage was not significantly different between groups, suggesting that there was no major attending physician bias. Analyses of the appreciation scores and of the change score did not detect any significant investigator bias. CONCLUSIONS: Although the study cannot be completely shielded from minor biases, the data presented here provide evidence that the dietary modifications per se were protective, not other (including psychosocial) changes resulting from the participation to the trial.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Alcohol_Drinking_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Anticoagulants_MeSH S_administration_&_dosage_MeSH Anticoagulants_administration_&_dosage_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH P_Bias_(Epidemiology)_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH P_Diet_MeSH M_Female_MeSH M_France_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Questionnaires_MeSH M_Recurrence_MeSH M_Smoking_MeSH 
****** 9133121
----K 1
----T [Pathogenesis of venous congestion symptoms after Fontan operation]
----A To evaluate a possible common pathogenetic denominator, we compared hemodynamic data of 18 patients who had an uneventful long-term course after a Fontan procedure, with the respective data of patients who developed symptoms of central venous congestion either in the immediate postoperative period (n = 10) or during late follow-up (n = 6). We found a coincidence of increased early postoperative venous pressures (CVP; 17.1 +/- 2.9 mm Hg) with relatively high cardiac indices (3.6 +/- 0.6 l/min.m-2) as compared to 2.4 l/min.m-2 in the group of patients with a symptom-free long-term course but no significant difference in total pulmonary resistance between the two groups. The increased CVP (17.2 +/- 2.9 mm Hg) in patients with late chronic central venous congestion is primarily due to increased total pulmonary resistance (552 +/- 131 dyn s/cm5.m-2). Both groups of patients with central venous congestion display a ratio of systemic to total pulmonary resistance lower than 4.5 whereas symptom-free patients have a significantly higher resistance ratio (6.8 +/- 2.3) and a highly significant increase in peripheral resistance to values of 2687 +/- 527 dyn s/cm5.m-2 as compared to 1486 +/- 340 dyn s/cm5.m-2 in the early postoperative group. Correspondingly, mean arterial pressure of the symptom-free patients is significantly elevated (93 +/- 11 mm Hg) as compared to a control group (81 +/- 11 mm Hg). Based on our theory an increase in systemic arterial resistance may lead to a fall in mean capillary filtration pressure and therefore counteract central venous congestion. To support this, we briefly present cases where pharmacologic enhancement of systemic arterial resistance was effective in the treatment of venous congestion whereas pharmacologic lowering of systemic resistance induced venous congestion.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Capillary_Permeability_MeSH S_drug_effects_MeSH Capillary_Permeability_drug_effects_MeSH S_physiology_MeSH Capillary_Permeability_physiology_MeSH M_Capillary_Resistance_MeSH S_drug_effects_MeSH Capillary_Resistance_drug_effects_MeSH S_physiology_MeSH Capillary_Resistance_physiology_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH S_physiology_MeSH Cardiac_Output_physiology_MeSH M_Catecholamines_MeSH S_administration_&_dosage_MeSH Catecholamines_administration_&_dosage_MeSH M_Central_Venous_Pressure_MeSH S_drug_effects_MeSH Central_Venous_Pressure_drug_effects_MeSH S_physiology_MeSH Central_Venous_Pressure_physiology_MeSH M_Child_MeSH M_English_Abstract_MeSH M_Female_MeSH P_Fontan_Procedure_MeSH M_Heart_Catheterization_MeSH M_Heart_Defects__Congenital_MeSH S_physiopathology_MeSH Heart_Defects__Congenital_physiopathology_MeSH S_surgery_MeSH Heart_Defects__Congenital_surgery_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Lung_MeSH S_blood_supply_MeSH Lung_blood_supply_MeSH M_Male_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH S_physiology_MeSH Vascular_Resistance_physiology_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 9050975
----K E
----T Comparison of different fixed antihypertensive combination drugs: a double-blind, placebo-controlled parallel group study.
----A OBJECTIVE: To compare the effects of fixed-dose preparations containing 180 mg sustained-release verapamil and 2 mg trandolapril, 100/25 mg atenolol/chlorthalidone, 20/12.5 mg lisinopril/hydrochlorothiazide and placebo in patients with essential hypertension. DESIGN: A 4-week placebo run-in period followed by a double-blind, placebo-controlled parallel group study lasting 8 weeks. SETTING: Office practices (21 centres). PATIENTS: Patients with essential hypertension (World Health Organization grades I or II); supine diastolic blood pressure 101-114 mmHg in week 4 of the run-in period; 215 patients were enrolled, of whom 205 were assigned randomly to double-blind therapy. MAIN OUTCOME MEASURES: Reduction in supine and standing blood pressures. RESULTS: All three active treatments with a single daily dose were significantly more effective than was placebo in reducing the blood pressure of seated subjects (P=0.0001). The reductions in sitting diastolic blood pressure (DBP) from baseline to the last visit with each active treatment were comparable: 13 mmHg [95% confidence interval (CI) 16-9] with sustained-release verapamil/trandolapril, 13 mmHg (16-9) with atenolol/chlorthalidone and 12 mmHg (15-8) with lisinopril/hydrochlorothiazide. Normalization of blood pressure (DBP < 90 mmHg) was observed in 48% of patients with sustained-release verapamil/trandolapril, in 46% with atenolol/chlorthalidone and in 40% with lisinopril/hydrochlorothiazide. Response rates (normalization of DBP or a reduction in DBP by > 10 mmHg) with each active treatment were 72% for sustained-release verapamil/trandolapril, 76% for atenolol/chlorthalidone and 69% for lisinopril/hydrochlorothiazide. All three active treatments were tolerated well. CONCLUSION: This study demonstrates that the low-dose combination sustained-release verapamil/trandolapril may be a suitable alternative for combinations containing a thiazide diuretic or a beta-blocker for longer term management of hypertensive patients for whom combination therapy is indicated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Drug_Tolerance_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH M_Lisinopril_MeSH S_administration_&_dosage_MeSH Lisinopril_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH 
****** 9052890
----K E
----T Effect of calcium channel or beta-blockade on the progression of diabetic nephropathy in African Americans.
----A beta-Blockers are known to slow the progression of diabetic nephropathy by lowering arterial pressure. Moreover, in individuals with diabetic nephropathy, antihypertensive agents that provide sustained reductions in proteinuria slow the rate of decline in renal function compared with agents without this antiproteinuric effect. To examine whether differential effects on proteinuria affect the progression of diabetic nephropathy, we conducted a randomized study that compared the effects of a heart rate-lowering calcium channel blocker, sustained-release verapamil, with those of a beta-blocker, atenolol, on the progression of diabetic renal disease. The primary end point of the study was a change in creatinine clearance slope. Thirty-four African Americans with the following inclusion criteria were randomized to one of the two groups: serum creatinine greater than 1.4 mg/dL, proteinuria greater than 1500 mg/d, longer than a 5-year history of both non-insulin-dependent diabetes mellitus and hypertension, and exclusion of other renal diseases. Goal blood pressure was less than 140/90 mm Hg. All subjects received loop diuretics as second line agents to help achieve the blood pressure goal. Twenty-four-hour urinary protein and sodium excretions as well as creatinine clearance were measured at 6-month intervals. Blood pressure was measured every 3 months. After a mean follow-up of 54+/-6 months, the calcium channel blocker group demonstrated both a slower rate of decline in creatinine clearance (-1.7+/-0.9 versus -3.7+/-1.4 mL/min per year per 1.73 m2, P<.01) and a greater reduction in proteinuria compared with the atenolol group. Additionally, a greater proportion of the atenolol group had a 50% or more increase in serum creatinine compared with the verapamil group (32+/-9% versus 16+/-7%, P<.05). These between-group differences could not be explained by differences in blood pressure control. These data support the concept that antihypertensive agents that persistently maintain reductions in both arterial pressure and proteinuria slow the progression of diabetic renal disease in African Americans to a greater extent than those agents without these effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Delayed-Action_Preparations_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Nephropathies_MeSH S_ethnology_MeSH Diabetic_Nephropathies_ethnology_MeSH S_prevention_&_control_MeSH Diabetic_Nephropathies_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Random_Allocation_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9054853
----K E
----T Loading manipulations improve the prognostic value of Doppler evaluation of mitral flow in patients with chronic heart failure.
----A BACKGROUND: Mitral flow velocity patterns (MFVPs) evaluated by Doppler echocardiography are strong predictors of survival in various cardiac diseases. However, MFVPs may change over time according to loading conditions. We performed this prospective study to assess whether changes in MFVP induced by loading manipulations provided additional prognostic information in 173 patients with chronic heart failure. METHODS AND RESULTS: Simultaneous Doppler echocardiographic and right-sided hemodynamic recordings were obtained at baseline in all patients, during nitroprusside infusion in the 98 patients who had a baseline restrictive (early-to-late flow velocity ratio > 1 and deceleration time < or = 130 ms) MFVP, and during passive leg lifting in the 75 patients who had a baseline nonrestrictive MFVP. Patients were categorized, according to changes in MFVP, into four groups: 61 patients with an irreversible restrictive, 37 with a reversible restrictive, 48 patients with a stable nonrestrictive, and 27 patients with an unstable nonrestrictive MFVP. Fifty patients experienced major cardiac events. Cox analysis revealed that MFVP was a strong predictor of events and that the response to loading manipulations improved its prognostic value. Patients with an irreversible restrictive MFVP had a higher event rate (51%) than patients with a reversible restrictive MFVP (19%). Among patients with a baseline nonrestrictive MFVP, those with a stable nonrestrictive MFVP had the lowest event rate (6%), whereas the event rate was 33% in patients with an unstable nonrestrictive MFVP. CONCLUSIONS: In patients with chronic heart failure, MFVPs provide independent prognostic information. Their prognostic value can be further increased by assessment of the changes induced in them by loading manipulations.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH P_Coronary_Circulation_MeSH M_Digitalis_Glycosides_MeSH S_therapeutic_use_MeSH Digitalis_Glycosides_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH P_Echocardiography__Doppler_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Heart_Rate_MeSH P_Hemodynamic_Processes_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Mitral_Valve_MeSH M_Nitroprusside_MeSH S_administration_&_dosage_MeSH Nitroprusside_administration_&_dosage_MeSH S_diagnostic_use_MeSH Nitroprusside_diagnostic_use_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Pulmonary_Circulation_MeSH M_Vascular_Resistance_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 9057069
----K E
----T Early captopril treatment reduces plasma endothelin concentrations in the acute and subacute phases of myocardial infarction: a pilot study.
----A It has been reported that endothelin-1 (ET-1) increases in acute myocardial infarction (AMI). Experimental studies showed that captopril administration reduces ET-1 secretion. In addition, it was reported that the increased ET-1 levels are a negative prognostic index. The study sought to verify whether captopril can reduce plasma ET levels in the acute and subacute phases of reperfused anterior AMI. Forty-five patients, hospitalized for suspected anterior AMI within 4 h from the onset of symptoms, suitable for thrombolysis (first episode), Killip class I-2, were randomized (double blind) into two groups: group A (23; seven women/16 men) received captopril (as first dose) 2-4 h after starting thrombolysis (the dose was then increased up to 25 mg every 8 h). Group B (22; five women/17 men) received placebo after thrombolysis. All the patients met the reperfusion criteria. The two groups were similar with regard to age, sex, CK peak, ejection fraction, end-systolic volume and risk factors. Plasma ET levels were measured at entry, and 2, 12, 24, 48, and 72 h after starting thrombolysis. Mean concentrations of ET +/- SD: Group A basal, 1.50 +/- 0.67; at 2h, 2.31 +/- 1.24; 12 h, 1.84 +/- 1.45; 24 h, 1.30 +/- 0.72; 48 h, o.95 +/- 0.50; 72 h, 0.60 +/- 0.15 fmol/ml; p < 0.001. Group B basal, 1.58 +/- 0.83; at 2 h, 2.38 +/- 1.35; 12 h, 2.33 +/- 1.71; 24 h, 1.80 +/- 1.41; 48h, 1.46 +/- 0.88; 72 h, 0.93 +/- 0.44 fmol/ml; p < 0.001. Difference between the two groups was significant at the beginning of the test (between 2 and 12 h, p[=]0.002). After that, the values of the plasma endothelin decreased in parallel, p < 0.001. Our data suggest that captopril affects plasma ET levels in the acute and subacute phases of AMI. Moreover, these results provide additional evidence for a beneficial effect of early captopril treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Endothelins_MeSH S_blood_MeSH Endothelins_blood_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Pilot_Projects_MeSH 
****** 9057730
----K E
----T Effect of long-acting and short-acting calcium antagonists on cardiovascular outcomes in hypertensive patients.
----A BACKGROUND: Short-acting calcium antagonists may increase coronary artery morbidity, mortality, and non-cardiovascular complications in hypertensive patients. We assessed whether this association was also true for long-acting calcium antagonists. METHODS: We did a case-control study, which was nested within a systematic hypertension control programme for a prospective cohort of 4350 people (first seen 1981-94). Cases (n = 189) were hypertensive patients who had had a first cardiovascular event, including all cardiovascular deaths and hospitalisations, between 1989 and 1995. Controls (n = 189) were individually matched to cases for sex, ethnic origin, age, type of previous antihypertensive treatment, year of entry into the study, and length of follow-up. We collected data on any prescribed drug regimen that was being taken on the event data for cases and on the same date for matched controls. Calcium antagonists were classified by duration of action. FINDINGS: Compared with those on beta-blocker monotherapy, patients on long-acting calcium antagonists (n = 136) had no increased risk of a cardiovascular event (adjusted odds ratio 0.76 [95% CI 0.41-1.43]), whereas patients on short-acting calcium antagonists (n = 27) were at significantly greater risk (adjusted odds ratio 3.88 [1.15-13.11], p = 0.029). Among 38 matched pairs who were both on calcium antagonists, the adjusted risk ratio for short-acting versus long-acting was 8.56 (1.88-38.97), p < 0.01. INTERPRETATION: Long-acting and short-acting calcium antagonists differ in cardiovascular outcomes. Consistent with earlier findings, the use of short-acting calcium antagonists was associated with increased risk of a cardiovascular event. This finding highlights the need to complete on-going clinical trials so that the relative cardiovascular impact of various antihypertensive agents can be assessed.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Cardiovascular_Diseases_MeSH S_chemically_induced_MeSH Cardiovascular_Diseases_chemically_induced_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Case-Control_Studies_MeSH M_Cohort_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Regression_Analysis_MeSH M_Risk_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 9067912
----K E
----T A short-term antihypertensive treatment-induced fall in glomerular filtration rate predicts long-term stability of renal function.
----A In long-term intervention studies on renal function outcome an initial decline in the glomerular filtration rate (GFR) may occur after starting therapy. If this initial GFR decline is the result of a treatment-induced hemodynamic change reflecting a fall in intraglomerular pressure, it should be reversible after treatment withdrawal, even after long-term treatment. In fact, it could be beneficial for renal function in the long term. We therefore studied systemic and renal hemodynamics in 40 non-diabetic patients with impaired renal function before treatment, during four years treatment with either atenolol or enalapril, and after withdrawal of that treatment. The acute change in GFR 12 weeks after start of treatment varied widely from -11 to + 11 ml/min (mean +/- SD -1.0 +/- 4.1 ml/min, NS). After four years of treatment, withdrawal for 12 weeks resulted in a rise in GFR of +2.2 +/- 5.4 ml/min, P = 0.011, again with a wide range of +14 to -6 ml/min). The initial fall in GFR was related to the rise after withdrawal (r = 0.32, P < 0.05). Interestingly, the acute treatment induced change in GFR correlated with the long-term slope, such that a patient with a greater initial decline in GFR showed a more stable course during the follow up (r = -0.36, P < 0.05). The patients were arbitrarily divided in group A (N = 20), with the largest initial treatment-induced fall in GFR, and group B (N = 20), with the smallest initial fall in GFR. Group A had a significantly less steep slope than group B (-0.41 +/- 1.52 vs. -2.09 +/- 2.79 ml/min/year, P = 0.023) during the four year follow-up. In group A GFR increased again after withdrawal of treatment (+3.8 +/- 5.6 ml/min, P = 0.011) whereas it did not change in group B (+0.5 +/- 4.0 ml/min, NS). As a consequence, GFR post-treatment was not different compared to pre-treatment in group A (-2.5 +/- 7.2 ml/min, NS), whereas it was 5.9 +/- 12.1 ml/min lower in group B (P = 0.023). Patients treated with enalapril had a similar response as patients treated with atenolol. In conclusion, an initial fall in GFR after starting antihypertensive treatment in patients with a mild to moderate renal function impairment (GFR 30 to 90 ml/min) is reversible even after years of treatment, suggesting that this therapy-induced fall is of hemodynamic and not of structural origin. This initial GFR fall was associated with a subsequent stable renal function. These data lead to the hypothesis that the initial fall in GFR in response to antihypertensive therapy reflects renal protection.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9068264
----K 1
----T Beta-blockers and nitrates in patients with peripheral arterial occlusive disease: long-term findings.
----A METHODS: The effect of 6 months' administration of celiprolol, atenolol and isosorbide dinitrate on peripheral arterial occlusive disease (PAOD), double-blind and placebo-controlled, was investigated in 56 patients with chronic ischaemic heart disease and stage IIb PAOD, using as criteria the walking distance and the change in resistance index in the femoral artery. The placebo group consisted of 14 patients with chronic ischaemic heart disease and the same stage of PAOD. RESULTS: Patients on 50 mg/day atenolol showed a significant reduction in both pain-free and maximal walking range compared with the controls. In contrast, those taking 200 mg/day celiprolol and those on 80 mg/day isosorbide dinitrate demonstrated significant increases in pain-free and maximal, walking distance compared with the control group. The colour duplex sonographically measured Doppler flow through the femoral artery showed a significant decrease both in the patients taking celiprolol and in those on isosorbide dinitrate, while in those receiving atenolol the resistance index increased significantly. CONCLUSIONS: The study shows that the beta-adrenoceptor blocker celiprolol also possesses a nitrate-like vasodilatory property and can be used in patients with chronic ischaemic heart disease and impaired peripheral arterial blood flow.
----P Biography Clinical_Trial Historical_Article Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Arterial_Occlusive_Diseases_MeSH S_drug_therapy_MeSH Arterial_Occlusive_Diseases_drug_therapy_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Celiprolol_MeSH S_adverse_effects_MeSH Celiprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_History_of_Medicine__17th_Cent__MeSH M_History_of_Medicine__18th_Cent__MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Long-Term_Care_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9071195
----K E
----T Effect of calcium channel blockade on skin blood flow in diabetic hypertension: a comparison of isradipine and atenolol.
----A In previous studies, using laser Doppler techniques, the authors have demonstrated a duration-dependent reduction in skin blood flow reserve at sites of nutritive (NUTR) perfusion that occurs in diabetes and correlates with the presence of diabetic retinopathy and proteinuria. They speculated that it might be possible to reverse this decrease in blood flow by using agents with peripheral vasodilating properties. They chose the calcium channel blocking agent isradipine as a prototype. As a contrast agent, they chose atenolol, which has an equivalent antihypertensive effect but minimal peripheral vasodilating properties. They studied 24 diabetic hypertensive patients in a randomized, two-way crossover design. They assigned patients randomly to one or the other active drug and titrated to a maximum tolerated maintenance dose. Skin blood flow was measured at the end of the titration and maintenance phases. Patients then entered a four-week washout period, followed by crossover to the alternative drug, and measurements were repeated. At baseline, the twenty-four-hour mean ambulatory systolic blood pressure was 150 +/- 2 mm Hg with a twenty-four-hour mean diastolic blood pressure of 93 +/- 1 mm Hg. Thermally stimulated skin blood flow reserve was about 50% lower in these patients as compared with an age-, sex-, and weight-matched group of 28 nondiabetic, nonhypertensive patients. There was no difference in skin blood flow between the two groups at basal skin temperature or at a controlled temperature of 35 degrees C. Both atenolol and isradipine successfully lowered blood pressure in the study patients. There was a slightly greater decrease in systolic blood pressure with isradipine and a greater decrease in heart rate with atenolol. Neither isradipine nor atenolol treatment affected skin blood flow values at the maximal 44 degrees C temperature. However, at basal skin temperature and at 35 degrees C, isradipine-treated patients had substantial increases in skin blood flow at NUTR sites. For example, skin blood flow at the knee at 35 degrees C with isradipine treatment was 3.1 +/- 0.4 mL/min/100 g compared with 1.1 +/- 0.2 with atenolol, 1.3 +/- 0.1 with placebo, and 0.9 +/- 0.1 for the nondiabetic controls (all P < 0.01). The authors found a twofold to threefold increase in basal skin blood flow at NUTR sites with isradipine treatment. This degree of increase is substantially greater than that previously demonstrated by their group using pentoxifylline. Locally reduced skin blood flow is a factor in promoting skin breakdown and delayed healing. Further study is needed to explore the possibility that isradipine treatment may enhance healing of diabetic skin ulcers.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diabetic_Angiopathies_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isradipine_MeSH S_pharmacology_MeSH Isradipine_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Skin_MeSH S_blood_supply_MeSH Skin_blood_supply_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9080239
----K E
----T Symptomatic and hemodynamic recovery following dobutamine stress echo: benefit of low-dose esmolol administration.
----A OBJECTIVES: We studied the use of esmolol in patients experiencing minor side effects of palpitations, anxiety, nervousness, and tremors associated with dobutamine stress echocardiography. BACKGROUND: Dobutamine stress echocardiography is frequently used in the assessment of coronary artery disease. Esmolol administration may enhance patient comfort. METHODS: Sixty consecutive patients who experienced minor side-effects during dobutamine stress echocardiography were given 0.3 mg/kg esmolol intravenously in the recovery period and compared retrospectively to sixty consecutive controls who underwent dobutamine stress echocardiography, who did not receive esmolol, during the same time period. Both groups were matched for age, ejection fraction, and peak dose of dobutamine. Heart rate and blood pressure were assessed during and after dobutamine administration. RESULTS: Both groups had similar baseline blood pressure (mmHg) (142 +/- 19/72 +/- 14 vs 139 +/- 20/72 +/- 14) and heart rate (beats per minute) (75 +/- 14 vs 75 +/- 17) (esmolol and control respectively, p = ns), but peak heart rate was higher in the esmolol group (126 +/- 14 vs. 116 +/- 14, p < 0.01). In the group who received esmolol, symptomatic relief paralleled the statistically significant decrease in heart rate which occurred within 1 minute of esmolol administration (99.7 +/- 15.3 vs 108.5 +/- 13.1 p < 0.0001); the heart rate in the esmolol group remained significantly lower than the control group for 5 minutes following esmolol administration (92.0 +/- 10.3 vs 96.7 +/- 11.8 p < 0.05). As a percentage of peak heart rate the esmolol group remained significantly lower than the control for 7 minutes (74% vs 80% p < 0.05). Esmolol induced a significant reversal of dobutamine-induced diastolic hypotension (diastolic blood pressure at peak 66 +/- 17 vs 8 min recovery 70 +/- 12, p < 0.03) that was not seen in controls (diastolic blood pressure at peak 64 +/- 18 vs 8 min recovery 65 +/- 14, p = ns). Systolic blood pressure and heart rate remained elevated in both groups 8 min into recovery compared to baseline, suggesting persistent dobutamine effect beyond the expected 2 min pharmacologic half-life of dobutamine. No side-effects from esmolol were seen despite it being used in 9 patients with EF < 35%. CONCLUSIONS: Esmolol is effective and well tolerated for the management of dobutamine-related minor side-effects. The mechanism of benefit, in addition to heart rate reduction, may involve a reversal of dobutamine-induced diastolic hypotension. Blood pressure and heart rate recovery are slower than expected from previously published pharmacokinetic data.
----P Journal_Article 
----M M_Adrenergic_beta-Agonists_MeSH S_diagnostic_use_MeSH Adrenergic_beta-Agonists_diagnostic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Dobutamine_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH S_drug_therapy_MeSH Hypotension_drug_therapy_MeSH S_physiopathology_MeSH Hypotension_physiopathology_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 9080918
----K E
----T Relationships of quality-of-life measures to long-term lifestyle and drug treatment in the Treatment of Mild Hypertension Study.
----A OBJECTIVES: To compare 5 antihypertensive drugs and placebo for changes in quality of life (QL). To assess the relationship of lifestyle factors and change in lifestyle factors to QL in participants with stage I diastolic hypertension. METHODS: The Treatment of Mild Hypertension Study (TOMHS) was a randomized, double-blind, placebo-controlled clinical trial with minimum participant follow-up of 4 years. It was conducted at 4 hypertension screening and treatment academic centers in the United States. The cohort consisted of 902 men and women with hypertension, aged 45 to 69 years, with diastolic blood pressures less than 100 mm Hg. Informed consent was obtained from each participant after the nature of the procedures had been fully explained. Sustained nutritional-hygienic intervention was administered to all participants to reduce weight, to reduce dietary sodium and alcohol intake, and to increase physical activity. Participants were randomized to take (1) acebutolol (n = 132); (2) amlodipine maleate (n = 131); (3) chlorthalidone (n = 126); (4) doxazosin mesylate (n = 134); (5) enalapril maleate (n = 135); or placebo (n = 234). Changes in 7 QL indexes were assessed based on a 35-item questionnaire: (1) general health; (2) energy or fatigue; (3) mental health; (4) general functioning; (5) satisfaction with physical abilities; (6) social functioning; and (7) social contacts. RESULTS: At baseline, higher QL was associated with older age, more physical activity, lower obesity level, male gender, non-African American race, and higher educational level. Improvements in QL were observed in all randomized groups, including the placebo group during follow-up; greater improvements were observed in the acebutolol and chlorthalidone groups and were evident throughout follow-up. The amount of weight loss, increase in physical activity, and level of attained blood pressure control during follow-up were related to greater improvements in QL. CONCLUSIONS: In patients with stage I hypertension, antihypertensive treatment with any of 5 agents used in TOMHS does not impair QL. The diuretic chlorthali-done and the cardioselective beta-blocker acebutolol appear to improve QL the most. Success with lifestyle changes affecting weight loss and increase in physical activity relate to greater improvements in QL and show that these interventions, in addition to contributing to blood pressure control, have positive effects on the general well-being of the individual.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Alcohol_Drinking_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Exercise_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Questionnaires_MeSH M_Sodium__Dietary_MeSH S_administration_&_dosage_MeSH Sodium__Dietary_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Weight_Loss_MeSH 
****** 9088769
----K E
----T Outcome of unstable angina in patients with diabetes mellitus.
----A This prospective hospital-based, case-control study compares the outcome of unstable angina in non-insulin dependent diabetic patients and non-diabetic control subjects. One hundred and sixty-two diabetic patients and 162 non-diabetic control patients with unstable angina were entered into the study. The 3-month mortality was 8.6% (95% confidence interval, CI = 4.4-12.9%) in diabetic patients and 2.5% (CI = 0.1-4.9%) in control patients (p = 0.014). The 1-year mortality was 16.7% (CI = 10.9%-22.4%) in diabetic patients and 8.6% (CI = 4.4%-12.9%) in non-diabetic patients (p = 0.029). Diabetic patients received beta-blockade and underwent coronary angiography and angioplasty less frequently than controls; the frequency of unstable angina, of acute myocardial infarction, and coronary artery bypass grafting was similar in both groups at 1 year of follow-up. It is concluded that diabetic patients with unstable angina have a higher mortality than non-diabetic patients and that this difference is largely accounted for by early (first 3 months) mortality.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_epidemiology_MeSH Angina__Unstable_epidemiology_MeSH S_mortality_MeSH Angina__Unstable_mortality_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH M_Angioplasty_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Confidence_Intervals_MeSH M_Coronary_Angiography_MeSH M_Coronary_Artery_Bypass_MeSH S_statistics_&_numerical_data_MeSH Coronary_Artery_Bypass_statistics_&_numerical_data_MeSH M_Coronary_Disease_MeSH S_genetics_MeSH Coronary_Disease_genetics_MeSH M_Diabetic_Angiopathies_MeSH S_epidemiology_MeSH Diabetic_Angiopathies_epidemiology_MeSH S_mortality_MeSH Diabetic_Angiopathies_mortality_MeSH S_therapy_MeSH Diabetic_Angiopathies_therapy_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH 
****** 9088811
----K E
----T Attenuation of the haemodynamic responses to noxious stimuli in patients undergoing cataract surgery. A comparison of magnesium sulphate, esmolol, lignocaine, nitroglycerine and placebo given i.v. with induction of anaesthesia.
----A A study was conducted on 100 middle-aged to elderly patients (n = 52, healthy; n = 48, suffering from either diabetes, hypertension, ischaemic heart disease or a combination of these diseases) undergoing cataract extraction to assess the effects of laryngoscopy and tracheal intubation, anaesthesia and surgery, eye bandaging and tracheal extubation, saline (control), magnesium sulphate 40 mg kg-1, esmolol 4.0 mg kg-1, lignocaine 1.5 mg kg-1 and glyceryl trinitrate 7.5 micrograms kg-1 given i.v. at induction of anaesthesia on heart rate (HR), blood pressure (BP), rate-pressure product (RPP) and pressure-rate quotient (PRQ). Anaesthesia was standardized. Haemodynamic responses and requirements for atropine, ephedrine and labetalol to maintain HR and BP during surgery were similar in healthy and diseased patients, and in the test drug groups. Differences produced by the test drugs were evident until 5 min following intubation. Esmolol prevented rises in HR and RPP. Glyceryl trinitrate prevented a rise in BP, but was associated with tachycardia and a fall in PRQ to < 1.0. Magnesium sulphate and lignocaine did not prevent responses to laryngoscopy and tracheal intubation, and were associated with rises in RPP. Application of the eye dressing and tracheal extubation at the end of surgery each caused significant increases in HR, BP and RPP in all groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH P_Anesthesia_MeSH S_adverse_effects_MeSH Anesthesia_adverse_effects_MeSH M_Anesthetics__Local_MeSH S_therapeutic_use_MeSH Anesthetics__Local_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH P_Cataract_Extraction_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Intraoperative_Complications_MeSH S_prevention_&_control_MeSH Intraoperative_Complications_prevention_&_control_MeSH M_Intubation__Intratracheal_MeSH S_adverse_effects_MeSH Intubation__Intratracheal_adverse_effects_MeSH M_Lidocaine_MeSH S_therapeutic_use_MeSH Lidocaine_therapeutic_use_MeSH M_Magnesium_Sulfate_MeSH S_therapeutic_use_MeSH Magnesium_Sulfate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9120160
----K E
----T Left ventricular remodeling with carvedilol in patients with congestive heart failure due to ischemic heart disease. Australia-New Zealand Heart Failure Research Collaborative Group.
----A OBJECTIVES: The aim of this study, a substudy of the Australia-New Zealand trial of carvedilol in patients with heart failure due to ischemic heart disease, was to determine the effects of this treatment on left ventricular size and function with the use of quantitative two-dimensional (2D) echocardiography. BACKGROUND: Beta-adrenergic blocking drugs have been shown to improve left ventricular ejection fraction in patients with heart failure due to either ischemic heart disease or idiopathic dilated cardiomyopathy. However, the effects of such treatment on left ventricular size remain uncertain. METHODS: One hundred twenty-three patients from 10 centers in New Zealand and Australia participated in the 2D echocardiographic substudy. Echocardiography was performed before randomization and was repeated after 6 and 12 months of treatment. Left ventricular end-diastolic and end-systolic volumes were measured from apical four- and two-chamber views with the use of a modified Simpson's rule method. RESULTS: After 12 months, heart rate was 8 beats/min lower in the carvedilol than in the placebo group, whereas left ventricular end-diastolic and end-systolic volumes were increased in the placebo group but reduced in the carvedilol group. At 12 months, left ventricular end-diastolic volume index was 14 ml/m2 less in the carvedilol than in the placebo group (p = 0.0015); left ventricular end-systolic volume index was 15.3 ml/m2 less (p = 0.0001), and left ventricular ejection fraction was 5.8% greater (p = 0.0015). CONCLUSIONS: In patients with heart failure due to ischemic heart disease, carvedilol therapy for 12 months reduced left ventricular volumes, increased left ventricular ejection fraction and prevented progressive left ventricular dilation. These changes demonstrate a beneficial effect of carvedilol on left ventricular remodeling in heart failure. The observed changes may explain in part the improved clinical outcomes produced by treatment with carvedilol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_ultrasonography_MeSH Myocardial_Ischemia_ultrasonography_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9098273
----K 4
----T Effects on intraocular pressure and side effects of 0.005% latanoprost applied once daily, evening or morning. A comparison with timolol. Scandinavian Latanoprost Study Group.
----A PURPOSE: To compare the effect on intraocular pressure (IOP) and side effects of 0.005% latanoprost applied once daily, morning or evening, with 0.5% timolol applied twice daily. METHODS: A 6-month randomized, double-masked, multicenter study with three parallel groups was undertaken. Two hundred sixty-seven patients were randomized, 84 to timolol, 89 to latanoprost in the morning for 3 months and then in the evening for another 3 months, and 94 to latanoprost with the treatment schedule reversed. RESULTS: After 6 months, timolol reduced diurnal IOP from 24.6 to 17.9 mmHg (27%); latanoprost applied in the morning, from 25.5 to 17.7 mmHg (31%); and latanoprost applied in the evening, from 24.8 to 16.2 mmHg (35%). The efficacy of latanoprost applied in the evening was statistically superior to latanoprost applied in the morning and to timolol (P < 0.001). Latanoprost induced a slight increase in conjunctival hyperemia in 31.4% of treated patients, compared with 15.9% for timolol. Sporadic episodes of mild punctate corneal epithelial erosions were three times as frequent in latanoprost-treated eyes as in timolol-treated eyes. The most significant ocular side effect was increased pigmentation of the iris observed in five and suspected in seven more latanoprost-treated eyes. All these eyes had a mixed green-brown or blue/gray-brown iris color. Timolol reduced heart rate by 3 beats/minute (P < 0.005). CONCLUSIONS: The effect on diurnal IOP of latanoprost applied once daily in the evening is superior to that of timolol. The main difference in side effects is increased pigmentation of the iris induced by latanoprost, most likely due to stimulation of melanogenesis in iris stromal melanocytes.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Evaluation_MeSH M_Eye_Color_MeSH S_drug_effects_MeSH Eye_Color_drug_effects_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9104896
----K E
----T Use of evidence-based medical therapy in patients undergoing percutaneous coronary revascularization in the United States, Europe, and Canada. Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT-I) and Canadian Coronary Atherectomy Trial (CCAT) investigators.
----A The objective of this study was to examine whether there are international variations in the use of evidence-based medical therapy in patients undergoing percutaneous coronary revascularization. We analyzed the medical therapy of patients in the United States (US) (n = 878), Europe (n = 134), and Canada (n = 274) who underwent percutaneous coronary revascularization in either the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT-I) (enrollment from August 1991 to April 1992) or the Canadian Coronary Atherectomy Trial (CCAT) (enrollment from July 1991 to August 1992). We found that at the time of hospital admission, Canadian patients had the highest rates of treatment with aspirin (95% vs 57% US and 78% Europe; p = 0.002), calcium antagonists (75% vs 48% US and 43% Europe; p 0.0001), beta blockers (60% vs 32% US and 46% Europe; p = 0.02), and combination anti-ischemic therapy (67% vs 43% US and 56% Europe; p = 0.0001). By discharge, however, Canadian patients had the lowest rates of treatment with nitrates (12% vs 40% US and 44% Europe; p = 0.0001) and combination anti-ischemic therapy (29% vs 53% US and 47% Europe; p < 0.01). At both admission and discharge, rates of treatment with angiotensin-converting enzyme inhibitors and lipid-lowering agents were < 15% in all 3 regions. We conclude that significant international variations exist in the use of evidence-based medical therapy in patients undergoing percutaneous coronary revascularization.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH P_Atherectomy__Coronary_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Canada_MeSH S_epidemiology_MeSH Canada_epidemiology_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Europe_MeSH S_epidemiology_MeSH Europe_epidemiology_MeSH M_Evidence-Based_Medicine_MeSH S_statistics_&_numerical_data_MeSH Evidence-Based_Medicine_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 9104905
----K E
----T Effect of antithrombotic therapy on risk of sudden coronary death in patients with congestive heart failure.
----A Data from epidemiologic, autopsy, Holter monitoring, and electrophysiologic studies support the hypothesis that acute myocardial ischemia, even in the absence of myocardial infarction, is a critical component of the pathophysiology of sudden coronary death. Acute myocardial ischemia superimposed upon ventricles damaged from previous infarctions has been demonstrated to enhance the generation of lethal ventricular arrhythmias. This is a retrospective analysis of 6,797 participants in the Studies of Left Ventricular Dysfunction prevention and treatment trials. Both univariate and multivariate Cox proportional-hazards modeling were used to study the association of anticoagulant and antiplatelet therapy with the risk for sudden cardiac death. The following covariates were adjusted for in the analysis: age, ejection fraction, gender, atrial fibrillation, diabetes, a history of angina, prior infarction, prior revascularization, and the regular use of beta blockers, diuretics, digoxin, antiarrhythmic agents, or enalapril. The overall incidence of sudden cardiac death per 100 patient-years of follow-up was 2.24%. In multivariate analysis, antiplatelet and anticoagulant monotherapy each remained independently associated with a reduction in the risk of sudden cardiac death: antiplatelet therapy with a 24% reduction (relative risk [RR] 0.76; 95% confidence interval [CI] 0.61-0.95) and antiplatelet monotherapy with a 32% reduction (RR 0.68; 95% CI 0.48-0.96). Thus, in patients with moderate to severe left ventricular systolic dysfunction resulting from coronary artery disease, antiplatelet and anticoagulant therapy are each associated with a reduction in the risk of sudden cardiac death.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Proportional_Hazards_Models_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 9105649
----K E
----T Inhibitor index: a novel method for measuring pharmacological inhibition of angiotensin-converting enzyme.
----A Research into the exact mechanism and site of action of ACE inhibiting compounds has been hampered by methodological difficulties concerning the quantitation of ACE inhibition in tissues. This paper describes an attempt to address this difficulty. ACE activity in serum and uncentrifuged skeletal muscle homogenates was measured with a fluorometric assay before and during treatment in 24 fosinopril-treated and 26 atenolol-treated hypertensives. The absolute difference in activity between the higher and the lower of two different sample dilutions divided by the mean activity was taken to represent competitive inhibition in the sample, "inhibitor index". The reduction in muscle ACE activity coinciding with fosinopril treatment was not statistically significant (-2.6%, p = 0.68). The inhibitor index, however, increased by 46% (p = 0.045) and no change was seen in the atenolol-treated group (-12%, p = 0.51). The change in muscle inhibitor index (but not the reduction in serum ACE activity) correlated inversely with the change in blood pressure (r = -0.50, p = 0.034) and serum aldosterone (r = -0.54, p = 0.031) in the fosinopril group, but not in the atenolol group. In a second study, serum inhibitor index increased by 0.28 (95% CI 0.24-0.32) in 12 trandolapril-treated, but was unchanged in 11 atenolol-treated patients (+0.0097, 95% CI -0.029-0.048). In conclusion, the present study indicates that the inhibitor index described recognizes physiologically relevant ACE inhibition. The value of the method needs to be investigated further.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiology_MeSH S_methods_MeSH Cardiology_methods_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fluorometry_MeSH M_Fosinopril_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle__Skeletal_MeSH S_enzymology_MeSH Muscle__Skeletal_enzymology_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH S_metabolism_MeSH Peptidyl-Dipeptidase_A_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9107160
----K E
----T Nonselective beta-adrenergic blockade with carvedilol does not hinder the benefits of exercise training in patients with congestive heart failure.
----A BACKGROUND: Long-term beta-adrenergic blockade does not appear to be associated with drug-induced training in patients with congestive heart failure (CHF); whether exercise training can increase peak aerobic capacity in patients with CHF who are treated with beta-adrenergic blockers is currently unknown. METHODS AND RESULTS: We studied 23 patients with CHF who were treated with carvedilol or propranolol in addition to ACE inhibitors, furosemide, and digoxin. Of the patients treated with carvedilol, 8 underwent exercise training and 8 remained sedentary. All 7 patients treated with propranolol underwent exercise training. Peak oxygen consumption (mL.kg-1.min-1) was serially measured in trained and sedentary patients. Peak reactive hyperemia (mL.min-1.100 mL-1) was determined in the calf and forearm immediately before and after 12 weeks of training. The peak oxygen consumption of trained patients treated with either carvedilol or propranolol increased from 12.9 +/- 1.4 to 16.0 +/- 1.6 (P < .001) and 12.4 +/- 1.0 to 15.7 +/- 0.9 (P < .001) mL.kg-1.min-1, respectively, whereas it did not change in the sedentary patients. Peak reactive hyperemia increased significantly in the calves but not the forearms of trained patients. CONCLUSIONS: Long-term, nonselective beta-adrenergic blockade with carvedilol or propranolol does not prevent patients with CHF from deriving systemic and regional benefits from physical training.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adaptation__Physiological_MeSH S_drug_effects_MeSH Adaptation__Physiological_drug_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aerobiosis_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics__Sulfamyl_MeSH S_administration_&_dosage_MeSH Diuretics__Sulfamyl_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH P_Exercise_Therapy_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Furosemide_MeSH S_administration_&_dosage_MeSH Furosemide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Furosemide_therapeutic_use_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_rehabilitation_MeSH Heart_Failure__Congestive_rehabilitation_MeSH M_Human_MeSH M_Hyperemia_MeSH S_etiology_MeSH Hyperemia_etiology_MeSH M_Leg_MeSH S_blood_supply_MeSH Leg_blood_supply_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Receptors__Adrenergic__beta_MeSH S_physiology_MeSH Receptors__Adrenergic__beta_physiology_MeSH 
****** 9107241
----K E
----T Randomised trial of transjugular-intrahepatic-portosystemic shunt versus endoscopy plus propranolol for prevention of variceal rebleeding.
----A BACKGROUND: The transjugular-intrahepatic-portosystemic shunt is a new interventional treatment for portal hypertension. The aim of our study was to compare the transjugular shunt with endoscopic treatment for the prophylaxis of recurrent variceal bleeding. METHODS: Between March, 1993, and March, 1996, 126 patients with variceal bleeding were randomly assigned either transjugular shunt (n = 61) or endoscopic treatment (n = 65). Patients were followed up for a median of 14 (IQR 8-25) months and 13 (8-25) months, respectively. In 31 (51%) of the shunted patients, simultaneous transjugular-variceal embolisation was done at the time of shunt placement. Endoscopic treatment consisted of sclerotherapy and/or banding ligation and was combined with propranolol medication. FINDINGS: Technical success was achieved in all patients assigned to the shunt group. During follow-up, the cumulative 1-year variceal rebleeding rates in the shunted and endoscopically treated patients were 15% and 41% and the 2-year rates were 21% and 52% (p = 0.001), respectively. In nine (12%) patients from the endoscopic group treatment failed and the patients received the transjugular-shunt treatment. A total of 19 bleeding episodes from any source occurred in 15 patients in the shunt group compared with 100 episodes in 33 patients in the endoscopic group. There was no difference in survival with estimated 1-year survival rates for shunted and endoscopically treated patients of 90% and 89%, and 2-year survival rates of 79% and 82%, respectively. The incidence of clinically significant hepatic encephalopathy after 1 year was higher in the shunt group (36% vs 18%, p = 0.011). INTERPRETATION: These results suggest, that the transjugular shunt is more effective than endoscopic treatment in prevention of variceal rebleeding but has a considerable risk of hepatic encephalopathy. Survival is similar in the two groups.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Embolization__Therapeutic_MeSH M_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hepatic_Encephalopathy_MeSH M_Human_MeSH M_Ligation_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH M_Survival_Rate_MeSH 
****** 9107560
----K I
----T Design of the cardiac insufficiency bisoprolol study II (CIBIS II). The CIBIS II Scientific Committee.
----A Clinical research in chronic heart failure has recently focused on the stimulated neuro-hormonal compensatory mechanisms that could contribute to auto-aggravation of the disease. On the basis of such a hypothesis, and apart from the inhibition of the renin angiotensin system, the antagonism of beta-receptors has evolved as a promising approach for improving quality of life and prognosis. However, the definite proof of beta-adrenoceptor blockade induced benefit on survival remains to be demonstrated. On the basis of CIBIS I data, the objective of the Cardiac Insufficiency Bisoprolol Study II (CIBIS II) is to evaluate effects of the selective beta-1 adrenoceptor blocker, bisoprolol, on mortality (primary endpoint) in patients with ischaemic or non-ischaemic chronic heart failure. Eligible patients will be symptomatic ambulatory patients with left ventricular ejection fraction < or = 35% in NYHA functional class III or IV, receiving a background treatment of diuretics and angiotensin converting enzyme inhibitors. A total of 2,500 patients are planned to be included with a mean follow up of at least 3 years. Secondary endpoints include hospitalisations, cardiovascular mortality and combination of both as well as permanent treatment withdrawal. Bisoprolol will be titrated up to 10 mg, starting with 1.25 mg daily. Randomization began in November 1995. CIBIS II results will represent a basis for definite conclusions on the evaluation of beta-adrenoceptor blockade induced benefit with bisoprolol in chronic heart failure.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Research_Design_MeSH 
****** 9113491
----K I
----T Sudden cardiac death in patients with hypertension. An association with diuretics and beta-blockers?
----A The cornerstones of current antihypertensive treatment are diuretics and beta-blockers and the efficacy of these drugs in preventing cardiovascular disease is undisputed. This article focuses on the effect of these 2 drug classes on the incidence of sudden death. Numerous studies have shown that thiazide diuretics have a strong, dosage-dependent potassium-depleting effect, and it has been postulated that this may explain why the reduction in risk of coronary heart disease, observed in hypertension trials, was less pronounced than expected. In 7 trials that included sudden death as an end-point; a pooled risk-ratio of sudden death of 1.5 (95% confidence interval 1.1 to 2.0) was observed when non-potassium-sparing diuretics were compared with placebo. Two recent case-control studies have also strongly indicated that the use of thiazides increases the risk of sudden death. Evidence from trials using potassium-sparing diuretic combinations suggests that these may be better tolerated than thiazide monotherapy. Although it was suggested in the 2 recent case-control studies that recipients of beta-blockers are also at an increased risk of sudden death, further studies are required to confirm this finding, particularly since these drugs have several well-documented cardioprotective effects.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH P_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Potassium_MeSH S_urine_MeSH Potassium_urine_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9114765
----K E
----T Effects of atenolol versus enalapril on cardiovascular fitness and serum lipids in physically active hypertensive men.
----A An ideal drug regimen for physically active hypertensive patients should not offset exercise-induced improvements in cardiovascular health or fitness. In this randomized, double-blind, placebo-controlled, crossover study of 39 physically active men with uncomplicated essential hypertension, we compared the effects of atenolol and enalapril on cardiovascular fitness and serum lipids. Drugs (atenolol, 50 or 100 mg once daily; enalapril, 10 or 20 mg once daily) were each administered for 4 weeks and each active drug period was preceded by 4 weeks of placebo therapy. Both drugs effectively (p < 0.001) lowered resting blood pressure when measured at the time of theoretical peak (i.e., 3 to 4 hours postdrug) and trough (i.e., 24 hours postdrug) drug blood levels. Atenolol reduced maximal oxygen uptake (by 7.3%, p < 0.001) 3 to 4, but not 24, hours after drug ingestion; no changes occurred with enalapril. Similarly, whereas serum lipids were essentially unchanged with enalapril, serum triglycerides (18.9% increase), high-density lipoprotein cholesterol (10.6% decrease), and ratio of low-density to high-density lipoprotein cholesterol (15.4% increase) were adversely impacted (p < or = 0.05) with atenolol. It is concluded that in contrast to enalapril, atenolol adversely impacts cardiovascular fitness and serum lipids and lipoproteins in physically active hypertensive men.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_Test_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH P_Physical_Fitness_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9114777
----K E
----T Effectiveness of digitalis with or without acebutolol in preventing atrial arrhythmias after coronary artery surgery.
----A In this study, a beta-adrenergic blocker in combination with digoxin provided marginal protection against atrial fibrillation/flutter after coronary artery surgery. The economic comparison of patients who did and did not develop atrial fibrillation/flutter indicates that prevention of these arrhythmias can have a significant impact on length of hospital stay and cost of this common surgical procedure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Atrial_Flutter_MeSH S_etiology_MeSH Atrial_Flutter_etiology_MeSH S_prevention_&_control_MeSH Atrial_Flutter_prevention_&_control_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 9129845
----K E
----T Prediction of left ventricular dysfunction in coronary artery disease from clinical and exercise test findings.
----A We studied the ability to predict depressed left ventricular ejection fraction (LVEF) from clinical and exercise test findings prior to surgery in consecutive patients who underwent coronary artery bypass grafting (CABG) from 1988 to 1991 (n = 663). Multivariate analysis showed a history of myocardial infarction, pathological Q-wave in resting ECG, systolic blood pressure at maximal exercise and the degree of mitral regurgitation as significant independent predictors of impaired LVEF. The relative risk (RR) of depressed LVEF was markedly increased for a previous history of myocardial infarction (RR 3.3, p < 0.0001) and a pathological Q-wave in resting ECG (RR 2.4, p < 0.0001). All associations found between depressed LVEF and exercise test results were poor, and of little value for discriminating patients with depressed LVEF. Thus, clinical data appear to be better markers of low LVEF than the information obtained from the exercise test.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Animals_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hamsters_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Predictive_Value_of_Tests_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH M_Ventricular_Pressure_MeSH 
****** 9129883
----K I
----T Effects of beta-blocker therapy on mortality in patients with heart failure. A systematic overview of randomized controlled trials.
----A AIMS: Several randomized trials have reported that beta-blocker therapy improves left ventricular function and reduces the rate of hospitalization in patients with congestive heart failure. However, most trials were individually too small to assess reliably the effects of treatment on mortality. In these circumstances a systematic overview of all trials of beta-blocker therapy in patients with congestive heart failure may provide the most reliable guide to treatment effects. METHODS AND RESULTS: Details were sought from all completed randomized trials of oral beta-blocker therapy in patients with heart failure of any aetiology. In particular, data on mortality were sought from all randomized patients for the scheduled treatment period. The typical effect of treatment on mortality was estimated from an overview in which the results of all individual trials were combined using standard statistical methods. Twenty-four randomized trials, involving 3141 patients with stable congestive heart failure were identified. Complete data on mortality were obtained from all studies, and a total of 297 deaths were documented during an average of 13 months of follow-up. Overall, there was a 31% reduction in the odds of death among patients assigned a beta-blocker (95% confidence interval 11 to 46%, 2P = 0.0035), representing an absolute reduction in mean annual mortality from 9.7% to 7.5%. The effects on mortality of vasodilating beta-blockers (47% reduction SD 15), principally carvedilol, were non-significantly greater (2P = 0.09) than those of standard agents (18% reduction SD 15), principally metoprolol. CONCLUSIONS: Beta-blocker therapy is likely to reduce mortality in patients with heart failure. However, large-scale, long-term randomized trials are still required to confirm and quantify more precisely the benefit suggested by this overview.
----P Journal_Article Review Review__Tutorial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 9133504
----K E
----T Silent myocardial ischemia: some good news.
----A 
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Myocardial_Revascularization_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Pilot_Projects_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH S_standards_MeSH Randomized_Controlled_Trials_standards_MeSH M_Research_Design_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9133508
----K E
----T Effect of single-drug therapy on reduction of left ventricular mass in mild to moderate hypertension: comparison of six antihypertensive agents. The Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A BACKGROUND: Antihypertensive drugs may differ in their ability to reduce LV mass. Covariates other than drug selection, such as pretreatment LV mass, body weight, the magnitude of blood pressure reduction, race, and age may modify the response of LV mass to therapy. METHODS AND RESULTS: Patients with mild to moderate hypertension (diastolic blood pressure, 95 to 109 mm Hg) were randomly allocated to treatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-masked trial. Patients achieving the goal diastolic blood pressure of <90 mm Hg during drug titration entered a 1-year maintenance period. Longitudinal analysis examined changes from baseline echocardiogram in LV mass at 8 weeks and at 1 year, statistically adjusted for pretreatment LV mass, systolic blood pressure, body weight, sodium excretion, physical activity, race, and age. Significant reductions at 1 year in adjusted LV mass were seen for patients in the highest tertile of pretreatment LV mass treated with hydrochlorothiazide (mean, -42.9; 95% confidence limits, -65.5, -20.2 g), captopril (mean, -38.7; 95% confidence limits, -61.0, -16.4 g), and atenolol (mean, -28.1; 95% confidence limits, -50.9, -5.3 g). These treatment effects differed from those of prazosin, diltiazem, or clonidine. CONCLUSIONS: Antihypertensive drugs have disparate effects on LV mass independent of the magnitude of blood pressure reduction. Patients with adequate blood pressure control on captopril, hydrochlorothiazide, and atenolol show a reduction of LV mass after 1 year of treatment, whereas patients on diltiazem, clonidine, or prazosin do not.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Clonidine_MeSH S_pharmacology_MeSH Clonidine_pharmacology_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_epidemiology_MeSH Hypertrophy__Left_Ventricular_epidemiology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Prazosin_MeSH S_therapeutic_use_MeSH Prazosin_therapeutic_use_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_United_States_Department_of_Veterans_Affairs_MeSH 
****** 9148648
----K I
----T Effect of antihypertensive drug treatment on cardiovascular outcomes in women and men. A meta-analysis of individual patient data from randomized, controlled trials. The INDANA Investigators.
----A BACKGROUND: Trials of drug therapy for hypertension have shown that such therapy has a clear overall benefit in preventing cardiovascular disease. Although these trials have included slightly more women than men, it is still not clear whether treatment benefit is similar for both sexes. OBJECTIVE: To quantify the average treatment effect in both sexes and to determine whether available data show significant differences in treatment effect between women and men. DESIGN: Subgroup meta-analysis of individual patient data according to sex. Analysis was based on seven trials from the INDANA (INdividual Data ANalysis of Antihypertensive intervention trials) database and was adjusted for possible confounders. PATIENTS: 20,802 women and 19,975 men recruited between 1972 and 1990. INTERVENTIONS: Primarily beta-blockers and thiazide diuretics. RESULTS: In women, treatment effect was statistically significant for stroke (fatal strokes and all strokes) and for major cardiovascular events. In men, it was statistically significant for all categories of events (total and specific mortality, all coronary events, all strokes, and major cardiovascular events). The odds ratios for any category of event did not differ significantly between men and women. In absolute terms, the benefit in women was seen primarily for strokes; in men, treatment prevented as many coronary events as strokes. Graphical analyses suggest that these results could be completely explained by the difference in untreated risk. CONCLUSIONS: In terms of relative risk, treatment benefit did not differ between women and men. The absolute risk reduction attributable to treatment seemed to depend on untreated risk. These findings underline the need to predict accurately the untreated cardiovascular risk of an individual person in order to rationalize and individualize antihypertensive treatment.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9137841
----K I
----T Migraine prophylactic drugs: proof of efficacy, utilization and cost.
----A OBJECTIVES: In order to understand the pattern of utilization of migraine prophylactic drugs by US physicians, we reviewed the scientific rigor of published trials of anti-migraine medications, assessed their cost, and tested the correlation, if any, between utilization, scientific rigor and cost. MATERIALS AND METHODS: Scientific rigor of published reports. We identified all placebo-controlled, randomized, double-blind trials of migraine prophylactic agents through Medline search, major Headache textbooks and proceedings of major scientific meetings where headache-related topics are discussed. We excluded trials that did not include placebo treatment during the active phase of the study. The trials were reviewed and rated for scientific rigor using a 5-point scale (scientific score [ss]; 1 = low, 5 = good), blinded to the physicians' utilization data and cost of the drugs. Studies that did not show benefit of the active drug over placebo were scored -1 to -5, thus allowing for the reverse logic of negative studies. US physicians utilization. Neurologists and primary care physicians (PCP) completed phone-mail-phone questionnaires which inquired about first and second choices of migraine prophylaxis. These choices were averaged to obtain a weighted average percent usage of each drug. Cost. The average wholesale price (AWP) of each drug was obtained from data published by Adelman and Von Seggern, and from the Amerisource (7/9/96) catalog. STATISTICAL ANALYSIS: Spearman's correlation coefficient was used to assess the relationship between the average ss, physician use, and cost of each drug. RESULTS: Propranolol (ss = 1.44), amitriptyline (ss = 2.33) and verapamil (ss = 1.00) were the three preferred migraine prophylactic drugs by both neurologists and PCPs. Approximately 10% of neurologists said that divalproex (ss = 3.75) would be their first or second choice. The selective serotonin reuptake blockers were favored by 13.21% of PCPs. All other prophylactic drugs were felt to be first or second line of treatment by less than 10% of either neurologists or PCPs. Except for one study (ss = 1) that showed that propranolol reduced the migraine frequency by 76% over placebo, trials of the three most preferred medications failed to demonstrate that the active drug is > 50% better than placebo, i.e. the difference in headache frequency when on placebo vs active drug is > 50%. Of the drugs available in the United States, flurbiprofen and metoprolol achieved the best ss (5.00 and 4.33, respectively) but their efficacy over placebo (23% and 14-33%, respectively) and cost ($67.2 and $65.6) were unfavorable. Neurologists and PCPs chose migraine prophylaxis on the basis of scientific merit (r = 0.644, p = 0.018; r = 0.576, p = 0.05, respectively) but not cost (r = -0.254, p = 0.45; r = -0.255, p = 0.455). CONCLUSION: The three most commonly chosen migraine prophylactic agents have not been shown irrefutably to prevent migraine. Furthermore, their benefit, if any, does not exceed 50% over placebo. The well-conducted recent trials that demonstrated the efficacy of divalproex in migraine prevention are steps in the right direction of finding the "ideal migraine preventative agent". Until that drug is discovered, it is difficult to argue that one migraine prophylactic medication is superior to another and accordingly should be used as a first line of treatment.
----P Journal_Article Review Review__Academic 
----M M_Adult_MeSH M_Amitriptyline_MeSH S_economics_MeSH Amitriptyline_economics_MeSH S_pharmacology_MeSH Amitriptyline_pharmacology_MeSH S_therapeutic_use_MeSH Amitriptyline_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Propranolol_MeSH S_economics_MeSH Propranolol_economics_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Verapamil_MeSH S_economics_MeSH Verapamil_economics_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9140801
----K E
----T Antihypertensive treatment with moexipril plus HCTZ vs metoprolol plus HCTZ in patients with mild-to-moderate hypertension.
----A Combination therapy with the new ACE inhibitor moexipril plus hydrochlorothiazide (HCTZ) results in significant blood pressure (BP) reductions. This study compares the efficacy and safety of moexipril plus HCTZ to that of a standard combination treatment in patients with mild-to-moderate hypertension. After a 1 month placebo run-in period, 140 hypertensive patients whose sitting diastolic BP (DBP) averaged 95-114 mm Hg were randomized to receive either once daily moexipril 7.5 mg/HCTZ 12.5 mg or metoprolol 100 mg/HCTZ 12.5 mg for the following 12-week double-blind treatment period. At biweekly visits BP was controlled sphygmomanometrically and the occurrence of adverse events (AE) was documented. At study endpoint adjusted mean reductions in sitting systolic/diastolic BP seen with both combinations were -17.6 mm Hg/-12.8 mm Hg and -17.2 mm Hg/-13.9 mm Hg in the moexipril/HCTZ and metoprolol/HCTZ groups, respectively. The response rate to both kinds of combinations were very similar, 69% and 74% in the moexipril/HCTZ and metoprolol/HCTZ groups, respectively. The percentage of patients which experienced one or more AEs were 46% in the moexipril/HCTZ and 61% in the metoprolol/HCTZ group. Headache and cough which are the most frequently reported AEs after treatment with ACE inhibitors were seen in 9% and 10% of the patients in the moexipril/HCTZ group compared to 10% and 4% in the metoprolol/HCTZ group. The study indicates that the combination of moexipril 7.5 mg plus HCTZ 12.5 mg is as efficacious and safe as metoprolol 100 mg plus HCTZ 12.5 mg in the treatment of mild-to-moderate hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isoquinolines_MeSH S_administration_&_dosage_MeSH Isoquinolines_administration_&_dosage_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 9141231
----K 1
----T Effects of atenolol as add-on therapy to fosinopril in heart failure.
----A Several trials have demonstrated functional benefit with beta-blockers in patients with chronic heart failure. The aim of this observational study was to investigate if additional beneficial effects can be obtained from beta-blockade in a heart failure population that is already receiving high-dose ACE-inhibitor therapy. Atenolol is a long-acting cardioselective beta-blocking agent and is devoid of additional vasodilatory properties. Twenty-five male patients with class II or III heart failure and background therapy of digitalis, furosemide and 20 mg fosinopril per day were treated with 40 mg fosinopril per day and additional 75 mg atenolol per day (beta-blocker group) or with 40 mg fosinopril per day alone (control group). At the end of one year, changes in left ventricular function, exercise parameters and plasma neurohumoral variables reflecting vasoconstriction (noradrenaline, big endothelin) were measured and compared in the two treatment groups. Nineteen patients completed the study. Drop-outs were due to death (4 patients) and non-compliance (2 patients) with no significant difference between the groups. There was a beta-blocker related improvement in left ventricular ejection fraction (p < 0.05 between groups) and an increase in peak oxygen consumption in the control group only (p < 0.05 between groups). Thus, in a heart failure population receiving high-dose ACE inhibitor background therapy beta-blockade with atenolol produced additional benefit by reversing left ventricular dysfunction.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fosinopril_MeSH S_administration_&_dosage_MeSH Fosinopril_administration_&_dosage_MeSH S_adverse_effects_MeSH Fosinopril_adverse_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 9143861
----K E
----T Metabolic effects of carvedilol in hypertensive patients.
----A OBJECTIVE: Fifty-six patients with essential hypertension were recruited to study the metabolic effects of carvedilol, a non-selective beta-adrenoceptor-blocker with alpha 1-adrenoceptor blocking properties. METHODS: The study started with a single-blind, 4-6-week placebo-treatment period followed by an open 6-month active treatment period. There was an option to increase the dose from 25 mg carvedilol to 50 mg daily after 6 weeks. Metabolic investigations were carried out at the end of the placebo period and at the end of the active treatment period. RESULTS: The results show that during carvedilol treatment blood pressure was efficiently lowered. The increase in very low density lipoprotein triglyceride concentration was 13%. Despite this modest increase high density lipoprotein cholesterol was reduced by 11%. The metabolic clearance rate of glucose at the hyper-insulinemic clamp test (adjusted for the prevailing insulin and glucose concentrations) decreased by 17%. At the i.v. glucose tolerance test the insulin area under the curve was increased by 18% and the glucose area by 10%. CONCLUSION: The alpha 1-adrenoceptor-blocking characteristics of carvedilol probably explain the moderate changes of lipoprotein concentrations and insulin sensitivity gained compared with what is usually obtained with a non-selective beta-adrenoceptor-blocker.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_metabolism_MeSH Adrenergic_alpha-Antagonists_metabolism_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_metabolism_MeSH Adrenergic_beta-Antagonists_metabolism_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_metabolism_MeSH Antihypertensive_Agents_metabolism_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_metabolism_MeSH Carbazoles_metabolism_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_metabolism_MeSH Propanolamines_metabolism_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9159306
----K E
----T Short-term effects of blood pressure control and antihypertensive drug regimen on glomerular filtration rate: the African-American Study of Kidney Disease and Hypertension Pilot Study.
----A The African-American Study of Kidney Disease and Hypertension pilot study randomized 94 nondiabetic black men and women (mean age, 53 years; 75% male) with presumed hypertensive nephrosclerosis and a baseline glomerular filtration rate (GFR) of 25 to 70 mL/min/1.73 m2 (mean, 52.3 mL/min/1.73 m2) to blood pressure control at either a low mean arterial pressure (MAP) goal of < or = 92 mm Hg or a usual MAP goal of 102 to 107 mm Hg and an antihypertensive drug regimen that included either a calcium antagonist (amlodipine), a beta-blocker (atenolol), or an angiotensin-converting enzyme (ACE) inhibitor (enalapril). After 3 months of follow-up (n = 90), the mean GFR was similar (53.0 mL/min/1.73 m2 v 53.7 mL/min/1.73 m2) to the baseline levels in participants randomized to the low MAP group (n = 44), whereas the mean GFR increased by 3.9 mL/min/1.73 m2 (P = 0.02) in participants randomized to the usual MAP group (n = 46). During the same period of time, the mean GFR increased significantly in participants randomized to the calcium channel blocker regimen (n = 28) (5.7 mL/min/ 1.73 m2; P = 0.01) but not in participants randomized to the beta-blocker regimen (n = 31) (1.7 mL/min/1.73 m2; P = 0.10) or the ACE inhibitor regimen (n = 31) (1.1 mL/min/1.73 m2; P = 0.52). Changes in GFR at 3 months were significantly different among the three treatment groups (P = 0.04). We conclude that the magnitude of short-term effects of blood pressure control and antihypertensive drug regimens on GFR should be considered when estimating sample size for clinical trials designed to evaluate the effects of these interventions on long-term changes in GFR slope.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Diseases_MeSH S_drug_therapy_MeSH Kidney_Diseases_drug_therapy_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_United_States_MeSH 
****** 9163999
----K E
----T [Arterial hypertension: current large therapeutic trials]
----A In this review, the design and objectives of ongoing clinical trials in essential hypertension are discussed along with the main results obtained from previously published therapeutic trials. In a meta-analysis of 14 of the major primary prevention trials in hypertension, the difference in diastolic blood pressure between the intervention groups and the control groups was only 5-6 mmHg. This difference was associated with significant reductions in all stroke events (42 per cent), all coronary heart disease events (14 per cent) and in cardiovascular mortality (21 per cent). In elderly hypertensive patients, available studies have shown that antihypertensive treatment reduces the incidence of non-fatal cardiovascular events without significantly modifying cardiovascular mortality. Most of these results were obtained with beta-blockers or diuretics. Despite official recommendation as first line monotherapy, none of the three new antihypertensive classes has been shown to have beneficial effects on hard primary endpoints such as cardiovascular morbidity and mortality. Several ongoing large scale randomized controlled trials vs. beta-blockers or diuretics are addressing this important issue. Moreover, other effects of antihypertensive treatment such as the 'J-curve phenomenon', the rate of change in the carotid wall thickness or the exact beneficial effects in elderly patients are being investigated in some of these studies.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteriosclerosis_MeSH S_drug_therapy_MeSH Arteriosclerosis_drug_therapy_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Morbidity_MeSH 
****** 9164696
----K E
----T Current management of aneurysmal subarachnoid hemorrhage guidelines from the Canadian Neurosurgical Society.
----A Published medical evidence pertaining to the management of aneurysmal subarachnoid hemorrhage (SAH) was critically reviewed in order to prepare practice guidelines for this condition. SAH should be considered as a possible cause of all sudden and/or unusual headaches, and every attempt should be made to recognize mild SAHs, as they are still frequently misdiagnosed. The first test for SAH is computed tomography (CT), followed by lumbar puncture when the CT is negative for intracranial bleeding (the case in only several per cent of patients within 24 hours of aneurysm bleeding). Urgent cerebral angiography is necessary to detect the underlying cerebral aneurysm. The advantage of rapid diagnosis of SAH followed by early aneurysm repair is minimizing the risk of catastrophic aneurysm rebleeding. Early surgery for aneurysm repair is often possible and is recommended, unless the aneurysm location or size renders it technically difficult to expose in clot-laden subarachnoid cisterns beneath an acutely swollen brain. Aneurysm ablation is optimally accomplished with open microsurgery and clipping of the aneurysm neck, although other options include proximal parent artery occlusion, "trapping" of the aneurysmal segment of the artery, and embolization of thrombogenic materials (e.g., platinum "microcoils") directly into the aneurysm dome using endovascular techniques. Neurological outcome following SAH is also optimized through the prevention of secondary SAH complications, and further management specific for ruptured cerebral aneurysms can include anticonvulsants, neuroprotectants, and various agents and techniques to prevent or reverse delayed-onset cerebral vasospasm. All patients with aneurysmal SAH should be treated with the calcium antagonist nimodipine, and in certain circumstances patients should receive anticonvulsants. Induced arterial hypertension, hypervolemia and in some instances percutaneous balloon angioplasty are recommended to reverse vasospasm causing symptomatic cerebral ischemia prior to cerebral infarction.
----P Guideline Journal_Article Practice_Guideline 
----M M_Human_MeSH M_Intracranial_Aneurysm_MeSH S_therapy_MeSH Intracranial_Aneurysm_therapy_MeSH M_Subarachnoid_Hemorrhage_MeSH S_therapy_MeSH Subarachnoid_Hemorrhage_therapy_MeSH 
****** 9165181
----K E
----T Effect of atenolol on birth weight.
----A To investigate the possible harmful effects of early antihypertensive drug therapy with atenolol versus other therapies on pregnancy outcome, we reviewed the records of 398 women referred to our antenatal hypertension clinic between 1980 and 1995. Babies born to women taking atenolol were significantly lighter than babies born to women taking other beta blockers, other antihypertensive drugs, or no therapy, suggesting that atenolol might be detrimental in early pregnancy.
----P Journal_Article 
----M M_Analysis_of_Variance_MeSH M_Anthropometry_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Birth_Weight_MeSH S_drug_effects_MeSH Birth_Weight_drug_effects_MeSH M_Female_MeSH M_Fetal_Growth_Retardation_MeSH S_chemically_induced_MeSH Fetal_Growth_Retardation_chemically_induced_MeSH M_Gestational_Age_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Placenta_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9168080
----K I
----T Beta blockade to prevent atrial dysrhythmias following coronary bypass surgery.
----A BACKGROUND: Atrial fibrillation and atrial flutter (AF) frequently complicate coronary artery bypass surgery (CABG) and increase hospital stay as well as morbidity. Studies of drug prophylaxis to prevent AF with beta-adrenergic blocking agents administered in fixed doses have had conflicting results. METHODS: One hundred patients were randomized to receive metoprolol or placebo following CABG. A dosing algorithm was used to achieve clinically significant beta-adrenergic blockade. RESULTS: There was no significant difference between the incidence of AF in the metoprolol (24%) and placebo (26%) groups. However, the incidence of AF in all patients having CABG at this institution declined over the period of the study from 31% to 23% (P < .025), in association with the adoption of a continuous technique of cardioplegia delivery. CONCLUSIONS: Metoprolol is not efficacious for the prevention of post-CABG AF even when dosage is titrated to achieve clinical evidence of beta blockade. It is likely that the adoption of a continuous cardioplegia technique caused a reduction in our incidence of post-CABG AF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Coronary_Artery_Bypass_MeSH S_methods_MeSH Coronary_Artery_Bypass_methods_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Heart_Arrest__Induced_MeSH S_methods_MeSH Heart_Arrest__Induced_methods_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 9169997
----K E
----T Effect of high-performance liquid chromatography on plasma angiotensin II measurements in treated and untreated normotensive and hypertensive patients.
----A BACKGROUND: Angiotensin II (Ang II) levels are normally very low in human plasma, approximately 5 pg/ml. They are usually measured by radioimmunoassay after extraction and concentration. An additional high-performance liquid chromatography (HPLC) step is reportedly necessary for accurate measurement but it is laborious and time-consuming, severely limiting the number of samples that can be assayed. OBJECTIVE: To investigate whether the HPLC step was necessary for measuring Ang II in human plasma samples in our laboratory using our own Ang II antiserum. DESIGN: Human plasma Ang II levels, measured with and without the HPLC step, were compared in two different studies. Since the action of renin is the rate-limiting step in the production of Ang II in plasma, the relationships of plasma renin activity (PRA) to Ang II levels measured with and without HPLC were also evaluated. In the first study, 108 blood samples were collected from 29 hypertensive patients during placebo or treatment with the Ang II antagonist BMS-186295. In the second study blood samples were collected from 12 normal subjects before and during beta-adrenergic blockade. RESULTS: In samples collected during angiotensin II antagonism, which predictably increased plasma Ang II levels, a highly significant relationship between the Ang II measurements with and without HPLC was found (y = 0.99x + 1.7; r = 0.97, P < 0.001). The y intercept of 1.7 pg/ml suggested that the nonspecific immunoreactivity was close to 2 pg/ml in samples assayed without the HPLC step. During beta-adrenergic blockade, which predictably suppressed plasma renin levels, highly significantly linear relationships between HPLC and non-HPLC Ang II measurements (y = 1.3x + 1.6; r = 0.93. P < 0.001, n = 16) and between non HPLC Ang II and PRA (y = 1.9x + 1.7; r = 0.73, P < 0.001, n = 108) were again found. The relationship between PRA and HPLC Ang II was also highly significant (y = 1.4x + 0.04; r = 0.92, P < 0.001, n = 16), but the y intercept was significantly lower (P < 0.001), approaching zero, indicating the removal of nonspecific immunoreactivity during the HPLC step. CONCLUSIONS: These results demonstrate once more that, when using polyclonal antibody 182, the accuracy of the Ang II measurement in human plasma is improved by the inclusion of a HPLC step, especially for samples with Ang II levels in the normal-to-low range. They also show that plasma Ang II and PRA increase or decrease proportionally during treatment with Ang II antagonists or beta-adrenergic blockade, respectively.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH S_blood_MeSH Angiotensin_II_blood_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Chemical_Analysis_MeSH S_methods_MeSH Blood_Chemical_Analysis_methods_MeSH S_statistics_&_numerical_data_MeSH Blood_Chemical_Analysis_statistics_&_numerical_data_MeSH M_Blood_Pressure_MeSH M_Chromatography__High_Pressure_Liquid_MeSH S_methods_MeSH Chromatography__High_Pressure_Liquid_methods_MeSH S_statistics_&_numerical_data_MeSH Chromatography__High_Pressure_Liquid_statistics_&_numerical_data_MeSH M_Evaluation_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Radioimmunoassay_MeSH S_methods_MeSH Radioimmunoassay_methods_MeSH S_statistics_&_numerical_data_MeSH Radioimmunoassay_statistics_&_numerical_data_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Sensitivity_and_Specificity_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 9170400
----K I
----T Fibrinolytic variables and cardiovascular prognosis in patients with stable angina pectoris treated with verapamil or metoprolol. Results from the Angina Prognosis study in Stockholm.
----A BACKGROUND: Disturbed fibrinolytic function may influence the progression of coronary atherosclerosis and contribute to thrombotic cardiovascular (CV) events. METHODS AND RESULTS: In the Angina Prognosis Study in Stockholm (APSIS), patients with stable angina pectoris were studied prospectively during double-blind treatment with metoprolol or verapamil. Various measures of fibrinolytic function were studied in 631 (of 809) patients. During a median follow-up time of 3.2 years (2132 patient-years), 32 patients suffered a CV death, 21 had a nonfatal myocardial infarction (MI), and 77 underwent revascularization. Plasma levels of tissue plasminogen activator (TPA) activity and antigen (ag), plasminogen activator inhibitor (PAI-1) activity at test, and TPA responses to exercise were determined at baseline and after 1 month's treatment and were related to subsequent fatal and nonfatal CV events. Univariate Cox regression analysis revealed that elevated levels of TPA-ag at rest (P < .05), high PAI-1 activity (P < .05), and low TPA-ag responses to exercise (P < .05) were associated with increased risk of subsequent CV death. After adjustment for baseline risk factors, TPA-ag independently predicted CV death or MI. In addition, PAI-1 activity independently predicted CV death or MI in male patients. Verapamil treatment was associated with a 10% decrease of TPA-ag levels and metoprolol treatment with a 2% increase (P < .001 for treatment difference). CONCLUSIONS: Plasma TPA-ag levels at rest, and among male patients PAI-1 activity as well, independently predict subsequent CV death or MI in patients with stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_System_MeSH S_physiopathology_MeSH Cardiovascular_System_physiopathology_MeSH M_Female_MeSH P_Fibrinolysis_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9182472
----K E
----T Metabolic and cardiovascular effects of carvedilol and atenolol in non-insulin-dependent diabetes mellitus and hypertension. A randomized, controlled trial.
----A BACKGROUND: Diabetic patients are considered less suitable than nondiabetic patients for beta-blocker therapy because of the risk for worsened glucose and lipid metabolism and more severe hypoglycemic attacks. OBJECTIVE: To compare the metabolic and cardiovascular effects of carvedilol with those of atenolol in diabetic patients with hypertension. DESIGN: Randomized, double-blind, 24-week trial. SETTING: University hospital clinic. PATIENTS: 45 patients with non-insulin-dependent diabetes mellitus and hypertension. INTERVENTION: After a 4- to 6-week run-in period during which placebo was given in a single-blind manner, patients were randomly assigned to carvedilol or atenolol. MEASUREMENTS: An oral glucose tolerance test; assessment of insulin sensitivity and hormonal responses to insulin hypoglycemia; and assessment of lipid levels, blood pressure, left ventricular mass, and lipid peroxidation. RESULTS: Changes in systolic and diastolic blood pressure and left ventricular mass index were similar with carvedilol and atenolol (P > 0.2). Fasting plasma glucose and insulin levels decreased with carvedilol and increased with atenolol. Responses to carvedilol were greater than those to atenolol, as follows: increase in total glucose disposal, 9.54 mumol/kg of body weight per minute (95% CI, 7 to 11.9 mumol/kg per minute); decrease in plasma glucose response to oral glucose, 61 mmol/L x 180 minutes (CI, -101 to -21 mmol/L x 180 minutes); decrease in insulin response to oral glucose, 6.2 nmol/L x 180 minutes (CI, -9.8 to -2.6 nmol/L x 180 minutes); decrease in triglyceride level, 0.56 mmol/L (CI, -0.75 to -0.37 mmol/L; P < 0.001); increase in high-density lipoprotein cholesterol level, 0.13 mmol/L (CI, 0.09 to 0.17 mmol/L; P < 0.001); and decrease in lipid peroxidation, 0.25 mumol/L (CI, -0.34 to -0.16 mumol/L). CONCLUSIONS: By improving glucose and lipid metabolism and reducing lipid peroxidation, carvedilol may offer advantages in patients with diabetes and hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_blood_MeSH Diabetic_Angiopathies_blood_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipid_Peroxidation_MeSH S_drug_effects_MeSH Lipid_Peroxidation_drug_effects_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Single-Blind_Method_MeSH 
****** 9174677
----K I
----T Carvedilol versus verapamil in chronic stable angina: a multicentre trial.
----A OBJECTIVE: In a multicentre, double-blind, parallel group study, the anti-anginal and the anti-ischaemic efficacy of 12 weeks of therapy with the vasodilating beta-adrenoceptor-blocker carvedilol 25 mg b.i.d. was compared with verapamil 120 mg t.i.d. METHODS: During a 2-week placebo run-in period, patients were required to have two treadmill exercise tests (modified Bruce Protocol) differing by not more than 15% with regard to total exercise time (TET). Of 313 patients enrolled, 248 were randomized and 212 completed the study according to the protocol. RESULTS: The primary variable TET was analysed using the Cox Proportional Hazards Model to take into account censored values due to the patient stopping the exercise test for reasons other than angina. Forty-three per cent of patients allocated to carvedilol and 36% to verapamil did not stop with angina at the final visit. There was no difference in the TET between the groups, the risk ratio being 1.14 in favour of carvedilol (90% CI 0.85-1.52). TET increased from 378 s at baseline to 436 s at the final visit in the carvedilol group and from 386 to 438 s in the verapamil group. Results for time to angina and time to 1 mm ST-segment depression were similar. Compared to verapamil, carvedilol significantly reduced HR, systolic BP and rate pressure product at peak exercise. Analysis of 48 h Holter monitor data showed a greater reduction of HR and PVCs with carvedilol. Lown grading improved in both groups. Adverse events were reported by 48% (3.2% serious adverse events) of patients taking carvedilol and 58% (5.7% serious adverse events) taking verapamil. CONCLUSION: Carvedilol is at least as effective as verapamil in the management of chronic stable angina and demonstrated a favourable adverse event profile.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9175566
----K E
----T Changes in left ventricular mass during treatment with minoxidil and cilazapril in hypertensive patients with left ventricular hypertrophy.
----A Attainment of the regression of hypertension-associated left ventricular hypertrophy (LVH) seems to be a desirable goal of blood pressure (BP)-reducing therapy. Since antihypertensive drugs of differing types may exhibit markedly different abilities to modulate LVH, we examined the effects of the angiotensin-converting enzyme inhibitor cilazapril, and the potassium channel activator minoxidil, alone or in combination with each other, on the left ventricular mass (LVM) in patients with severe essential hypertension who had LVH detected by echocardiography. All patients received the same base therapy of bopindolol and guanfacine. After a run-in period, they were treated with: (1) cilazapril (n = 10); (2) minoxidil, combined with a diuretic (n = 10); or (3) both cilazapril and monoxidil (n = 6) for 12 months. The LVM index (LVMI; LVM per body surface area) was estimated every 3 months by means of echocardiography. Each kind of therapy decreased the arterial pressures to a similar degree. The 1-year treatment with the cilazapril-based regimen resulted in a significantly diminished LVMI (from a mean +/- s.d. of 173 +/- 38 to 152 +/- 22 g/m2; P < 0.05). On the other hand, the minoxidil-based therapy led to a significant increase in LVMI (from 148 +/- 19 to 170 +/- 35 g/m2; P < 0.05). There were no significant LVMI changes in patients receiving the combined, cilazapril + minoxidil-based treatment (172 +/- 34 vs the pretreatment 183 +/- 54 g/m2). The results confirm that long-term treatment with cilazapril is effective both in reducing BP and in reducing LVM. In spite of yielding a satisfactory reduction of BP, minoxidil therapy, even in combination with a diuretic and a beta-blocker, may lead to an aggravation of pre-existing LVH; this effect of minoxidil could be prevented by the simultaneous administration of cilazapril.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Cilazapril_MeSH S_administration_&_dosage_MeSH Cilazapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Cilazapril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_metabolism_MeSH Hypertrophy__Left_Ventricular_metabolism_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Minoxidil_MeSH S_administration_&_dosage_MeSH Minoxidil_administration_&_dosage_MeSH S_therapeutic_use_MeSH Minoxidil_therapeutic_use_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9181278
----K E
----T Proteinuria in mild to moderate hypertension: results of the VA cooperative study of six antihypertensive agents and placebo. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A The prevalence and natural history of severe proteinuria in mild to moderate hypertension are not completely defined. We screened 1635 men with a history of hypertension and randomized 1292 with untreated diastolic blood pressure (DBP) 95-109 mmHg to single-drug treatment with either hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem-SR, prazosin, or placebo in a double-blind prospective trial. Twenty-seven of 1635 patients (1.7%) satisfying clinical criteria for primary hypertension were found to have developed proteinuria > 1000 mg/24 hours and were removed from the study. Follow-up data were obtained on 19 of these 27 patients. One patient was found to have focal segmental sclerosis and progressed to end-stage renal disease. Three other patients developed severe (serum creatinine > 3.5 mg/dl) chronic renal failure (one with diabetic nephropathy), one progressed from serum creatinine 1.4 to 2.2 mg/dl, but 14 of the 19 remained with stable serum creatinine < 2.0 mg/dl on follow-up for 6-9 years. Data were available for 1076 of 1155 (93%) treated study patients at end titration, 522/600 (87%) at one year and 322/444 (73%) at two years. There were significant associations for proteinuria with obesity and higher systolic blood pressure. There was a trend toward significant difference in mean 24-hour protein excretion rates at baseline between black (127 mg) and white (139 mg) patients (p = 0.07). There were no statistically significant changes in urinary protein excretion/24 hours between or within the different treatment groups (including placebo). Eighteen patients were removed from the study during the active treatment phase for proteinuria > 1000 mg/24 hours: hydrochlorothiazide 4, placebo 3, diltiazem 3, prazosin 3, atenolol 2, clonidine 2, and captopril 1. We conclude: (1) the prevalence of severe (> 1 g/24 hours) proteinuria in the hypertensive population is significant but does not necessarily imply a poor prognosis; (2) mean 24-hour urinary protein excretion rates did not vary in response to the different classes of antihypertensive drugs; and (3) there was no drug-specific increase in proteinuria detected in this study.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Continental_Population_Groups_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_complications_MeSH Hypertension__Renal_complications_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Renal_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Proteinuria_MeSH S_epidemiology_MeSH Proteinuria_epidemiology_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 9185024
----K E
----T Calcium channel blockers and cardiac mortality in the treatment of hypertension: a report from the Department of Health Hypertension Care Computing Project (DHCCP).
----A OBJECTIVE: A case control study has reported a 60% higher risk of myocardial infarction in hypertensives treated with a calcium channel blocker (CCB). We examined the Department of Health Hypertension Care Computing Project (DHCCP) data to see if we could confirm or refute this suggestion. DESIGN: Two case control studies, matched and unmatched, plus two longitudinal studies from 1 year of presentation, one for all subjects given a CCB for more than 1 year compared with those not given this drug, and the second comparing survival on the different drugs initially given between 3 and 12 months of follow-up. SUBJECTS: A total of 9328 subjects were included in the analyses and 2154 died. Of these, 6406 received one or more of the following index drugs: 26% a calcium channel blocker (CCB); 84% a diuretic; 29% alpha methyldopa; 12% a beta-blocker (BB); and 11% an angiotensin-converting enzyme (ACE) inhibitor. The CCBs were nifedipine, diltiazem or verapamil. RESULTS: In the case control studies a group given diuretics +/- other treatments (but not including one of the index drugs) provided a reference group with a relative risk (RR) of 1.0. In the matched case control study the adjusted RR for a CCB without a diuretic was 1.32 (95% CI 0.64-2.70) for IHD mortality and 1.05 (95% CI 0.60-1.84) for cardiovascular mortality. Similar results were observed for methyldopa, BBs and ACE inhibitors. The results in the unmatched case control analysis were also similar. The longitudinal study comparing all those treated for over 1 year with a CCB with all other treatments showed a RR for total mortality of 1.03 (95% CI 0.85-1.25). The longitudinal study of total mortality according to treatment initiated at 3-12 months found results of a similar magnitude for CCBs, methyldopa and BBs. CONCLUSIONS: The reference diuretic group had less severe cardiovascular disease than other groups. Treatment with a CCB, BB or methyldopa was associated with an excess mortality in comparison with this reference group. The excess was similar in the different drug groups.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adult_MeSH M_Age_Distribution_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Incidence_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_chemically_induced_MeSH Myocardial_Ischemia_chemically_induced_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Risk_Factors_MeSH M_Sex_Distribution_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 9244644
----K E
----T [Effectiveness and tolerability of bisoprolol vs. nifedipine in uremic patients with ischemic cardiopathy in dialysis treatment]
----A The effects of bisoprolol on transient myocardial ischemia have been compared with those of nifedipine in patients with coronary artery disease in end-stage renal failure maintained on haemodialysis. We also evaluated the tolerability of both drugs. Sixty patients (42 males, 18 females, mean age 52 +/- 4 years) in renal failure maintained on haemodialysis, with coronary artery disease and more than four significant episodes of transient myocardial ischemia (> or = 1 min) during 48-hour Holter monitoring, were included in the study. All cardiovascular drugs were discontinued > or = 6 days before this 48-hour ambulatory ECG monitoring, with the exception of sublingual nitrates allowed for relief of anginal attacks. Patients were then randomized to receive either bisoprolol or nifedipine for 2 weeks. After a 15-day wash-out period, they were crossed over to receive either bisoprolol or nifedipine for other 2 weeks. Statistical analysis was carried out using the Student's t test. A p value < 0.01 was considered significant. Both bisoprolol and nifedipine reduced number and duration of transient ischemic episodes as well as the total ischemic burden. Reductions were statistically significant for both antianginal drugs. Only bisoprolol was effective in silent ischemia (p < 0.001). It also reduced heart rate (p < 0.001), while nifedipine raised it (p < 0.001). Both drugs reduced systolic and diastolic blood pressure. The circadian variations of transient ischemic episodes showed two peaks in the 24 hours. Both peaks were reduced with bisoprolol. Nifedipine brought a clear overall reduction in the number of episodes but the circadian pattern was unchanged. During the study, 10 patients taking bisoprolol and 12 patients taking nifedipine had drug adverse effects. No one of them had to be withdrawn from treatment. In conclusion, bisoprolol seems to be more useful than nifedipine because its effects, in transient ischemic episodes, are greatly superior to those of nifedipine, and because it is effective also in silent ischemia. Both drugs showed a good tolerability in these patients. Bisoprolol, reducing the two daily peaks of ischemic episodes frequency, has a protective role towards mortality due to coronary artery disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Renal_Dialysis_MeSH M_Uremia_MeSH S_complications_MeSH Uremia_complications_MeSH S_therapy_MeSH Uremia_therapy_MeSH 
****** 9191511
----K E
----T PROTECT (Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial): a randomized, double-blind clinical trial of diltiazem versus atenolol in secondary prophylaxis post non-Q wave myocardial infarction.
----A OBJECTIVE: To describe the rationale and design of the Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial (PROTECT). DESIGN: A multicentre, randomized, double-blind, parallel-group comparison of once daily beta-therapy versus heart rate lowering calcium channel blocker therapy, in the reduction of one-year nonfatal reinfarction and cardiovascular death (combined primary end-point) initiated 24 to 96 h post non-Q wave myocardial infarction. SETTING: One hundred and twenty hospitals across Canada. PATIENTS: Over 7500 women and men aged 21 years or older with enzyme-confirmed non-Q wave infarction and without significant left ventricular systolic dysfunction will be recruited over two years. INTERVENTIONS: Once daily beta-blocker therapy (oral atenolol, 50 to 200 mg) versus once daily calcium channel blocker therapy (oral diltiazem 120 to 360 mg) with follow-up for up to three years. CONCLUSIONS: The PROTECT will be the largest all-Canadian cardiovascular trial to date and will compare two commonly prescribed agents for secondary prophylaxis following non-Q wave infarction. The scientific question addressed by the PROTECT is of major public health importance and the results of the study will directly affect current clinical practice.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Recurrence_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9191619
----K I
----T Safety and efficacy of first-line antihypertensives.
----A 
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Placebos_MeSH M_Randomized_Controlled_Trials_MeSH M_Safety_MeSH M_Treatment_Outcome_MeSH 
****** 9199952
----K 1
----T Identification of viable myocardium early after acute myocardial infarction under beta-blockade by enoximone echocardiography.
----A The influence of the beta-blocker metoprolol on the capacity either of low-dose dobutamine echocardiography or the recently introduced enoximone echocardiography to detect viable dysfunctioning myocardium after myocardial infarction was investigated. Initial clinical experience would suggest that the phosphodiesterase III inhibitor enoximona could be an alternative pharmacological stimulation, inducing an increase in contractility in the presence or absence of beta-receptor stimulation. Ten patients with a baseline low-dose dobutamine-echocardiographic test (up to 10 micrograms/kg/min) positive for myocardial viability in > or = 1 segment(s), performed 4-5 days after a first acute myocardial infarction treated with rtPA, were randomized after the administration of intravenous metoprolol (15 mg in three 5-mg boluses) either to dobutamine (up to 15 micrograms/kg/min) or to an enoximone intravenous bolus (1 mg/kg over 5 min) under echocardiographic monitoring, in a crossover sequence, with a 24-h interval. The infarct related artery was patent (TIMI grade 2 o 3) in all the patients. Follow-up echocardiograms were performed 5-7 weeks later. Resting asynergy was found in 40 segments; of these, 17 were viable. All the viable segments remained unresponsive during the post-metoprolol dobutamine infusion, while improved their contractility during enoximone echocardiography. Two patients suffering from early post-infarction angina underwent coronary angioplasty successfully. Eight out of ten patients (2 revascularized and 6 not) showed contractile recovery in a total of 14 segments at the follow-up echocardiogram. Sensitivity, specificity and overall accuracy in predicting reversible dysfunction after acute myocardial infarction for enoximone echocardiography were 93, 85, and 88%, respectively. Our results support the value of enoximone echocardiography in the identification of myocardial viability after myocardial infarction, in patients treated with beta-blockers, which interfere heavily with the results of dobutamine echocardiography.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acute_Disease_MeSH M_Adrenergic_beta-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Agonists_adverse_effects_MeSH S_diagnostic_use_MeSH Adrenergic_beta-Agonists_diagnostic_use_MeSH S_pharmacology_MeSH Adrenergic_beta-Agonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Cardiotonic_Agents_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH M_Dobutamine_MeSH S_adverse_effects_MeSH Dobutamine_adverse_effects_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH S_pharmacology_MeSH Dobutamine_pharmacology_MeSH M_Echocardiography_MeSH S_drug_effects_MeSH Echocardiography_drug_effects_MeSH M_Enoximone_MeSH S_adverse_effects_MeSH Enoximone_adverse_effects_MeSH S_diagnostic_use_MeSH Enoximone_diagnostic_use_MeSH S_pharmacology_MeSH Enoximone_pharmacology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_diagnostic_use_MeSH Metoprolol_diagnostic_use_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Myocardial_Infarction_MeSH S_pathology_MeSH Myocardial_Infarction_pathology_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH 
****** 9200392
----K E
----T Treatment of medically and surgically refractory angina pectoris with high thoracic epidural analgesia: initial clinical experience.
----A Surgical sympathectomy can relieve symptoms of angina in patients with refractory angina. However, in these high-risk patients this thoracic surgery may result in significant morbidity and mortality rates. Similar sympathetic blockade can now be produced with high thoracic epidural analgesia (HTEA). From September 1995 to August 1996, we treated 10 consecutive patients with HTEA. These eight men and two women, aged 58 +/- 5 years, with extensive three-vessel coronary disease and ejection fractions of 40% +/- 5%, had New York Heart Association (NYHA) class IV angina despite medical therapy, including nitrates, beta-blockade, calcium channel blockade, and narcotics. HTEA was performed at the T1 through T4 levels with a catheter placed either percutaneously or surgically, with radiographic confirmation of catheter placement with an epidurogram or computed tomography scan. Bupivacaine (0.25% to 0.5%), an amide local anesthetic, was given as a bolus through the epidural catheter and then maintained either as a continuous infusion or an intermittent rebolus. The epidural catheter remained in place for 7 days in four patients, 14 days in three patients, and > or =90 days in three patients. Before consideration for HTEA, each patient was deemed unsuitable for or refused coronary bypass surgery and percutaneous coronary angioplasty and had NYHA class IV symptoms of angina. Seven of 10 patients required intravenous nitroglycerin and heparin and were unable to be discharged from the intensive care unit because of anginal symptoms. Two of these seven patients also required an intraaortic balloon pump for symptom control. After HTEA, all 10 patients had improved symptoms, with five patients improving to NYHA class II symptoms and five improving to NYHA class III. All seven patients receiving intravenous nitroglycerin, heparin, or intraaortic balloon pump support had these modalities discontinued. Six of these seven patients were subsequently discharged from the hospital. One patient died from a non-HTEA related cause. There were no HTEA-related deaths. There were three catheter-related complications necessitating catheter removal during 12 months of HTEA use. Local infection developed in one patient, one had catheter occlusion caused by fibrosis, and one patient had chronic back pain exacerbation from a paraspinous muscle spasm. No patient had a myocardial infarction or a significant arrhythmia. In patients with otherwise intractable angina pectoris, HTEA is an effective modality that produces symptomatic relief of angina pectoris and allows increased activity level.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Analgesia__Epidural_MeSH S_adverse_effects_MeSH Analgesia__Epidural_adverse_effects_MeSH S_instrumentation_MeSH Analgesia__Epidural_instrumentation_MeSH M_Analgesics_MeSH S_administration_&_dosage_MeSH Analgesics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Analgesics__Opioid_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Anesthetics__Local_MeSH S_administration_&_dosage_MeSH Anesthetics__Local_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anesthetics__Local_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_surgery_MeSH Angina_Pectoris_surgery_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Bupivacaine_MeSH S_administration_&_dosage_MeSH Bupivacaine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Bupivacaine_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_complications_MeSH Cardiac_Output__Low_complications_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Female_MeSH M_Heparin_MeSH S_therapeutic_use_MeSH Heparin_therapeutic_use_MeSH M_Human_MeSH M_Intensive_Care_MeSH M_Intra-Aortic_Balloon_Pumping_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Patient_Discharge_MeSH M_Radiography__Interventional_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH M_Survival_Rate_MeSH M_Thoracic_Vertebrae_MeSH M_Tomography__X-Ray_Computed_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9200654
----K E
----T Long-term effect of lisinopril and atenolol on kidney function in hypertensive NIDDM subjects with diabetic nephropathy.
----A The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic. We performed a prospective, randomized, parallel study for 42 months, double blind for the first 12 months and single blind thereafter. Forty-three (21 lisinopril and 22 atenolol) hypertensive NIDDM patients with diabetic nephropathy were enrolled. Data from 36 patients (17 lisinopril and 19 atenolol, 60 +/- 7 years of age, 27 men) who completed at least 12 months of the study period are presented. At baseline, the two groups were comparable: glomerular filtration rate (51Cr-EDTA plasma clearance) was 75 +/- 6 and 74 +/- 8 ml x min(-1) x 1.73 m(-2), mean 24-h ambulatory blood pressure (A&D TM2420) was 110 +/- 3 and 114 +/- 2 mmHg, and 24-h urinary albumin excretion rate was 961 (range 331-5,727) and 1,578 (476-5,806) mg/24 h in the lisinopril and atenolol groups, respectively. The mean follow-up time was similar, 37 and 35 months in the lisinopril and atenolol groups, respectively. Mean ambulatory blood pressure was equally reduced in the two groups, 12 +/- 2 and 10 +/- 2 mmHg in the lisinopril and atenolol groups, respectively. Glomerular filtration rate declined in a biphasic manner with a faster initial (0 to 6 months) change of 1.25 +/- 0.49 and 0.81 +/- 0.29 ml x min(-1) x month(-1) followed by a slower sustained decline (6 to 42 months) of 0.59 +/- 0.10 and 0.54 +/- 0.13 ml x min(-1) x month(-1) in the lisinopril and atenolol groups, respectively. No significant differences were observed in either initial or sustained decline in glomerular filtration rate between the two groups. Urinary albumin excretion was reduced (% reduction of baseline) more in the lisinopril than in the atenolol group, at 55 (95% CI 29-72) and 15% (-13 to 34), respectively (P = 0.01). In conclusion, the relentless decline in kidney function characteristically found in hypertensive NIDDM patients with diabetic nephropathy can be reduced equally effectively by two antihypertensive treatments, the beta-blocker atenolol and the ACE inhibitor lisinopril.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Albuminuria_MeSH S_drug_therapy_MeSH Albuminuria_drug_therapy_MeSH S_physiopathology_MeSH Albuminuria_physiopathology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Nephropathies_MeSH S_complications_MeSH Diabetic_Nephropathies_complications_MeSH S_physiopathology_MeSH Diabetic_Nephropathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Follow-Up_Studies_MeSH M_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Renal_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiology_MeSH Kidney_physiology_MeSH M_Lisinopril_MeSH S_adverse_effects_MeSH Lisinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Rabbits_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9205815
----K E
----T Pharmacokinetics of beta-adrenoceptor blockers in obese and normal volunteers.
----A AIMS: Obesity can modify the pharmacokinetics of lipophilic drugs. As beta-adrenoceptor blockers (BB) are often prescribed for obese patients suffering from hypertension or coronary heart disease, this study compares the pharmacokinetics of lipophilic beta-adrenoceptor blockers in obese and control subjects. METHODS: Nine obese (157 +/- 24% of ideal body weight (IBW) mean +/- s.d.) and nine non-obese healthy volunteers (98 +/- 10% IBW), aged 32 +/- 9 years, were included in the study. Subjects were randomly given a single i.v. infusion of one of the following racemic beta-adrenoceptor blockers, whose doses (expressed as base per kg of IBW) were: propranolol (0.108 mg), labetalol (0.99 mg) and nebivolol (0.073 mg). The plasma concentrations of unchanged drugs were measured by h.p.l.c. The ionisation constants and lipophilicity parameters of beta-adrenoceptor blockers were assessed. RESULTS: The pharmacokinetic data for the three drugs were qualitatively similar. There was a trend towards a greater total distribution volume (Vss) in obese patients than in controls. However, Vss expressed per kg body weight was slightly smaller in obese patients. The relationship between Vss and lipophilicity of five beta-adrenoceptor was studied by combining the current results with those previously obtained with a moderately lipophilic drug (bisoprolol) and a hydrophilic one (sotalol). The Vss of the five drugs was positively and well-correlated (r2 = 0.90; P < 0.01) with their distribution coefficient at pH 7.4 (log D7.4), but not with their partition coefficients. The linear regression coefficients for lean and obese subjects were very similar. CONCLUSIONS: Lipophilic beta-adrenoceptor blockers seem to diffuse less into adipose than into lean tissues. All electrical forms of the drugs (i.e. cations, neutral forms, or zwitterions) present at physiological pH contribute to their tissue distribution, in both obese and lean subjects. Their tissue distribution in obese patients could be restricted by the sum of hydrophobic forces and hydrogen bonds they elicit with macromolecules in lean tissues.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adipose_Tissue_MeSH S_metabolism_MeSH Adipose_Tissue_metabolism_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_chemistry_MeSH Adrenergic_beta-Antagonists_chemistry_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Area_Under_Curve_MeSH M_Benzopyrans_MeSH S_administration_&_dosage_MeSH Benzopyrans_administration_&_dosage_MeSH S_chemistry_MeSH Benzopyrans_chemistry_MeSH S_pharmacokinetics_MeSH Benzopyrans_pharmacokinetics_MeSH S_pharmacology_MeSH Benzopyrans_pharmacology_MeSH M_Binding_Sites_MeSH M_Bisoprolol_MeSH S_blood_MeSH Bisoprolol_blood_MeSH S_pharmacokinetics_MeSH Bisoprolol_pharmacokinetics_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Blood_Chemical_Analysis_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Chromatography__High_Pressure_Liquid_MeSH M_Comparative_Study_MeSH M_Ethanolamines_MeSH S_administration_&_dosage_MeSH Ethanolamines_administration_&_dosage_MeSH S_chemistry_MeSH Ethanolamines_chemistry_MeSH S_pharmacokinetics_MeSH Ethanolamines_pharmacokinetics_MeSH S_pharmacology_MeSH Ethanolamines_pharmacology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrogen-Ion_Concentration_MeSH M_Infusions__Intravenous_MeSH M_Labetalol_MeSH S_administration_&_dosage_MeSH Labetalol_administration_&_dosage_MeSH S_chemistry_MeSH Labetalol_chemistry_MeSH S_pharmacokinetics_MeSH Labetalol_pharmacokinetics_MeSH S_pharmacology_MeSH Labetalol_pharmacology_MeSH M_Male_MeSH M_Obesity_MeSH S_blood_MeSH Obesity_blood_MeSH S_metabolism_MeSH Obesity_metabolism_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_chemistry_MeSH Propranolol_chemistry_MeSH S_pharmacokinetics_MeSH Propranolol_pharmacokinetics_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Regression_Analysis_MeSH M_Sotalol_MeSH S_blood_MeSH Sotalol_blood_MeSH S_pharmacokinetics_MeSH Sotalol_pharmacokinetics_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH M_Stereoisomerism_MeSH M_Tissue_Distribution_MeSH 
****** 9205847
----K E
----T When, and when not, to use digoxin in the elderly.
----A Digitalis has been widely used in the treatment of cardiac disease for more than 200 years. The present article reviews the current role of digitalis in the management of heart failure and atrial fibrillation (AF) in light of recent study findings. Generally, first-line therapy for the management of heart failure due to systolic dysfunction should include an ACE inhibitor and a diuretic. In patients who remain symptomatic despite the use of these drugs, the addition of digoxin should be considered. Because digoxin has been shown to reduce the number of hospital admissions attributable to worsening heart failure, more liberal use of digoxin in the management of heart failure may be justified. Digoxin may be adequate as monotherapy for ventricular rate control in patients with chronic AF, particularly in sedentary and elderly patients. A beta-blocker or calcium antagonist (either alone or in combination with digoxin) is indicated when digoxin is ineffective for ventricular rate control. Digoxin is ineffective in restoring sinus rhythm, preventing paroxysms or controlling rate in paroxysmal AF. The elderly are at an increased risk of digoxin toxicity. Low dosages of digoxin appear to be effective in the treatment of heart failure due to systolic dysfunction and may reduce the incidence of digitalis toxicity in these patients. In elderly patients with AF and inadequate rate control who are receiving digitalis monotherapy, adding another atrioventricular nodal blocking drug may be more appropriate than increasing the digoxin dose, in order to avoid toxic digoxin levels.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aging_MeSH S_physiology_MeSH Aging_physiology_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH S_pharmacology_MeSH Digoxin_pharmacology_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Dosage_Forms_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9205939
----K E
----T The effects of atenolol and zofenopril on plasma atrial natriuretic peptide are due to their interactions with target organ damage of essential hypertensive patients.
----A The effects of 10 weeks of treatment with atenolol (n = 9) or the converting enzyme inhibitor zofenopril (n = 25) on plasma atrial natriuretic peptide (ANP) were studied in 34 essential hypertensive patients. After 4 weeks on placebo, pretreatment ANP, 56 +/- 7 pg/ml, was slightly but not significantly higher than that of 29 controls (41 +/- 4) and correlated with age (r = 0.44), ECG score for left ventricular hypertrophy (LVH) (r = 0.51) and serum creatinine (r = 0.67), and negatively with creatinine clearance (r = -0.39). Atenolol reduced blood pressure (BP) by 0 +/- 6/8 +/- 2 mm Hg (ns/P < 0.01), and zofenopril by 14 +/- 4/6 +/- 2 (P < 0.01/P < 0.01), not significantly different between the two agents. Heart rate was decreased by atenolol (-16 +/- 4 bpm, P < 0.01) but not by zofenopril (+1 +/- 2 bpm, ns). Atenolol increased ANP in all patients but one (delta = +42 +/- 9 pg/ml, P < 0.01), while zofenopril did not change it significantly (-6 +/- 6 pg/ml), due to 15 patients exhibiting decreases and 10 increases in plasma ANP. The effect of atenolol on ANP positively correlated with duration of hypertension (r = 0.74), ECG score for LVH (r = 0.73) and serum creatinine (r = 0.68). Individual changes in ANP by zofenopril negatively correlated with pretreatment ANP (r = -0.69), ECG score for LVH (r = -0.44) and serum creatinine (r = -0.41). No correlations were found between BP, heart rate or their changes by treatment and the effect of either agent on plasma ANP. Multiple linear regression showed that the change in ANP was explained by the therapeutic agent used, the pretreatment plasma level of ANP, and the ECG score for LVH (F = 12.5, P < 0.001, r2 = 0.56). We conclude that the effect of antihypertensives on plasma ANP is independent of their action on BP, but dependent on an interaction between the type of drug employed and those clinical characteristics of the patient that reflect pre-existing hypertensive target organ damage.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Captopril_analogs_&_derivatives_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH 
****** 9207336
----K I
----T Antihypertensives and the risk of serious hypoglycemia in older persons using insulin or sulfonylureas.
----A CONTEXT: Beta-Blockers and angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents for patients with diabetes mellitus. However, beta-blockers attenuate some components of the autonomic response to hypoglycemia and could increase the risk of hypoglycemia. ACE inhibitors may increase insulin sensitivity and predispose users to hypoglycemia. OBJECTIVE: To determine whether use of cardioselective beta-blockers, nonselective beta-blockers, ACE inhibitors, thiazide diuretics, calcium channel blockers, or other antihypertensive drugs alters the risk of developing serious hypoglycemia among older persons prescribed insulin or sulfonylureas. DESIGN: Retrospective cohort study. SETTING: Tennessee Medicaid Program. PATIENTS: A total of 13,559 elderly (mean age, 78+/-7 years) Medicaid enrollees, who were prescribed insulin (n=5171, 38%) or sulfonylureas (n=8368, 62%) from 1985 through 1989. These enrollees contributed a total of 33,107 person-years of insulin or sulfonylurea use for follow-up. MEASUREMENTS: Hospitalization, emergency department admission, or death associated with hypoglycemic symptoms and a concomitant blood glucose determination of less than 2.8 mmol/L (50 mg/dL). RESULTS: We identified 598 persons with an episode of serious hypoglycemia during the study period. The rate of serious hypoglycemia was 2.01 per 100 person-years among those who were not prescribed antihypertensives. Crude rates of serious hypoglycemia were highest among users of ACE inhibitors (2.47 per 100 person-years) and lowest among users of cardioselective beta-blockers (1.23 per 100 person-years). However, when we controlled for demographic characteristics and markers of comorbidity, there was no statistically significant increase or decrease in risk of serious hypoglycemia among users of any class of antihypertensive agents compared with nonusers of antihypertensive drugs. Using nonselective beta-blockers as the reference group, each of these agents was associated with a lower, but not statistically significant, risk of hypoglycemia. CONCLUSIONS: In this population, specific antihypertensive drug therapy had little impact on the risk of hypoglycemia in older diabetic patients. Therapy should be chosen based on other considerations of safety and effectiveness.
----P Journal_Article 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH M_Drug_Interactions_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypoglycemia_MeSH S_chemically_induced_MeSH Hypoglycemia_chemically_induced_MeSH S_etiology_MeSH Hypoglycemia_etiology_MeSH M_Insulin_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH M_Poisson_Distribution_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Sulfonylurea_Compounds_MeSH S_pharmacology_MeSH Sulfonylurea_Compounds_pharmacology_MeSH S_therapeutic_use_MeSH Sulfonylurea_Compounds_therapeutic_use_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9207617
----K I
----T Effect of beta-blockade on mortality in patients with heart failure: a meta-analysis of randomized clinical trials.
----A OBJECTIVES: We sought to evaluate the current evidence for an effect of beta-blockade treatment on mortality in patients with congestive heart failure (CHF). BACKGROUND: Although numerous small studies have suggested a benefit with beta-blocker therapy in patients with heart failure, a clear survival benefit has not been demonstrated. A recent combined analysis of several studies with the alpha- and beta-adrenergic blocking agent carvedilol demonstrated a significant survival advantage; however, the total number of events was small. Furthermore, it is unclear if previous studies with other beta-blockers are consistent with this finding. METHODS: Randomized clinical trials of beta-blockade treatment in patients with CHF from January 1975 through February 1997 were identified using a MEDLINE search and a review of reports from scientific meetings. Studies were included if mortality was reported during 3 or more months of follow-up. RESULTS: We identified 35 reports, 17 of which met the inclusion criteria. These studies included 3,039 patients with follow-up ranging from 3 months to 2 years. Beta-blockade was associated with a trend toward mortality reduction in 13 studies. When all 17 reports were combined, beta-blockade significantly reduced all-cause mortality (random effect odds ratio [OR] 0.69, 95% confidence interval [CI] 0.54 to 0.88). A trend toward greater treatment effect was noted for nonsudden cardiac death (OR 0.58, 95% CI 0.40 to 0.83) compared with sudden cardiac death (OR 0.84, 95% CI 0.59 to 1.2). Similar reductions in mortality were observed for patients with ischemic (OR 0.69, 95% CI 0.49 to 0.98) and nonischemic cardiomyopathy (OR 0.69, 95% CI 0.47 to 0.99). The survival benefit was greater for trials of the drug carvedilol (OR 0.54, 95% CI 0.36 to 0.81) than for noncarvedilol drugs (OR 0.82, 95% CI 0.60 to 1.12); however, the difference did not reach statistical significance (p = 0.10). CONCLUSIONS: Pooled evidence suggests that beta-blockade reduces all-cause mortality in patients with CHF. Additional trials are required to determine whether carvedilol differs in its effect from other agents.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Mortality_MeSH S_trends_MeSH Mortality_trends_MeSH M_Odds_Ratio_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9207639
----K E
----T Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.
----A OBJECTIVES: This study was undertaken to define and better understand the characteristics and outcomes of patients with diabetes treated for acute myocardial infarction with contemporary thrombolysis. BACKGROUND: Although thrombolysis has substantially improved survival of patients with myocardial infarction, diabetes mellitus remains an independent predictor for a poor prognosis. METHODS: We characterized the contemporary relation between diabetes and outcome after myocardial infarction treated with thrombolytic agents from a large international cohort. Of 41,021 patients randomized to receive accelerated tissue-type plasminogen activator (t-PA), streptokinase or a combination of both agents in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries study, there were 5,944 patients with diabetes and 34,888 patients without diabetes. RESULTS: Patients with diabetes were older and more likely to be female, to present with anterior wall infarction, to receive thrombolysis later and to have triple-vessel coronary artery disease. Mortality at 30 days was highest among diabetic patients treated with insulin (12.5%) compared with non-insulin-treated diabetic (9.7%) and nondiabetic (6.2%) patients (p < 0.001). Mortality was lowest among those with diabetes receiving accelerated t-PA, which is consistent with the results of the overall patient cohort. Although stroke occurred more frequently among diabetic (1.9%) than nondiabetic patients (1.4%, p < 0.001), there was no significant difference in the rates of intracranial hemorrhage. Cardiac failure, shock, atrioventricular block and atrial flutter/ fibrillation were more common among diabetic patients. The proportion of patients undergoing revascularization was similar between patients with and without diabetes, although diabetic patients were more likely to undergo coronary artery bypass graft surgery (10.4% vs. 8.3%). Diabetes remained an independent predictor for mortality at 1-year follow-up (14.5% vs. 8.9%, p < 0.001). CONCLUSIONS: Diabetes, alone and in association with its comorbidities, portends a substantially worse 30-day and 1-year prognosis for patients with myocardial infarction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Odds_Ratio_MeSH M_Plasminogen_Activators_MeSH S_therapeutic_use_MeSH Plasminogen_Activators_therapeutic_use_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Streptokinase_MeSH S_therapeutic_use_MeSH Streptokinase_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9212681
----K 1
----T [Prevention of cardiac events by beta-blocking agents in elderly patients after myocardial infarction]
----A We retrospectively analyzed the effect of beta-blocking agents on the incidence of cardiac events in elderly patients who had had myocardial infarction. A total of 1169 patients who had had a myocardial infarction (age, 60.2 +/- 11.4 years) were followed for a mean of 18.0 +/- 19.7 months and the incidence of cardiac events (fatal or nonfatal myocardial infarction, sudden cardiac death, and death due to congestive heart failure) was computed. There were 21 cardiac events in 653 patients who received beta-blocking agents (3.2%) and 39 events in 516 patients who did not receive beta-blocking agents (7.6%, p < 0.01). Among patients less than 50 years old, the incidences of cardiac events were 4.1% in those who received beta-blocking agents and 7.6% in those who did not; among those 50 to 59 years old the incidences were 3.0% and 7.5%, respectively; among those 60 to 69 years old they were 4.3% and 6.0%, respectively; and among those 70 years old or older they were 0.8% and 11.4%, respectively (p < 0.01). We found that beta-blocking agents prevented cardiac events both in elderly and in younger patients after myocardial infarction.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH 
****** 9213203
----K E
----T Assessment of antihypertensive effect by blood pressure monitoring: applications to bisoprolol and lisinopril in a double-blind study.
----A The aim of this study was to evaluate the antihypertensive effect of drugs according to the initial ambulatory blood pressure (BP) level. After a 15-day placebo run-in period, 105 patients with moderate essential hypertension (mean age, 52 years) underwent 24-h BP monitoring (spacelabs: 1 measure/15 min). Patients were subdivided into two groups: the "High" group, with 24-h mean values of systolic BP (SBP) > 137 or diastolic BP (DBP) > 87 mm Hg, and the "Low" group, with SBP < or = 137 and DBP < or = 87 mm Hg. All patients received, in a random and double-blind design, either bisoprolol (10 mg q.d.) or lisinopril (20 mg q.d.) for 8 weeks. At the end of this active treatment period, office and ambulatory BP measurements were performed. Casual measurements revealed similar BP decreases in all subgroups receiving bisoprolol and lisinopril; BP monitoring showed that the antihypertensive effect depended on the baseline mean 24-h value; -15/-12 mm Hg for bisoprolol and -18/-13 mm Hg for lisinopril in the High group; -7/-6 mm Hg for bisoprolol and -6/-6 mm Hg for lisinopril in the Low group. This study shows that the antihypertensive effect depended on initial ambulatory BP values, with a lower BP decrease in the Low group. Assessment of the antihypertensive effect on ambulatory BP is useful in clinical trials.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH P_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 9215330
----K E
----T Use of digoxin, diuretics, beta blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers in older patients in an academic hospital-based geriatrics practice.
----A OBJECTIVE: To investigate the prevalence of and indications for digoxin use and the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension in an academic hospital-based geriatrics practice. DESIGN: A retrospective analysis of charts from 528 unselected older patients, seen from June 1995 through July 1996 at an academic hospital-based geriatrics practice, was performed to investigate the prevalence of digoxin use and indications for digoxin use, the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension. SETTING: An academic hospital-based, primary care geriatrics practice staffed by fellows in a geriatrics training program and full-time faculty geriatricians. PATIENTS: A total of 416 women and 112 men, mean age 81 +/- 8 years (range 58 to 101), were included in the study. MEASUREMENTS AND MAIN RESULTS: Ninety-two of the 528 patients (17%) were taking digoxin. Recorded indications for digoxin were atrial fibrillation with or without congestive heart failure (CHF) in 39% of patients, CHF with sinus rhythm and abnormal left ventricular ejection fraction (LVEF) in 18% of patients, a clinical assessment of CHF with sinus rhythm and no recorded measurement of LVEF in 20% of patients, paroxysmal atrial fibrillation in 14% of patients, and coronary artery disease (CAD) in 9% of patients. Of 121 patients with previous myocardial infarction, 23 (19%) were prescribed beta blockers, and 54 (45%) were taking calcium channel blockers. Of 173 patients with CAD, 41 (24%) were treated with beta blockers, and 79 (46%) were taking calcium channel blockers. LVEF was not recorded in the charts of 90 of 121 patients (74%) with prior myocardial infarction and of 125 of 173 patients (72%) with CAD. Of 480 older patients with hypertension, 154 (37%) were treated with diuretics, 55 (13%) were treated with beta blockers, 160 (38%) were treated with ACE inhibitors, and 197 (47%) were treated with calcium channel blockers. CONCLUSIONS: In 528 older patients seen in an academic hospital-based geriatrics practice, the prevalence of digoxin use was 19%. Appropriate indications for digoxin were documented clearly in the charts of 53 of 92 patients (57%). Calcium channel blockers were used more often than beta blockers in patients with previous myocardial infarction or CAD. Calcium channel blockers were the most frequently used antihypertensive drugs.
----P Journal_Article 
----M M_Academic_Medical_Centers_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Ambulatory_Care_Facilities_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Geriatrics_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9217564
----K E
----T Myocardial infarction in newly diagnosed hypertensive Medicaid patients free of coronary heart disease and treated with calcium channel blockers.
----A PURPOSE: A retrospective cohort analysis of 1,406 newly diagnosed hypertensive patients, aged 18 to 59, without prior coronary heart disease and initially treated with calcium channel blockers (CCBs) or eight other drug regimens was conducted to evaluate the relative risk of acute myocardial infarction (AMI) among patients on CCBs alone or with a diuretic. MATERIALS AND METHODS: Administrative claims data from Pennsylvania's Medicaid program were the data source. Patients were followed up from 1987 to 1994. RESULTS: There was a highly significant trend towards prescribing CCBs between 1988 and 1991 (P = 0.0001). A total of 67 AMIs occurred, 33 of which were during original drug therapy. Compared with those treated with beta blockers, the relative risk of AMI among patients treated only with CCBs was 0.49 (95%) confidence interval [CI] 0.11 to 2.20). Compared with diuretic therapy, the AMI relative risk associated with CCB therapy was 0.60 (95% CI 0.16 to 2.32) when patient drug regimen was classified based on the first six prescriptions. Several alternative drug regimen classification schemes were tested to evaluate the sensitivity of relative risk of AMI to classification of drug therapy. CONCLUSIONS: The measurement of relative risk of AMI was highly dependent on the study design, including patient selection criteria and classification of patient drug therapy. Previous findings of elevated risk of AMI from CCB antihypertensive therapy could not be confirmed.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Medicaid_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_chemically_induced_MeSH Myocardial_Infarction_chemically_induced_MeSH M_Proportional_Hazards_Models_MeSH M_Retrospective_Studies_MeSH M_United_States_MeSH 
****** 9217673
----K E
----T The secondary prevention of coronary artery disease.
----A Randomized clinical trials demonstrate the efficacy of medical secondary prevention in coronary disease patients. The magnitude of risk reduction with exercise, diet, lipid modification, and smoking cessation is similar to other medical therapies for coronary disease such as aspirin, beta blockers, as well as coronary bypass surgery, (Table VI) In contrast to these therapies, however, secondary prevention stabilizes angiographic progression in about 50% of patients and induces regression in about 25% of patients. Both symptoms and perceived quality of life also are beneficially altered by secondary prevention programs, although possibly not by the magnitude reported for bypass surgery. These clinical trial results have led the American Heart Association, and the American College of Cardiology to strongly endorse secondary prevention. A reasonable projection based on these clinical trial data is that widespread use of these recommendations in the 12 million established coronary disease patients would significantly reduce coronary mortality and morbidity.
----P Journal_Article Review Review__Tutorial 
----M M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_therapy_MeSH Diabetes_Mellitus_therapy_MeSH M_Exercise_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_therapy_MeSH Hyperlipidemia_therapy_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Smoking_Cessation_MeSH M_Stress__Psychological_MeSH S_therapy_MeSH Stress__Psychological_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Weight_Loss_MeSH 
****** 9218667
----K I
----T Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension. SHEP Cooperative Research Group.
----A CONTEXT: Heart failure is often preceded by isolated systolic hypertension, but the effectiveness of antihypertensive treatment in preventing heart failure is not known. OBJECTIVE: To assess the effect of diuretic-based antihypertensive stepped-care treatment on the occurrence of heart failure in older persons with isolated systolic hypertension. DESIGN: Analysis of data from a multicenter, randomized, double-blind, placebo-controlled clinical trial. PARTICIPANTS: A total of 4736 persons aged 60 years and older with systolic blood pressure between 160 and 219 mm Hg and diastolic blood pressure below 90 mm Hg who participated in the Systolic Hypertension in the Elderly Program (SHEP). INTERVENTION: Stepped-care antihypertensive drug therapy, in which the step 1 drug is chlorthalidone (12.5-25 mg) or matching placebo, and the step 2 drug is atenolol (25-50 mg) or matching placebo. MAIN OUTCOME MEASURES: Fatal and nonfatal heart failure. RESULTS: During an average of 4.5 years of follow-up, fatal or nonfatal heart failure occurred in 55 of 2365 patients randomized to active therapy and 105 of the 2371 patients randomized to placebo (relative risk [RR], 0.51; 95% confidence interval [CI], 0.37-0.71; P<.001; number needed to treat to prevent 1 event [NNT], 48). Among patients with a history of or electrocardiographic evidence of prior myocardial infarction (MI), the RR was 0.19 (95% CI, 0.06-0.53; P=.002; NNT, 15). Older patients, men, and those with higher systolic blood pressure or a history of or electrocardiographic evidence of MI at baseline had higher risk of developing heart failure. CONCLUSION: In older persons with isolated systolic hypertension, stepped-care treatment based on low-dose chlorthalidone exerted a strong protective effect in preventing heart failure. Among patients with prior MI, an 80% risk reduction was observed.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH M_Systole_MeSH 
****** 9218922
----K E
----T Valsartan, a new angiotensin II antagonist for the treatment of essential hypertension: efficacy and safety compared to hydrochlorothiazide.
----A OBJECTIVE: To compare the antihypertensive efficacy of a new angiotensin II antagonist, valsartan, with a reference therapy, hydrochlorothiazide (HCTZ). METHODS: In this double-blind study, 167 adult out-patients with mild-to-moderate essential hypertension were randomly allocated in equal number to receive valsartan 80 mg or HCTZ 25 mg for 12 weeks. In patients whose blood pressure (BP) remained uncontrolled after 8 weeks of monotherapy, atenolol 50 mg was added to the initial treatment. Patients were assessed at 4, 8 and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic BP (SDBP) at 8 weeks. Secondary variables included change in sitting systolic BP (SSBP) and responder rates (percentage of patients with SDBP < 90 mmHg or drop > or = 10 mmHg compared to baseline) at 8 weeks. RESULTS: Valsartan and HCTZ were both effective at lowering diastolic and systolic blood pressure at all time points. Similar falls were seen in both groups with no significant differences between treatments. For the primary variable (decrease in SDBP) there was no significant difference between treatments. For SSBP there was also no significant difference observed. Responder rates at 8 weeks were 74% for valsartan and 62% for HCTZ (P = 0.10). Both treatments were well tolerated, both as monotherapy, and when combined with atenolol 50 mg per day. CONCLUSION: The data show valsartan 80 mg to be as effective as HCTZ in the treatment of mild-to-moderate hypertension. The results also show valsartan to be well tolerated when taken alone or in combination with atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Valine_MeSH S_adverse_effects_MeSH Valine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 9219043
----K E
----T Paroxetine and pindolol: a randomized trial of serotonergic autoreceptor blockade in the reduction of antidepressant latency.
----A A double-blind, randomized, placebo-controlled, parallel group study was performed in 80 adult outpatients meeting ICD-10 criteria for major depression and with a Montgomery-Asberg Depression Rating Scale (MADRS) score of at least 18 at baseline. All patients received paroxetine (20 mg once a day) plus either pindolol (2.5 mg three times a day) or matching placebo for 6 weeks. Analysis of the day 14 MADRS scores on an intent-to-treat basis revealed a treatment-by-centre interaction, with a significant effect of pindolol being demonstrable at only one centre. At this centre, 25% of the paroxetine plus pindolol group and 0% of the paroxetine plus placebo group showed a decrease of at least 50% from baseline MADRS by day 4 (p < 0.05). At day 14, the proportions were 73% and 7%, respectively (p < 0.001). Analysis of covariance on a "perprotocol" population demonstrated a significant accelerator effect of pindolol at days 4 and 7 in the absence of a treatment-by-centre interaction, but a centre effect was apparent at later time-points. The results suggest that the latency of antidepressant action can be reduced with pindolol augmentation. A large multicentre study is in progress to investigate this effect further.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Depressive_Disorder_MeSH S_diagnosis_MeSH Depressive_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH S_psychology_MeSH Depressive_Disorder_psychology_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Paroxetine_MeSH S_administration_&_dosage_MeSH Paroxetine_administration_&_dosage_MeSH S_adverse_effects_MeSH Paroxetine_adverse_effects_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH M_Psychiatric_Status_Rating_Scales_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_administration_&_dosage_MeSH Serotonin_Uptake_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Uptake_Inhibitors_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9222734
----K I
----T Medical prophylaxis of haemorrhage from oesophageal varices in patients with liver cirrhosis.
----A Haemorrhage from oesophageal varices is a life-threatening event in patients with liver cirrhosis. About 40-80% of patients surviving the first bleeding suffer a recurrence within 1 year. This high recurrence rate substantially contributes to the mortality in patients with liver cirrhosis. Therefore, various treatment regimens in both primary and secondary prophylaxis were studied. Most experience in medical primary prophylaxis was collected with beta-blockers, mainly propranolol. Treating patients with oesophageal varices with propranolol significantly reduces the incidence of first variceal bleeding. However, the effect on mortality is marginal, and primary prophylaxis is generally not recommended in these patients. Several studies support the hypothesis that medical prophylaxis with beta-blockers is more effective in reducing the rate of first oesophageal bleeding in patients with a high risk of haemorrhage, such as those with very large varices with red spots. A score to assess an individual patient's risk of variceal bleeding would be helpful, but until such a score has been validated, no general rule for this treatment decision can be given. In secondary prophylaxis, both beta-blockers and endoscopic therapy (sclerotherapy or ligation of the varices) are effective in lowering the rate of rebleeding. However, the effect on mortality was not significant in most studies. Several studies comparing the efficacy of medical prophylaxis and endoscopic treatment showed advantages of the endoscopic therapy with a greater reduction in recurrent bleeding episodes. However, medical prophylaxis with beta-blockers has the important advantage of being immediately effective, whereas endoscopic procedures provide the best protection against recurrent bleeding after complete obliteration of the varices. Therefore, in the first weeks and months of endoscopic therapy, additional treatment with beta-blockers may further reduce the risk of rebleeding. Only half of all studies on this topic reported a significant advantage with this combined therapy. Therefore, it seems reasonable to restrict this approach to patients with a high risk of rebleeding, such as patients with large sclerotherapy-derived oesophageal ulcers.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_complications_MeSH Gastrointestinal_Hemorrhage_complications_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH P_Sclerotherapy_MeSH M_Treatment_Outcome_MeSH 
****** 9224506
----K E
----T Pharmacological treatment of portal hypertension.
----A 
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Balloon_Dilatation_MeSH M_Clinical_Trials_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH M_Lypressin_MeSH S_analogs_&_derivatives_MeSH Lypressin_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Lypressin_therapeutic_use_MeSH M_Metoclopramide_MeSH S_therapeutic_use_MeSH Metoclopramide_therapeutic_use_MeSH M_Molsidomine_MeSH S_therapeutic_use_MeSH Molsidomine_therapeutic_use_MeSH M_Octreotide_MeSH S_therapeutic_use_MeSH Octreotide_therapeutic_use_MeSH M_Portasystemic_Shunt__Surgical_MeSH M_Sclerotherapy_MeSH M_Somatostatin_MeSH S_therapeutic_use_MeSH Somatostatin_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Vasopressins_MeSH S_therapeutic_use_MeSH Vasopressins_therapeutic_use_MeSH 
****** 9289367
----K 1
----T [The effects of mid- and long-term administration (3-4 years) of carvedilol in patients with idiopathic dilated cardiomyopathy]
----A Carvedilol has been shown to determine a significant improvement in left ventricular function, symptoms, clinical course and prognosis of patients with chronic heart failure. However, these results were obtained in medium-term studies of < 1 year duration. We report the results obtained with long-term (3-4 years) carvedilol administration to 40 patients with idiopathic dilated cardiomyopathy who were initially recruited in a 4-month double-blind placebo-controlled trial. In the initial 4-month double-blind trial, 20 patients were randomized to placebo and 20 to carvedilol treatment. All patients, except one who was not on ACE-inhibitors, were on digoxin, furosemide and ACE-inhibitors. Carvedilol or placebo doses were progressively titrated, at weekly intervals, up to the maximal doses of 25 mg bid. After the initial 4-month double-blind phase, all patients were followed long term. Mean follow-up duration was 52 +/- 12 months (range 48-61). Among the 20 patients initially randomized to carvedilol administration, 4 died (3 for cardiac and 1 for extracardiac causes) and 2 underwent heart transplant. Among the 20 patients initially randomized to placebo, 5 died for cardiac causes, 3 underwent heart transplant and 4 were started on carvedilol because of progressive heart failure during the initial 4 months of the study. The remaining 8 patients, who were kept on digoxin, furosemide and ACE-inhibitors, were used as control group. Each patient underwent an assessment of clinical conditions (NYHA functional classification and Minnesota Living with Heart Failure questionnaire), equilibrium radionuclide ventriculography, and maximal cardiopulmonary bicycle exercise testing. Exams were performed before treatment, after 4 and 12 months, and at the end of the follow-up period. No significant difference between the carvedilol and control group was present at baseline. Compared with baseline, patients in the control group presented a significant increase in left ventricular end-diastolic volume after long-term follow-up (from 126 +/- 62 to 138 +/- 43 and 158 +/- 52 ml/m2 after 12 and 48 months, respectively). No significant difference, compared to baseline values, was noted. Patients on carvedilol presented a persistent improvement in left ventricular function. This was shown by the progressive increment in left ventricular ejection fraction from 22 +/- 6 to 34 +/- 11, 37 +/- 11 and 37 +/- 13%, after 4, 12 and 48 months, respectively (p < 0.001) with a concomitant reduction in left ventricular end-diastolic volume from 147 +/- 54 to 101 +/- 44 ml/m2 at the end of the follow-up (p < 0.05). NYHA functional class remained significantly improved, in comparison with baseline (2.6 +/- 0.5 to 1.9 +/- 0.3, 1.9 +/- 0.8 and 2.0 +/- 1.0 after 4, 12 and 48 months, respectively; p < 0.01). Maximal functional capacity, assessed as peak VO2 was not significantly changed after 4 months (from 15.2 +/- 3.6 to 16.4 +/- 4.0 ml/kg/min) and showed a tendency towards a further improvement after 12 months and at the end of the follow-up (17.3 +/- 5.6 and 17.2 +/- 5.3 ml/kg/min, respectively). These results show that the favorable effects of carvedilol administration on left ventricular function and clinical symptoms are maintained also after long-term treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 9226286
----K E
----T Heart rate variability after acute myocardial infarction in patients treated with atenolol and metoprolol.
----A Heart rate variability (HRV) reflects autonomous activity that influences the heart. It has been shown that HRV is depressed during acute myocardial infarction (AMI) and that it recovers with time. Beta-blockers reduce mortality after AMI and changes in sympathico-vagal activity have been suggested to be of importance. Under certain animal experimental conditions, metoprolol has been reported to increase vagal tone more than atenolol, which could have clinical implications. The purpose of the present study was to compare the effects of atenolol and metoprolol treatments on HRV during 6 weeks after AMI and to follow the post MI changes in HRV in patients on betablockers. METHODS: In an open, randomised cross-over study, 28 patients were randomised to 3+3 weeks' treatment with atenolol or metoprolol starting 2-5 days after AMI. Twenty-four hour Holter recordings were made before randomisation and after 3 and 6 weeks. HRV was analysed as HR, SDRR, SDANN, SD, rMSSD and pNN50 in the time domain and as coefficient of component variance (CCV) of HF and LF, and as LF/HF ratio in the frequency domain. RESULTS: The average daily dose in our study population was 106 mg of metoprolol and 54 mg of atenolol. There were trends toward lower heart rates daytime, lower LF/HF ratio daytime and higher rMSSD on atenolol compared to metoprolol. In the total group of 28 patients we found during the first 3 weeks, a significant increase of SDNN, SDANN (p<0.0001) and LF/HF ratio daytime and CCV-HF night-time (p<0.01). All differences and trends were unchanged between 3 and 6 weeks. CONCLUSIONS: There was no evidence of more increased vagal tone with metoprolol compared to atenolol as has been suggested from animal models. In patients also on chronic treatment with beta blockers, an increase of HRV was seen during the first weeks post MI.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Random_Allocation_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9229549
----K E
----T The 32nd annual meeting of the European Association for the Study of Diabetes. Treatment of type I diabetes, hypoglycemia, retinopathy, nephropathy, and the genetics of complications.
----A 
----P Congresses 
----M P_Diabetes_Mellitus_MeSH S_genetics_MeSH Diabetes_Mellitus_genetics_MeSH S_therapy_MeSH Diabetes_Mellitus_therapy_MeSH M_Diabetic_Nephropathies_MeSH S_genetics_MeSH Diabetic_Nephropathies_genetics_MeSH S_therapy_MeSH Diabetic_Nephropathies_therapy_MeSH M_Diabetic_Retinopathy_MeSH S_genetics_MeSH Diabetic_Retinopathy_genetics_MeSH S_therapy_MeSH Diabetic_Retinopathy_therapy_MeSH M_Human_MeSH M_Hypoglycemia_MeSH S_genetics_MeSH Hypoglycemia_genetics_MeSH S_therapy_MeSH Hypoglycemia_therapy_MeSH 
****** 9230162
----K I
----T Effect of propranolol versus no propranolol on total mortality plus nonfatal myocardial infarction in older patients with prior myocardial infarction, congestive heart failure, and left ventricular ejection fraction > or = 40% treated with diuretics plus angiotensin-converting enzyme inhibitors.
----A At 32-month follow-up of older patients with prior myocardial infarction, congestive heart failure, and a left ventricular ejection fraction > or = 40% treated with diuretics plus angiotensin-converting enzyme inhibitors, and also with digoxin if atrial fibrillation was present, propranolol caused a 35% significant reduction in total mortality and a 37% significant decrease in total mortality plus nonfatal myocardial infarction compared with no propranolol. At 1-year follow-up, propranolol caused a significantly greater increase in left ventricular ejection fraction (6%) and a significantly greater reduction in left ventricular mass (34 g) than did no propranolol (2% and 20 g, respectively).
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Mortality_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH 
****** 9230823
----K 4
----T A 1-year study of brimonidine twice daily in glaucoma and ocular hypertension. A controlled, randomized, multicenter clinical trial. Chronic Brimonidine Study Group.
----A OBJECTIVE: Brimonidin tartrate is a highly selective alpha 2-agonist. This study investigates the safety and efficacy of 0.2% brimonidine administered twice daily for 1 year in patients with glaucoma or ocular hypertension. METHODS: The study design was a multicenter, double-masked, randomized, parallel-group, active-controlled comparison clinical trial. Subjects instilled 0.2% brimonidine or 0.5% timolol maleate twice daily for 12 months. Subjects were examined at baseline, week 1, and months 1, 2, 3, 6, 9, and 12. A subset of subjects was examined at week 2. RESULTS: Of 443 subjects enrolled in this study, 374 met the entry criteria; 186 received brimonidine and 188 received timolol. Brimonidine-treated subjects showed an overall mean peak reduction in intraocular pressure (IOP) of 6.5 mm Hg; timolol-treated subjects had a mean peak reduction in IOP of 6.1 mm Hg. Brimonidine lowered mean peak IOP significantly more than timolol at week 2 and month 3 (P < .03); no significant difference was observed between the groups for this variable at other visits throughout the 1-year course of the study. No evidence of tachyphylaxis was seen in either group. Allergy was seen in 9% of subjects treated with brimonidine. Dry mouth was more common in the brimonidine-treated group than in the timolol-treated group (33.0% vs 19.4%), but complaints of burning and stinging were more common in the timolol-treated group (41.9%) than in the brimonidine-treated patients (28.1%). Headache, fatigue, and drowsiness were similar in the 2 groups. In general, the tolerance to medication was acceptable. CONCLUSIONS: Brimonidine is safe and effective in lowering IOP in glaucomatous eyes. Brimonidine provides a sustained long-term ocular hypotensive effect, is well tolerated, and has a low rate of allergic response.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Ophthalmic_Solutions_MeSH M_Pupil_MeSH S_drug_effects_MeSH Pupil_drug_effects_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Visual_Acuity_MeSH S_drug_effects_MeSH Visual_Acuity_drug_effects_MeSH 
****** 9231814
----K E
----T Safety of nifedipine in patients with hypertension: a meta-analysis.
----A Our objective was to compare cardiovascular event rates in patients with mild or moderate hypertension who received nifedipine with active drug controls. We performed a MEDLARS search using the MeSH heading "hypertension" and the text word "nifedipine" to identify all articles that were published between 1966 and August 1995 in English, French, German, Italian, and Spanish languages and that involved human subjects. The computerized search was supplemented by a manual search of article bibliographies. Review of 1880 citations revealed 98 randomized controlled clinical trials that met protocol criteria. Articles were extracted independently by two doctors who were blinded for author, institution, and treatment regimen, using a structured, pretested extraction form. Differences of opinion were resolved by consensus. Fourteen events occurred in 5198 exposures (0.27%) to nifedipine and 24 events in 5402 exposures (0.44%) to other active drug controls. Unadjusted odds ratios for nifedipine versus controls were 0.49 (95% confidence interval [CI], 0.22-1.09) for definitive events (death, nonfatal myocardial infarction or stroke, revascularization procedure) and 0.61 (95% CI, 0.31-1.17) for all events (definitive plus increased angina). The odds ratio for nifedipine monotherapy (sustained- or extended-release in 91% of exposures) was nonsignificantly higher for definitive and all events (odds ratio, 1.40; 95% CI, 0.49-4.03 and odds ratio, 1.39; 95% CI, 0.59-3.32, respectively). The odds ratio for nifedipine in combination with another drug was significantly lower for definitive and all events (odds ratio, 0.09; 95% CI, 0.01-0.66 and odds ratio, 0.15; 95% CI, 0.03-0.65, respectively). Differences in odds ratio for nifedipine monotherapy and combined therapy were statistically significant (P=.02 for definitive events and P=.001 for all events). Results support the safety of sustained- and extended-release nifedipine in the treatment of mild or moderate hypertension when it is used in combination with other drugs.
----P Clinical_Trial Journal_Article Meta-Analysis Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_MEDLARS_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Odds_Ratio_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_United_States_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9234823
----K E
----T The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study: rationale, design, and methods. The LIFE Study Group.
----A The treatment of hypertension mainly with diuretics and beta blockers reduces cardiovascular mortality and morbidity, largely due to a decreased incidence of stroke, whereas the beneficial effects of antihypertensive therapy on the occurrence of coronary events have been less than expected from epidemiological studies. Furthermore, treated hypertensive patients still have a higher cardiovascular complication rate, compared with matched normotensives. This is particularly evident in patients with left ventricular hypertrophy (LVH), a major independent risk indicator for cardiovascular disease. In addition to elevating blood pressure, angiotensin II (A-II) exerts an important influence on cardiac structure and function, stimulating cell proliferation and growth. Thus, to further reduce morbidity and mortality when treating hypertensive patients, it may be important to effectively block the effects of A-II. This can be achieved directly at the A-II receptor level by losartan, the first of a new class of antihypertensive agents. It therefore seems pertinent to investigate whether selective A-II receptor blockade with losartan not only lowers blood pressure but also reduces LVH more effectively than current therapy, and thus improves prognosis. The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of the beta-blocker atenolol on the reduction of cardiovascular morbidity and mortality in approximately 8,300 hypertensive patients (initial sitting diastolic blood pressure 95 to 115 mm Hg or systolic blood pressure 160 to 200 mm Hg) with electrocardiographically documented LVH. The study, which will continue for at least 4 years and until 1,040 patients experience one primary endpoint, has been designed with a statistical power that will detect a difference of at least 15% between groups in the incidence of combined cardiovascular morbidity and mortality. It is also the first prospective study with adequate power to link reversal of LVH to reduction in major cardiovascular events. The rationale of the study, which will involve more than 800 clinical centers in Scandinavia, the United Kingdom, and the United States, is discussed, and the major features of its design and general organization are described. On April 30, 1997, when inclusion was stopped, 9,218 patients had been randomized.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Imidazoles_MeSH S_therapeutic_use_MeSH Imidazoles_therapeutic_use_MeSH M_Losartan_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Research_Design_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9236404
----K E
----T Low-molecular-weight heparins for unstable angina. A better mousetrap?
----A 
----P Comment Editorial 
----M M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Drug_Administration_Schedule_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Half-Life_MeSH M_Heparin_MeSH S_adverse_effects_MeSH Heparin_adverse_effects_MeSH M_Heparin__Low-Molecular-Weight_MeSH S_pharmacokinetics_MeSH Heparin__Low-Molecular-Weight_pharmacokinetics_MeSH S_therapeutic_use_MeSH Heparin__Low-Molecular-Weight_therapeutic_use_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Injections__Subcutaneous_MeSH M_Thrombophlebitis_MeSH S_prevention_&_control_MeSH Thrombophlebitis_prevention_&_control_MeSH 
****** 9236433
----K I
----T Beneficial effects of intravenous and oral carvedilol treatment in acute myocardial infarction. A placebo-controlled, randomized trial.
----A BACKGROUND: Evidence of efficacy and safety of beta-blockers after thrombolysis for acute myocardial infarction (AMI) is equivocal. Newer beta-blockers such as carvedilol have not been tested in this setting. METHODS AND RESULTS: This study investigated the effects of acute (intravenous) and long-term (6 months, oral) treatment with carvedilol versus placebo in 151 consecutive patients with AMI. Exercise ECG, ambulatory monitoring, and two-dimensional echocardiography were performed before hospital discharge and at 3 and 6 months. All patients were followed up and cardiovascular events recorded. The Cox proportional hazards model was used to compare time from randomization with the occurrence of a cardiovascular event, and Kaplan-Meier survival curves were calculated. Carvedilol was found to be safe, and it significantly reduced cardiac events compared with placebo (18 on carvedilol and 31 on placebo, P < .02). Fifty-four patients had heart failure at study entry; 34 received carvedilol. There were no adverse effects of carvedilol therapy and no excess events in this subgroup. Carvedilol produced significant reductions in heart rate (P < .0001), blood pressure (P < .005) at rest, and rate-pressure product at peak exercise (P < .003), but exercise capacity was unchanged. Left ventricular ejection fraction was not altered significantly by carvedilol, but stroke volume was higher at pre-hospital discharge examination (63 versus 53 mL; P < .01). Diastolic filling of the left ventricle (E/A ratio) was also improved (1.2 versus 0.9; P < .001). In a subgroup with left ventricular ejection fraction < 45% (n = 49 patients; 24 on carvedilol and 25 on placebo), carvedilol showed attenuation of remodeling. CONCLUSIONS: Carvedilol was well tolerated and safe to use in patients immediately after AMI, including those with heart failure, and significantly improved outcome.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH M_Comparative_Study_MeSH M_Dizziness_MeSH S_chemically_induced_MeSH Dizziness_chemically_induced_MeSH M_Echocardiography_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH M_Proportional_Hazards_Models_MeSH M_Recurrence_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH 
****** 9243145
----K E
----T More favourable haemodynamic effects from metoprolol than from captopril in patients with dilated cardiomyopathy.
----A AIM: The object of this study was to investigate and compare the haemodynamic effects of treatment with a beta receptor blocker (metoprolol) or an angiotensin-converting-enzyme inhibitor (captopril) in 54 patients with idiopathic dilated cardiomyopathy. METHOD: All patients had cardiac catheterization performed at rest and during exercise, before and after 3 months of treatment. RESULTS: The mean dose of metoprolol was 135 mg.day-1 and of captopril 98 mg.day-1. After treatment there was a significant reduction in left ventricular filling pressure both at rest (from 16 to 12 mmHg) and during exercise (from 27 to 20 mmHg) in the metoprolol group. In the captopril group a significant reduction was seen only during exercise (25 to 20 mmHg), compared to baseline. The stroke volume increased significantly after 3 months of therapy in the metoprolol group, both at rest (53 to 70 ml) and during exercise (56 to 79 ml). In the captopril group the increase reached significance only during exercise (72 to 79 ml). Cardiac output was maintained in both groups. CONCLUSION: There were positive effects on left ventricular function in the metoprolol group as well as in the captopril group. Metoprolol reduced left ventricular filling pressure at rest and increased stroke volume both at rest and during exercise significantly more than captopril.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Pressure_MeSH S_drug_effects_MeSH Ventricular_Pressure_drug_effects_MeSH 
****** 9251545
----K E
----T Randomised, double blind, multicentre comparison of hydrochlorothiazide, atenolol, nitrendipine, and enalapril in antihypertensive treatment: results of the HANE study. HANE Trial Research Group.
----A OBJECTIVE: To compare the effectiveness and tolerability of hydrochlorothiazide, atenolol, nitrendipine, and enalapril in patients with mild to moderate hypertension. DESIGN: Randomised multicentre trial over 48 weeks with double blind comparison of treatments. SETTING: 48 centres in four countries. PATIENTS: 868 patients with essential hypertension (diastolic blood pressure 95-120 mm Hg) INTERVENTIONS: Initial treatment (step 1) consisted of 12.5 mg hydrochlorothiazide (n = 215), 25 mg atenolol (n = 215), 10 mg nitrendipine (n = 218), or 5 mg enalapril (n = 220) once daily. If diastolic blood pressure was not reduced to < 90 mm Hg within four weeks, doses were increased to 25 mg, 50 mg, 20 mg, 10 mg, respectively, once daily (step 2) and after two more weeks to twice daily (step 3). The eight week titration phase was followed by an additional 40 weeks for patients who had reached the target diastolic pressure. MAIN OUTCOME MEASURES: Blood pressure by means of an automatic device with repeated measurements. RESULTS: After eight weeks the response rate for atenolol (63.7%) was significantly higher than for enalapril (50.0%), hydrochlorothiazide (44.7%), or nitrendipine (44.5%). After one year atenolol was still more effective (48.0%) than hydrochlorothiazide (35.4%) and nitrendipine (32.9%), but not significantly better than enalapril (42.7%). The treatment related dropout rate was higher (P < 0.001) in the nitrendipine group (n = 28). CONCLUSIONS: There is no evidence of superiority for antihypertensive effectiveness or tolerability of the "new" classes of antihypertensives (calcium channel blockers and angiotensin converting enzyme inhibitors). As these drugs are now widely used as treatment of first choice, our results further emphasise the need for studies confirming that they also reduce morbidity and mortality, as has been shown for diuretics and beta blockers.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrendipine_MeSH S_adverse_effects_MeSH Nitrendipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nitrendipine_therapeutic_use_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9251876
----K I
----T Prophylactic treatment of migraine with bisoprolol: a placebo-controlled study.
----A The objective of the present study was to assess the efficacy of bisoprolol in migraine prophylaxis. A double-blind placebo-controlled study was conducted in 226 patients with migraine with or without aura, a migraine history of at least 2 years at least 3 documented attacks during the 28 days run-in period. The duration of treatment was 12 weeks following an initial 28 days' run-in period. Patients reported the number of attacks and their severity in a diary. Treatment with bisoprolol 5 mg resulted in a significant reduction in the frequency of migraine attacks (39% vs 22%) compared to placebo treatment (p < 0.05). Treatment had no effect on the duration and severity of the attacks. Bisoprolol was well tolerated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH 
****** 9253384
----K E
----T On reaching the tunnel at the end of the light.
----A 
----P Comment Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Data_Interpretation__Statistical_MeSH M_Human_MeSH M_Multicenter_Studies_MeSH S_methods_MeSH Multicenter_Studies_methods_MeSH S_statistics_&_numerical_data_MeSH Multicenter_Studies_statistics_&_numerical_data_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Treatment_Outcome_MeSH 
****** 9257080
----K I
----T Antiarrhythmic therapies for the prevention of sudden cardiac death.
----A Despite remarkable advances in cardiovascular therapeutics, sudden cardiac death remains a significant problem. In this review, data from clinical trials and other studies on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention of sudden cardiac death in high risk patients. Overall, routine prophylactic use of class I antiarrhythmic agents in high risk patients, mostly survivors of acute myocardial infarction, is associated with increased risk of death [61 trials, 23,486 patients: odds ratio (OR) 1.13; 95% confidence interval (CI) 1.01 to 1.27, p < 0.05]. Conversely, beta-blockers are associated with highly significant reductions in risk of death in postinfarction patients (56 trials, 53,521 patients: OR 0.81; 95% CI 0.75 to 0.87, p < 0.00001). Overall data from the amiodarone trials on high risk patients, including postinfarction patients, patients with congestive heart failure or survivors of cardiac arrest, suggest that this agent is effective in reducing the risk of death (14 trials, 5713 patients: OR 0.83; 95% CI 0.72 to 0.95, p = 0.01) although further studies are needed to better define which types of patients will potentially benefit most from this agent. No benefits were seen with calcium channel blockers (26 trials, 21,644 patients: OR 1.03; 95% CI 0.94 to 1.13, p = NS). The implantable cardioverter-defibrillator is a promising option for high risk patients, but definition of its role awaits the completion of ongoing clinical trials. Since causes of sudden death are heterogeneous, the clinician should pursue a multifactorial approach to its prevention. Primary and secondary prevention of cardiac ischaemia, through the treatment of cardiovascular risk factors and maximising the use of aspirin, beta-blockers, lipid-lowering drugs, and angiotensin converting enzyme inhibitors after acute myocardial infarction, should lead to a future decrease in the incidence of sudden cardiac death.
----P Journal_Article Review Review_Literature 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH M_Coronary_Artery_Bypass_MeSH S_methods_MeSH Coronary_Artery_Bypass_methods_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Defibrillators__Implantable_MeSH M_Human_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9259162
----K E
----T Reverse remodeling in heart failure with intensification of vasodilator therapy.
----A BACKGROUND: Heart failure therapy with beta-receptor blockade has been shown to effect a partial reversal of left ventricular (LV) remodeling in heart failure. HYPOTHESIS: We tested the hypothesis that, in the absence of beta blockade, uptitration of angiotensin-converting enzyme (ACE) inhibitor and nitrate therapy over conventional dosages would improve symptoms as well as LV function in patients with severe heart failure. METHODS: For patients with nonischemic or ischemic cardiomyopathy, intensive high-dose angiotensin-converting enzyme inhibitor and nitrate therapy was uptitrated. Echocardiograms were obtained semiannually and evaluated in a blinded fashion. Of 99 patients in the study, aged 55 +/- 13 years, with heart failure for 5.2 +/- 3.1 years, 74 were men, 69 were Caucasian, and 34 had ischemic cardiomyopathy. The final dosage of enalapril was 40 +/- 23 mg/day of isosorbide dinitrate it was 153 +/- 127 mg/day. RESULTS: Initial New York Heart Association classification improved from 2.8 +/- 0.9 to 1.7 +/- 0.9 (p < 0.001) in 2.7 years of follow-up. Of the 99 patients, 72 further improved their ejection fraction. For the whole group, ejection fraction increased from 21 +/- 9% to 30 +/- 13% in 6 months (p < 0.001), with a reduction in LV end-diastolic size from 6.6 +/- 0.9 to 6.3 +/- 1.0 cm (p = 0.002), a decrease in the severity of mitral regurgitation from mild/moderate to only mild. Resting heart rate declined with no change over time in systemic systolic blood pressure. Final ejection fraction for nonischemic patients (n = 65) was 36 +/- 16% versus 23 +/- 9% for the ischemic population. CONCLUSIONS: Uptitration of high-dose ACE inhibitor and nitrate therapy to higher doses is well tolerated in severe heart failure, further improves both clinical status and LV systolic function, and is more effective in nonischemic than in ischemic cardiomyopathy.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Cohort_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9260367
----K 1
----T Comparison of clinical efficacy and adverse effects between extended-release felodipine and atenolol in patients with mild and moderate essential hypertension.
----A BACKGROUND: Essential hypertension is a risk factor for cardiovascular disease. Atenolol, a cardio-selective beta-blocker, has been shown to be a safe and effective antihypertensive agent. The extended-release form of felodipine (felodipine ER), a vascular-selective dihydropyridine calcium blocker, is extensively used in Caucasians. However, its effectiveness, tolerability and adverse side-effect have not been assessed in Chinese populations. METHODS: Sitting blood pressure (BP), heart rate, body weight, adverse reaction and serum biochemistry were assessed in 70 patients with mild-moderate essential hypertension treated either with felodipine ER (37 patients), or atenolol (33 patients) for 10 weeks. Each patient was prescribed 5 mg of felodipine ER or 50 mg of atenolol once daily and this daily dosage was doubled to twice daily if necessary. RESULTS: Six patients who received felodipine ER and 3 who received atenolol withdrew from the treatment because of intolerable side effects. Within ten weeks, 81.1% of the patients had responded to a total daily dosage of 5-10 mg of felodipine ER and 81.8% to a daily dose of 50-100 mg of atenolol. By the end of treatment, the mean BP in the felodipine ER group had decreased from 176/104 mmHg at baseline to 145/85 mmHg, while the BP in the atenolol group had dropped from 173/103 mmHg to 145/84 mmHg (NS between the two groups). Heart rate declined in the atenolol group but did not change in patients who received felodipine ER. Overall, patients in the felodipine ER group had a higher rate of adverse reaction (70.3% vs. 39.4%; p < 0.001), and 16.2% of the patients in the felodipine ER group experienced symptoms of hypotension. CONCLUSION: Equivalent doses of felodipine ER and atenolol are effective first-line monotherapeutic agents for the treatment of mild-moderate essential hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 9263654
----K I
----T Clinical trials with implications regarding heart failure therapy.
----A Paradigms for the treatment of heart failure have changed substantially over the past several decades. It has been the performance of relatively large, carefully controlled and often mortality endpoint trials that has given us great insight into therapies that are advantageous, disadvantageous, or neutral with respect to outcomes in patients with heart failure. No longer is the care of a patient with ventricular dysfunction and heart failure solely rooted in the prescription of a diuretic and digoxin. Indeed, we have seen a rather radical evolution from this prescription practice to approaches that were thought to be contraindicated at one time, such as beta blocker and vasodilator therapy. Indeed, treatment paradigms today are shifting rapidly toward more complete attenuation of adrenergic processes known to be detrimental in this setting. It is important to review the recent clinical trials that have given us further insight into managing heart failure. Twenty trials published since 1995 have been selected because of the important insight they give us regarding the wide spectrum of therapeutic options available for individuals with heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Double-Blind_Method_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Meta-Analysis_MeSH P_Multicenter_Studies_MeSH S_methods_MeSH Multicenter_Studies_methods_MeSH P_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH 
****** 9296895
----K 1
----T [Changes in the quality of life influenced by treatment of primary arterial hypertension]
----A The quality of life (QL) in 90 male patients (age 41.2 +/- 41) suffering from Ist IInd hemodynamic WHO-stage of essential arterial hypertension has been studied during 3 months therapy. The patients have been divided into 3 groups treated with enalapril, atenolol and verapamil respectively. The Sickness Impact Profile, Bulpitt's test and Spitzer's test were used for evaluation of QL. Significant reduction in diastolic arterial blood pressure has been achieved during the treatment period. In the same time improvement in QL indices was observed, most evident in group of enalapril, moderate in group of verapamil and the minor in atenolol group. It is concluded that these three QL test (SIP, Bulpit, Spitzer) are very useful in monitoring of treatment of the essential arterial hypertension.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9280714
----K E
----T [Renal hemodynamics and proteinuria in chronic glomerulonephritis treated with beta-receptor blockers or ace inhibitors]
----A BACKGROUND AND OBJECTIVE: In patients with chronic glomerular nephropathy associated arterial hypertension and proteinuria are considered to be cardinal risk factors in the progressive deterioration of renal function. Treatment regimens which reduce proteinuria and hypertension improve prognosis. The effect of the new beta-receptor blockers compared to common ACE-Inhibitors is of special interest. PATIENTS AND METHODS: The studied cohort consisted of 11 patients with CGN, hypertension and proteinuria > 400 mg/24 h. Four drugs were given for 4 weeks, doubly blinded and randomized according to a "Latin-square design": Celiprolol (beta-1-antagonist, beta-2-agonist, 200 mg/d), Atenolol (selective beta-1-antagonist, 50 mg/d), Ramipril (ACE-inhibitor, 2.5 mg/d) and placebo. There was a two-week wash-out phase between each of the four treatment phases. At the end of each treatment phase glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by inulin and para-amino-hippuric acid (PAH) clearance. Proteinuria was determined in the course of a three-day collection period at the end of each treatment phase. During this period blood pressures were measured with a continuous 24-hour blood pressure monitor. RESULTS: Mean arterial blood pressure (MAP) was significantly reduced, compared with placebo, by all three antihypertensives (108 +/- 9 mm Hg with placebo, 98 +/- 12 mg Hg with atenolol, 101 +/- 11 mm Hg with celiprolol and 98 +/- 8 mm Hg with ramipril; P < 0.01). Celiprolol produced a significant rise In ERPF (322 +/- 109 ml/min with placebo, 391 +/- 110 ml/min with celiprolol: P < 0.05). GFR was slightly, but not significantly, reduced by celiprolol and atenolol. Filtration fraction remained unchanged with atenolol and celiprolol, while it was slightly, but not significantly, reduced with ramipril. Compared with the placebo, all three drugs significantly reduced proteinuria (P < 0.05): 1.8 +/- 1.3 g/24 h with placebo, 1.2 +/- 1.2 g/24 h with atenolol, 1.2 +/- 1.1 g/24 h with celiprolol and 1.4 +/- 1.4 g/24 h with ramipril. CONCLUSION: These data indicate that, in addition to ACE inhibitors, the new generation of beta-receptor blockers in particular, because of their vasodilator action, favourably influence proteinuria and renal blood flow in patients with CGN and arterial hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Glomerulonephritis_MeSH S_physiopathology_MeSH Glomerulonephritis_physiopathology_MeSH M_Human_MeSH M_Inulin_MeSH S_blood_MeSH Inulin_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH S_physiopathology_MeSH Proteinuria_physiopathology_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH M_Renal_Circulation_MeSH S_drug_effects_MeSH Renal_Circulation_drug_effects_MeSH M_Renal_Plasma_Flow__Effective_MeSH S_drug_effects_MeSH Renal_Plasma_Flow__Effective_drug_effects_MeSH M_Treatment_Outcome_MeSH M_p-Aminohippuric_Acid_MeSH S_blood_MeSH p-Aminohippuric_Acid_blood_MeSH 
****** 9269942
----K E
----T Characterization of bunazosin-sensitive alpha1-adrenoceptors in human renal medulla.
----A We studied the characteristics of bunazosin-sensitive alpha1-adrenoceptors in human renal medullae by using renal-clearance studies and radioligand-binding assay. In 12 patients with hypertension, renal-clearance studies demonstrated that bunazosin significantly increased renal blood flow from 683 +/- 82 (SD) to 829 +/- 103 ml/min (p < 0.05) and decreased renal vascular resistance from 0.18 +/- 0.02 to 0.14 +/- 0.02 mm Hg/(ml/min) (p < 0.05), but that prazosin had little effect on renal function. In a radioligand-binding assay, specific, saturable, and stereoselective [3H]bunazosin binding, with a single class of binding sites (Kd = 2.7 +/- 1.4 nM; Bmax = 44 +/- 16 fmol/mg protein; n = 11) was detected in membrane preparations of human renal medullae. The rank order of potency of antagonists that inhibited [3H]bunazosin-binding was bunazosin (Ki in nM = 49) > prazosin (57) > yohimbine (3,900) > propranolol (29,000), and that of agonists, l-norepinephrine (7,400) > l-epinephrine (19,000) > d-norepinephrine (71,000). The competition curves fit a one-site model. These findings suggest that bunazosin-sensitive alpha1-adrenoceptors exist in human renal medullae and participate in the regulation of renal hemodynamics.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_alpha-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_In_Vitro_MeSH M_Kidney_Function_Tests_MeSH M_Kidney_Medulla_MeSH S_drug_effects_MeSH Kidney_Medulla_drug_effects_MeSH S_metabolism_MeSH Kidney_Medulla_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prazosin_MeSH S_pharmacokinetics_MeSH Prazosin_pharmacokinetics_MeSH S_pharmacology_MeSH Prazosin_pharmacology_MeSH M_Quinazolines_MeSH S_pharmacokinetics_MeSH Quinazolines_pharmacokinetics_MeSH S_pharmacology_MeSH Quinazolines_pharmacology_MeSH M_Radioligand_Assay_MeSH M_Receptors__Adrenergic__alpha-1_MeSH S_agonists_MeSH Receptors__Adrenergic__alpha-1_agonists_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__alpha-1_antagonists_&_inhibitors_MeSH S_metabolism_MeSH Receptors__Adrenergic__alpha-1_metabolism_MeSH 
****** 9270085
----K E
----T Comparison of the combination of enalapril and a very low dose of hydrochlorothiazide with atenolol in patients with mild-to-moderate hypertension. Scandinavian Study Group.
----A The blood pressure lowering effect and tolerability of the angiotensin-converting enzyme inhibitor enalapril combined with a very low dose of hydrochlorothiazide (HCTZ) were compared with the selective betareceptor blocker atenolol in patients with mild-to-moderate hypertension. Three hundred seventy-four patients were randomized into a triple-blind, parallel, active-controlled 12-week study period comparing enalapril/HCTZ (20/6 mg) with atenolol (50 mg) after a 4-week placebo baseline period. Blood pressure (BP), clinical and laboratory safety, and metabolic laboratory variables were assessed. Enalapril/HCTZ as well as atenolol reduced both sitting and standing diastolic and systolic BP (P < .001), but enalapril/HCTZ had a more pronounced effect than atenolol on sitting systolic BP (P = .019); there was a trend toward more patients achieving target diastolic BP (<90 mm Hg, P = .053). No clinically important differences in safety and tolerability were observed.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 10169635
----K I
----T Randomized trial of carvedilol in treatment of congestive heart failure.
----A BACKGROUND: Members of the U.S. Cardevivol Study Group at Lovelace Scientific Resources, Albuquerque, NM, designed and carried out a large multicenter randomized clinical trial of Cardevilol vs placebo in patients with clinical heart failure and ejection fraction < 0.35. RESULTS: Derived exposure and death data at 50-day intervals to 400 days were used to construct tables of comparative mortality, all ages, both sexes and all durations to 400 days combined, in the Carvedilol and the placebo groups Derivation of expected mortality is explained in detail. CONCLUSIONS: Excess mortality, measured as mortality ratio or excess death rate, was much higher in the placebo than in the Cardevilol-treated group.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Survival_Analysis_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 9282610
----K E
----T Nifedipine, captopril, metoprolol and nifedipine with metoprolol in hypertensive crisis in non-intensive care setting.
----A In 102 cases of severe hypertension (DBP > or = 115 mm Hg), with or without acute complications, efficacy and safety of SL Nifedipine 10 mg (NIF), SL Captopril 25 mg (CAP), IV Metoprolol 15 mg (MET) and SL NIF + IV MET were studied in an inpatient trial. Maximum mean percent reduction in SBP was 13.3, 9.7, 15.7 and 19.9 and in DBP was 21.2, 13.9, 12.5 and 20.4 with NIF, CAP, MET and NIF + MET respectively. A safe DBP of < or = 110 mm Hg (Kaplan) was achieved in 90, 61, 72.2 and 95.2 percent of patients. A statistically significant fall in DBP was observed at 5 minutes with all regimens except CAP which was at 15 minutes. Mild side effects observed were palpitations and flushing (NIF n = 4), taste disturbances (CAP n = 3), heaviness of head (CAP n = 1) and giddiness (MET n = 2, NIF + MET n = 2). The trial data suggest that hypertensive crisis can be managed, without intensive care facility, with all four regimens; this implies significant cost containment.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Acute_Disease_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Safety_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9284428
----K E
----T [Large, long-term, randomized trials and meta-analysis of therapy of patients with hypertension]
----A Over the past few decades, numerous randomized controlled studies of the treatment of hypertension have been conducted in Western countries to determine whether blood pressure reduction reduces the risk of stroke and myocardial infarction. Diuretics and beta blockers, because they have been shown in clinical trials to reduce cardiovascular morbidity and mortality, are the preferred drugs of first choice. No direct evidence yet supports the theoretical advantages of calcium channel blockers and ACE inhibitors over diuretics and beta blockers. Because East Asian nations differ culturally from Western countries, it is very difficult to conduct a randomized trials, thus, there were no reports of large, long-term, randomized placebo-controlled clinical trials of hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Meta-Analysis_MeSH M_Randomized_Controlled_Trials_MeSH M_Time_Factors_MeSH 
****** 9285109
----K I
----T Sexual dysfunction as an obstacle to compliance with antihypertensive therapy.
----A Sexual dysfunction has been identified in numerous controlled trials to be a frequent accompaniment to antihypertensive therapy. Issues of cause and effect are confused because hypertension itself can cause sexual dysfunction. It seems probable, however, that use of certain classes of blood pressure-lowering agents, notably non-cardioselective beta blockers such as propranolol, thiazide diuretics such as chlorthalidone and centrally-acting adrenergic agonists, is associated with an increased risk of sexual dysfunction. The implications of these data for compliance with antihypertensive therapy are considered.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Patient_Compliance_MeSH M_Randomized_Controlled_Trials_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH 
****** 9292396
----K I
----T Coronary artery disease and antioxidants--is there a role for carvedilol?
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_metabolism_MeSH Coronary_Disease_metabolism_MeSH M_Free_Radical_Scavengers_MeSH S_therapeutic_use_MeSH Free_Radical_Scavengers_therapeutic_use_MeSH M_Human_MeSH M_Lipid_Peroxidation_MeSH S_drug_effects_MeSH Lipid_Peroxidation_drug_effects_MeSH M_Lipoproteins__LDL_MeSH S_metabolism_MeSH Lipoproteins__LDL_metabolism_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9293727
----K E
----T Emergency department management of acute myocardial infarction.
----A Myocardial infarction-remains one of the leading causes of death among adults in the United States despite the significant advances in therapy made during the past three decades. However, a significant reduction in mortality following acute myocardial infarction has been accomplished through an aggressive strategy directed toward early recognition and intervention. This approach requires that the emergency physician act promptly and choose appropriately from the ever-expanding therapeutic options. This paper summarizes the recent progress and treatment options in the management of acute myocardial infarction with regard to prehospital care, diagnostic challenges in the emergency department, conventional therapy and pharmacologic advances, newer interventional measures, and future trends.
----P Journal_Article Review Review__Tutorial 
----M M_Adult_MeSH M_Angioplasty_MeSH P_Emergency_Medical_Services_MeSH M_Human_MeSH P_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_surgery_MeSH Myocardial_Infarction_surgery_MeSH M_Patient_Selection_MeSH M_Thrombolytic_Therapy_MeSH M_Time_Factors_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 9296310
----K E
----T Comparison of temocapril and atenolol in the long-term treatment of mild to moderate essential hypertension.
----A This 1-year, dose-titration, General Practitioner (GP) study compared efficacy, tolerability and safety of oral temocapril (10-40 mg once daily) with atenolol (25-100 mg once daily) in mild to moderate adult hypertensives (diastolic blood pressure (DBP) 95-114 mmHg). A 12-week dose-titration period, randomized 3:1 temocapril: atenolol, preceded 40 weeks long-term treatment. An intent-to-treat population of 472 patients was analysed for efficacy after 12 weeks dose-titration. Sitting DBP fell significantly (p < 0.001) in both groups, by mean +/- standard deviation (SD) 15.9 +/- 5.7 mmHg on temocapril and by 16.6 +/- 5.9 mmHg on atenolol. Therapeutic equivalence was demonstrated using the two one-sided t-tests procedure according to Schuirmann (equivalence interval [theta 1 - theta 2] < or = 5 mmHg). Responders (DBP < or = 90 mmHg) represented 89.9% of temocapril and 94.0% of atenolol patients. The lower doses were effective in 70.9% of temocapril patients (10 or 20 mg) and in 63.7% of atenolol patients (25 or 50 mg), these doses being continued after the dose titration period. No clinically relevant changes in haematological, biochemical and urinalysis variables occurred. Adverse events were few, largely unrelated to treatment and comparable between groups. In conclusion, temocapril and atenolol proved to be therapeutically equivalent antihypertensives.
----P Clinical_Trial Clinical_Trial__Phase_III Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiazepines_MeSH S_adverse_effects_MeSH Thiazepines_adverse_effects_MeSH S_therapeutic_use_MeSH Thiazepines_therapeutic_use_MeSH 
****** 9298044
----K E
----T Comparison of manual versus automated blood pressure measurements in treated hypertensive patients.
----A This study assesses differences in blood pressure (BP) levels prospectively between office (manual) measurement and ambulatory blood pressure monitoring (ABPM) in 70 treated, essential, hypertensive patients. The objective was to determine whether ABPM is superior to office measurement for assessing adequacy of therapy. Twenty-four patients received monotherapy and 46 received multiple therapy. Thirty-five patients were administered medication in the morning only, whereas 33 were administered medication in the morning and evening both. Mean systolic BP by manual method was identical to that obtained by ABPM (141.98 +/- 14.98 mm Hg versus 141.46 +/- 16.33 mm Hg, respectively). However, mean diastolic BP by manual method was significantly higher than that obtained by ABPM. (90.38 +/- 9.01 mm Hg versus 86.69 +/- 10.65 mm Hg, respectively; P < 0.001). Significant correlations (P < 0.01) were found between the BP levels measured by these two methods, although individual readings differed by 10 mm Hg or more systolic and by 5 mm or more diastolic in many subjects. No significant differences were noted in BP levels measured by either method for patients treated by monotherapy or multiple therapy, and none were noted whether they were taking medication in the morning or in both the morning and evening. In addition, no differences were noted in BP levels using either method for race. Thus, this study shows that the office measurement is grossly similar to ABPM for assessment of adequacy of therapy in treated hypertensive patients whose blood pressure is controlled adequately. However, ABPM is found to be superior to office measurement in identifying hypertensive patients whose blood pressure is not controlled adequately or is uncontrolled.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_African_Continental_Ancestry_Group_MeSH M_Age_Factors_MeSH M_Atenolol_MeSH M_Blood_Pressure_Determination_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH S_instrumentation_MeSH Blood_Pressure_Monitoring__Ambulatory_instrumentation_MeSH S_methods_MeSH Blood_Pressure_Monitoring__Ambulatory_methods_MeSH M_Calcium_Channel_Blockers_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_European_Continental_Ancestry_Group_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Prospective_Studies_MeSH M_Systole_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 9340476
----K 1
----T [Cost effectiveness of bisoprolol in heart failure. Economic evaluation of the Cardiac Insufficiency Bisoprolol Study (CIBIS) for Germany]
----A BACKGROUND: The Cardiac Insufficiency Bisoprolol Study (CIBIS) demonstrates that, for patients with heart failure of different etiologies, the administration of the beta(1)-adrenoceptor blocker bisoprolol adjuvant to the standard therapy leads to a significant avoidance of hospital admissions. PHARMACOECONOMIC EVALUATION: The results of the CIBIS were evaluated pharmacoeconomically for the Federal Republic of Germany, and were restricted to direct costs only. The costs of bisoprolol medication and in-patient treatment of heart failure were considered, the latter forming the major part of costs incurred. CONCLUSION: Adjunctive therapy with bisoprolol is not only clinically beneficial to the patient with heart failure, but also economically advantageous.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_economics_MeSH Bisoprolol_economics_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cost-Benefit_Analysis_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Germany_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_National_Health_Programs_MeSH S_economics_MeSH National_Health_Programs_economics_MeSH M_Patient_Admission_MeSH S_economics_MeSH Patient_Admission_economics_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9307671
----K E
----T Calcium-channel antagonists in cardiovascular disease.
----A In the last 2 years there has been considerable controversy over the safety of certain calcium antagonists. This article discusses recent drug developments, summarizes the publications that sparked the controversy, highlights results of the l latest trials of calcium antagonists and considers the range of clinical conditions in which calcium antagonists may play a useful role.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9311358
----K I
----T A comparison of divalproex with propranolol and placebo for the prophylaxis of migraine without aura.
----A OBJECTIVE: To compare the efficacy of divalproex sodium (Depakote) with that of propranolol hydrochloride (and placebo) for the prophylaxis of migraine without aura. DESIGN: Single-investigator, randomized, single-blind, placebo-controlled study with 5 phases: baseline (weeks 1-4); placebo (weeks 5-8); first treatment, 1 agent (weeks 9-20); washout (weeks 21-24); and second treatment, crossover to other agent (weeks 25-36). SETTING: Private practice of a general neurologist with a special interest in headache disorders. PATIENTS: Of 37 patients (30 women and 7 men) selected, 32 completed the study. All received placebo, after which half were randomized to receive divalproex or propranolol, then crossed over after washout. INTERVENTION: Divalproex and propranolol doses were titrated during the initial 8 weeks of each 12-week treatment cycle. For divalproex, doses were titrated to 1500 mg/d in 23 patients, to 2000 mg/d in 2, and downward in 7; the mean valproate sodium trough level was 68.5 mg/L. Propranolol was titrated to 180 mg/d in 28 patients, to 240 mg/d in 1, and downward in 3. RESULTS: Migraine frequency was reduced in 19% (6/ 32) of placebo-treated, 66% (21/32) of divalproex-treated, and 63% (20/32) of propranolol-treated patients. Assessment of migraine-days per month revealed significant response to placebo in 22% (7/32) of patients, to divalproex in 66% (21/32), and to propranolol in 69% (22/32). When results were limited to the third month of each active-agent treatment phase, 75% (24/ 32) of patients receiving divalproex and 78% (25/32) of those receiving propranolol had reduction in migraine frequency. CONCLUSION: No significant difference was identified between divalproex and propranolol for the prophylaxis of migraine without aura.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_GABA_Agents_MeSH S_therapeutic_use_MeSH GABA_Agents_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_complications_MeSH Migraine_complications_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Sensation_Disorders_MeSH S_etiology_MeSH Sensation_Disorders_etiology_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Valproic_Acid_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH 
****** 9313591
----K E
----T Efficacy and safety of sotalol in patients with refractory atrial fibrillation or flutter.
----A Sotalol's usefulness in treatment of atrial fibrillation and atrial flutter is unproven. This study evaluated (1) the efficacy of sotalol in preventing recurrences of paroxysmal atrial fibrillation or atrial flutter and controlling ventricular rate (in chronic atrial fibrillation or relapse of paroxysmal atrial arrhythmias), (2) the safety of sotalol, and (3) predictors of sotalol efficacy. Thirty-three patients, 28 with paroxysmal and five with chronic atrial fibrillation or atrial flutter, received an average dose of 265 +/- 119 mg of oral sotalol per day. During a 10 +/- 12 month follow-up, recurrence rate for paroxysmal arrhythmia was 64%, with a 50% recurrence at 4.6 months. For patients with chronic atrial fibrillation, ventricular rates were well controlled with sotalol administration (136 +/- 33 beats/min versus 88 +/- 23 beats/min; p = 0.04). No patient with chronic atrial fibrillation converted to sinus rhythm during the study. Side effects necessitated sotalol discontinuation in three patients. By multivariate analysis, younger age, higher ejection fraction, and absence of hypertension independently predicted sotalol efficacy.
----P Clinical_Trial Journal_Article 
----M M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Atrial_Flutter_MeSH S_drug_therapy_MeSH Atrial_Flutter_drug_therapy_MeSH M_Chronic_Disease_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9315764
----K E
----T Antihypertensive treatment based on conventional or ambulatory blood pressure measurement. A randomized controlled trial. Ambulatory Blood Pressure Monitoring and Treatment of Hypertension Investigators.
----A CONTEXT: Ambulatory blood pressure (ABP) monitoring is used increasingly in clinical practice, but how it affects treatment of blood pressure has not been determined. OBJECTIVE: To compare conventional blood pressure (CBP) measurement and ABP measurement in the management of hypertensive patients. DESIGN: Multicenter, randomized, parallel-group trial. SETTING: Family practices and outpatient clinics at regional and university hospitals. PARTICIPANTS: A total of 419 patients (> or =18 years), whose untreated diastolic blood pressure (DBP) on CBP measurement averaged 95 mm Hg or higher, randomized to CBP or ABP arms. INTERVENTIONS: Antihypertensive drug treatment was adjusted in a stepwise fashion based on either the average daytime (from 10 AM to 8 PM) ambulatory DBP (n=213) or the average of 3 sitting DBP readings (n=206). If the DBP guiding treatment was above (>89 mm Hg), at (80-89 mm Hg), or below (<80 mm Hg) target, 1 physician blinded to the patients' randomization intensified antihypertensive treatment, left it unchanged, or reduced it, respectively. MAIN OUTCOME MEASURES: The CBP and ABP levels, intensity of drug treatment, electrocardiographic and echocardiographic left ventricular mass, symptoms reported by questionnaire, and cost. RESULTS: At the end of the study (median follow-up, 182 days; 5th to 95th percentile interval, 85-258 days), more ABP than CBP patients had stopped antihypertensive drug treatment (26.3% vs 7.3%; P<.001), and fewer ABP patients had progressed to sustained multiple-drug treatment (27.2% vs 42.7%; P<.001). The final CBP and 24-hour ABP averaged 144.1/89.9 mm Hg and 129.4/79.5 mm Hg in the ABP group and 140.3/89.6 mm Hg and 128.0/79.1 mm Hg in the CBP group. Left ventricular mass and reported symptoms were similar in the 2 groups. The potential savings in the ABP group in terms of less intensive drug treatment and fewer physician visits were offset by the costs of ABP monitoring. CONCLUSIONS: Adjustment of antihypertensive treatment based on ABP monitoring instead of CBP measurement led to less intensive drug treatment with preservation of blood pressure control, general well-being, and inhibition of left ventricular enlargement but did not reduce the overall costs of antihypertensive treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Belgium_MeSH M_Blood_Pressure_Determination_MeSH S_economics_MeSH Blood_Pressure_Determination_economics_MeSH S_methods_MeSH Blood_Pressure_Determination_methods_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH S_economics_MeSH Blood_Pressure_Monitoring__Ambulatory_economics_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Family_Practice_MeSH M_Female_MeSH M_Hospitals__University_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Outpatient_Clinics__Hospital_MeSH M_Statistics__Nonparametric_MeSH M_Survival_Analysis_MeSH 
****** 9315986
----K E
----T Effects of trazodone and fluoxetine in the treatment of major depression: therapeutic pharmacokinetic and pharmacodynamic interactions through formation of meta-chlorophenylpiperazine.
----A It has been suggested that (1) the clinical efficacy of the heterocyclic antidepressant trazodone in depression may, in part, be attributed to its metabolite meta-chlorophenylpiperazine (mCPP); and (2) the enhancement of the efficacy of trazodone by the addition of fluoxetine, a selective serotonin reuptake inhibitor, may, in part, be ascribed to fluoxetine-induced plasma concentrations of trazodone. After a washout period of 10 days, 27 inpatients with major depression were treated with trazodone 100 mg/day (orally). One week later (T0), fluoxetine 20 mg/day, placebo, or pindolol 7.5 mg/day was added. Plasma concentrations of mCPP and trazodone were determined at T0 and 2 and 4 weeks later. Although placebo pindolol had no significant effect on the plasma concentrations of mCPP and trazodone, there was a significant increase of the concentrations of these compounds associated with the combination of trazodone + fluoxetine. The results suggest that fluoxetine-induced increases in plasma mCPP and trazodone concentrations contribute to the clinical efficacy of the combination of fluoxetine + trazodone. It is suggested that desensitization of 5-HT2C receptor function by mCPP as well as fluoxetine may contribute to the antidepressant effects of this combination.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antidepressive_Agents__Second-Generation_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents__Second-Generation_administration_&_dosage_MeSH S_adverse_effects_MeSH Antidepressive_Agents__Second-Generation_adverse_effects_MeSH S_pharmacokinetics_MeSH Antidepressive_Agents__Second-Generation_pharmacokinetics_MeSH M_Comparative_Study_MeSH M_Depression__Involutional_MeSH S_blood_MeSH Depression__Involutional_blood_MeSH S_drug_therapy_MeSH Depression__Involutional_drug_therapy_MeSH S_psychology_MeSH Depression__Involutional_psychology_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_administration_&_dosage_MeSH Fluoxetine_administration_&_dosage_MeSH S_adverse_effects_MeSH Fluoxetine_adverse_effects_MeSH S_pharmacokinetics_MeSH Fluoxetine_pharmacokinetics_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Personality_Inventory_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_pharmacokinetics_MeSH Pindolol_pharmacokinetics_MeSH M_Piperazines_MeSH S_pharmacokinetics_MeSH Piperazines_pharmacokinetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Trazodone_MeSH S_administration_&_dosage_MeSH Trazodone_administration_&_dosage_MeSH S_adverse_effects_MeSH Trazodone_adverse_effects_MeSH S_pharmacokinetics_MeSH Trazodone_pharmacokinetics_MeSH M_Treatment_Outcome_MeSH 
****** 9316529
----K E
----T Improvement of postreceptor events by metoprolol treatment in patients with chronic heart failure.
----A OBJECTIVES: This study tested the hypothesis that metoprolol restores the reduction of the inotropic effect of the cyclic adenosine monophosphate (cAMP)-phosphodiesterase inhibitor milrinone, which is cAMP dependent but beta-adrenoceptor independent. BACKGROUND: Treatment with beta-adrenergic blocking agents has been shown to lessen symptoms and improve submaximal exercise performance and left ventricular ejection fraction in patients with heart failure. Restoration of the number of down-regulated beta-adrenoceptors has been suggested to be one mechanism of beta-blocker effectiveness. However, the reversal of postreceptor events, namely, an increase in inhibitory G-protein alpha-subunit concentrations, could also play a role. METHODS: Fifteen patients with heart failure due to dilated cardiomyopathy (left ventricular ejection fraction 24.6 +/- 1.5% [mean +/- SD], New York Heart Association functional class II or III) were treated with metoprolol (maximal dose 50 mg three times daily) for 6 months. Before and after metoprolol treatment, inotropic responses to milrinone (5 to 10 micrograms/kg body weight per min) were measured echocardiographically. For comparison, responses to milrinone were determined under control conditions and after accelerated application of 150 mg of metoprolol to inactivate beta-adrenoceptors in subjects with normal left ventricular function. RESULTS: In subjects with normal left ventricular function, treatment with metoprolol did not alter the increase in fractional shortening or pressure/dimension ratio of circumferential fiber shortening after application of milrinone. In patients with heart failure, treatment with metoprolol significantly increased left ventricular ejection fraction, fractional shortening and submaximal exercise tolerance and reduced heart rate, plasma norepinephrine concentrations and functional class. After metoprolol treatment, milrinone increased fractional shortening but had no effect before beta-blocker treatment. CONCLUSIONS: Milrinone increases inotropic performance independently of beta-adrenoceptors in vivo. Metoprolol treatment restores the blunted inotropic response to milrinone in patients with heart failure, indicating that postreceptor events (e.g., increase in inhibitory G-protein) are favorably influenced. This mechanism could contribute to the beneficial effects observed in the study patients and represents an important mechanism of how beta-blocker treatment influences the performance of the failing heart.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Drug_Synergism_MeSH M_Female_MeSH M_GTP-Binding_Protein_alpha_Subunits__Gi-Go_MeSH S_drug_effects_MeSH GTP-Binding_Protein_alpha_Subunits__Gi-Go_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Milrinone_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_therapeutic_use_MeSH Phosphodiesterase_Inhibitors_therapeutic_use_MeSH M_Pyridones_MeSH S_therapeutic_use_MeSH Pyridones_therapeutic_use_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH M_Receptors__Cyclic_AMP_MeSH S_drug_effects_MeSH Receptors__Cyclic_AMP_drug_effects_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9324103
----K E
----T Impact of alpha- versus beta-blockers on hypertensive target organ damage: results of a double-blind, randomized, controlled clinical trial.
----A In hypertensive disease, the extent of target organ damage determines the prognosis. We conducted a 6-month, double-blind randomized study to compare the effects of an alpha1-adrenoreceptor blocker (bunazosin) with those of a beta1-adrenoreceptor blocker (metoprolol) on early hypertensive target organ damage at a similar level of blood pressure reduction. The study consisted of 43 patients (29 men and 14 women) of varying ages (mean age 52 +/- 9 years) with essential hypertension World Health Organization stage I-II. Both the alpha- and the beta-blocker lowered blood pressure to a similar extent measured by 24-h blood pressure monitoring. The left ventricular mass was comparably reduced in both cohorts (alpha-blocker 284 +/- 80 v 259 +/- 67 g, P < .05, beta-blocker 282 +/- 74 v 254 +/- 70 g, P < .05). Treatment with the alpha-blocker led to reduced total peripheral resistance (22.9 +/- 8.0 v 19.9 +/- 5.3 U, P < .05), whereas therapy with the beta-blocker resulted in an elevated total peripheral resistance (25.5 +/- 8.4 v 28.5 +/- 9.3 U, P < .10; P < .05 for the difference in both groups). Renal plasma flow remained constant in the alpha-blocker treated group but decreased in the beta-blocker treated group (508 +/- 141 v 477 +/- 134 mL/min/1.73 m2, P < .05). Glomerular filtration rate as measured by inulin clearance tended to increase after treatment with the alpha-blocker (112 +/- 20 v 115 +/- 18 mL/min/1.73 m2, P < .10) in accordance with a decrease of serum creatinine (1.00 +/- 0.14 v 0.93 +/- 0.12 mg/dL, P < .001). Plasma cholesterol and LDL cholesterol was lowered after treatment with the alpha-blocker (238 +/- 48 v 312 +/- 37 mg/dL; P < .001, and 153 +/- 32 v 130 +/- 25 mg/dL; P < .05) while remaining unchanged in group treated with the beta-blocker. Left ventricular hypertrophy was similarily reduced with alpha- and with beta-blockade at a comparable reduction of 24-h blood pressure. Alpha-blockers effected a more favorable renal and systemic hemodynamic profile than beta-blockers, but only long-term prospective studies will answer the question whether these hemodynamic effects result into a better cardiovascular prognosis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_urine_MeSH Proteinuria_urine_MeSH M_Renal_Circulation_MeSH 
****** 9323940
----K 4
----T Efficacy of carteolol hydrochloride 1% vs timolol maleate 0.5% in patients with increased intraocular pressure. Nocturnal Investigation of Glaucoma Hemodynamics Trial Study Group.
----A PURPOSE: To evaluate the ocular hypotensive effect and safety of carteolol hydrochloride 1% vs timolol maleate 0.5%. METHODS: One hundred seventy-six patients with ocular hypertension or primary open-angle glaucoma were randomly assigned to receive either carteolol 1% twice a day or timolol maleate 0.5% solution twice a day in a randomized, double-masked, multicenter, parallel-group, active-control comparison trial during a 3-month period. RESULTS: After 12 weeks, carteolol 1% reduced the mean +/- SE intraocular pressure from 25.0 +/- 0.3 to 19.5 +/- 0.3 mm Hg; timolol maleate 0.5% reduced the mean intraocular pressure from 25.2 +/- 0.3 to 19.6 +/- 0.3 mm Hg. The mean difference in trough intraocular pressure between carteolol and timolol maleate of -0.14 mm Hg was not significantly (P = .745) different (95% confidence limits, -0.97 to 0.70 mm Hg). Trough pulse and blood pressure also showed no consistent statistically significant differences between groups. The 2-hour postdose pulse, however, demonstrated a greater decrease in the timolol maleate than in the carteolol group (P < .001). Systemic and ocular signs and symptoms were similar between the groups except that the number of treatment-emergent reports of bradycardia was greater in the timolol maleate group (P = .039), and the carteolol group reported fewer ocular symptoms than the timolol maleate group did (P < .01). CONCLUSIONS: Both carteolol 1% and timolol maleate 0.5% are highly effective in lowering intraocular pressure when measured at the end of the dosing interval. Carteolol 1% demonstrates an ocular hypotensive effect and safety profile similar to those of timolol maleate 0.5% solution.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carteolol_MeSH S_adverse_effects_MeSH Carteolol_adverse_effects_MeSH S_therapeutic_use_MeSH Carteolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9327317
----K E
----T Perioperative metoprolol reduces the frequency of atrial fibrillation after thoracotomy for lung resection.
----A OBJECTIVE: The association of atrial fibrillation with thoracic surgical procedures is well known, but nevertheless its cause is not well defined. Increased sympathetic activity may play a role in the development of atrial fibrillation, and reduced beta-receptor activity may be advantageous. The objective was to evaluate the effect of oral beta-blockade on the frequency of atrial fibrillation and to evaluate some possible causative factors. DESIGN AND SETTING: The study was prospective, randomized, and double-blind, and was conducted at Aarhus University Hospital. PARTICIPANTS: Thirty patients without previous or present cardiovascular history undergoing elective thoracotomy for lung resection. INTERVENTIONS: The patients received either 100 mg of metoprolol or placebo orally before surgery and once daily postoperatively. Anesthesia consisted of a thoracic epidural block combined with general intravenous anesthesia. Epidural morphine was continued postoperatively. MEASUREMENTS AND MAIN RESULTS: Patients were monitored with electrocardiograms (ECGs), capillary pulse oximetry, invasive hemodynamic monitoring, central venous oxygen saturation, arterial blood gases, serum electrolytes, and fluid balances. Atrial fibrillation developed in 23.3% of the patients, 6.7% after metoprolol compared with 40% in the placebo group. Atrial fibrillation developed a mean of 2.9 days postoperatively. The predominant hemodynamic findings were perioperative lower oxygen consumption and postoperative lower cardiac index after metoprolol. Patients developing atrial fibrillation had much higher oxygen consumption and postoperative cardiac index than other patients. CONCLUSION: Perioperative oral beta-blockade can reduce the frequency of atrial fibrillation without serious side effects. Increased sympathetic activity is one of the predominant factors in the cause of this complication.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH S_drug_effects_MeSH Oxygen_Consumption_drug_effects_MeSH M_Pneumonectomy_MeSH S_adverse_effects_MeSH Pneumonectomy_adverse_effects_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Thoracotomy_MeSH S_adverse_effects_MeSH Thoracotomy_adverse_effects_MeSH 
****** 9329280
----K E
----T Pattern of out-patient drug treatment of hypertension in Korle-Bu Teaching Hospital, Accra.
----A In a retrospective study of the pattern of drugs used in the initial treatment of hypertension, 300 case notes of hypertensive patients attending medical clinics at the Korle-Bu Teaching Hospital, Accra and whose treatment were initiated during the period 1973-1993, were reviewed. The mean age of patients was 55 years, mean pre-treatment systolic and diastolic pressures were 179.5 +/- 25. 5 and 108.5 +/- 14.2 mm Hg, respectively, with 85% of patients being female. The frequencies of individual drugs prescribed for the initial treatment of hypertension were: diuretics (90%), reserpine (46%), methyldopa (31%), and propranolol (30%). Single drug treatment was prescribed for 18%, two drugs for 60% and three or more (multiple drugs) for 22% of patients. The mean number of drugs per patient was 2.2 Patients prescribed multiple drugs had pre-treatment systolic and diastolic blood pressures which were significantly (p < 0.01) higher than those prescribed 2 drugs which were, in turn, higher (p < 0.001) than those prescribed single drugs. The results showed that during the period 1973-1993, diuretic based "stepped care" therapy was the main first line anti-hypertensive drug management regime. "Old" anti-hypertensive drugs were more commonly used than newer ones. The cost and availability drugs and the pretreatment blood pressure were probably the main determinants of the choice of the type and number of drugs prescribed.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Drug_Therapy__Combination_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Ghana_MeSH M_Hospitals__Teaching_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Outpatient_Clinics__Hospital_MeSH M_Retrospective_Studies_MeSH 
****** 9330125
----K I
----T Safety and efficacy of carvedilol in severe heart failure. The U.S. Carvedilol Heart Failure Study Group.
----A BACKGROUND: Many patients remain markedly symptomatic despite optimal current therapy for heart failure. Beta-blockers have often been viewed as contraindicated in this group because of their potential adverse short-term effects on cardiac function. METHODS AND RESULTS: One hundred thirty-one patients with severe congestive heart failure were enrolled into a double-blind, placebo-controlled study of the vasodilating beta-blocker carvedilol. All patients had symptomatic, advanced heart failure while on standard triple therapy, as evidenced by a mean ejection fraction of 0.22, marked reduction in distance traveled in a 6-minute corridor walk test, and severe impairment in quality of life measured by the Minnesota Living With Heart Failure Questionnaire. After a 2-week, open-label test of 6.25 mg twice daily carvedilol, 105 patients were randomized (2:1) to receive either carvedilol (up to 25 mg twice daily, n = 70) or matching placebo (n = 35) for 6 months while background therapy with digoxin, diuretics, and an angiotensin-converting enzyme inhibitor remained constant. Ten patients (8%) did not complete the open-label period because of adverse events and 11.4% in both the carvedilol and placebo groups dropped out in the double-blind phase. The study was terminated early by the Data Safety and Monitoring Board and follow-up evaluation was therefore aborted before the projected number of patients and follow-up time was achieved. Quality of life, which was the primary endpoint, improved similarly in the carvedilol and placebo groups, whereas the global assessment by the physicians and the patient exhibited a better response to carvedilol (P < .05). Hospitalization and mortality rate were too low to evaluate a difference, and exercise time and New York Heart Association classification did not change significantly in response to the drug. Left ventricular ejection fraction rose significantly (+0.09) in the carvedilol group compared with the placebo group (+0.02, P = .004). CONCLUSION: The beta-blocker carvedilol can be safely employed in patients with severe heart failure. Improved left ventricular function with a trend for some improvement in symptoms combined with the experience with the drug in the larger population of less severe patients in this multicenter trial suggests that carvedilol may have a favorable long-term effect in heart failure of diverse severity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9335414
----K E
----T Relations between fasting serum insulin, glucose, and dihydroepiandrosterone-sulfate concentrations in obese patients with hypertension: short-term effects of antihypertensive drugs.
----A A randomized, single-blind, placebo-controlled study was conducted in 82 obese patients with mild to moderate essential hypertension, to determine the incidence of hyperinsulinemia, the relations between fasting insulin and dihydroepiandrosterone-sulfate (DHEA-S) levels, and the short-term effects of antihypertensives on DHEA-S and insulin serum concentrations. Increased insulin/glucose ratios (IGR) suggestive of insulin resistance were found in half of our patients. Hyperinsulinemic and normoinsulinemic obese patients with hypertension had comparable fasting glucose and DHEA-S concentrations and comparable blood pressure (BP) levels. Thus no relations were found between fasting insulin and DHEA-S levels. Fasting hyperinsulinemia was found in only half of the obese subjects with hypertension, suggesting that not all obese patients with hypertension are at the same high cardiovascular risk. Short-term treatment with captopril, prazosin, verapamil, atenolol, or hydrochlorothiazide (HCTZ) reduced BP; greater BP reduction was observed with drugs with vasodilatory effects. Captopril, prazosin, and verapamil reduced fasting insulin levels, whereas atenolol and hydrochlorothiazide did not. The former drugs reduced fasting insulin levels that were either within normal limits or in the hyperinsulinemic range. None of the drug treatments produced significant increases in serum DHEA-S concentrations, although some of them considerably reduced fasting insulin levels. No relations between insulin and DHEA-S levels were observed either at baseline or at the end of the antihypertensive treatment. The BP reduction resulting from the peripheral vasodilation may explain the insulin-reducing action of captopril, verapamil, and prazosin. These results further emphasize the large heterogeneity present in the pathophysiologic mechanisms operating in obesity and hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Dehydroepiandrosterone_Sulfate_MeSH S_blood_MeSH Dehydroepiandrosterone_Sulfate_blood_MeSH M_Fasting_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_blood_MeSH Obesity_blood_MeSH S_complications_MeSH Obesity_complications_MeSH M_Placebos_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9336024
----K E
----T Drug management of hypertensive disorders of pregnancy.
----A Drugs used in the acute and long-term management of hypertension in pregnancy and the preeclampsia-eclampsia syndrome have been reviewed and their therapeutic effects and maternal and fetal adverse effects have been considered. The review also focuses on recent developments in the areas of prevention and management of pre-eclampsia-eclampsia syndrome. Although a number of new drugs have emerged, as potentially useful in the management of hypertension in pregnancy and pre-eclampsia-eclampsia syndrome, some remain at the cornerstone of therapy; for example, methyldopa for long-term treatment of chronic hypertension, hydralazine or nifedipine for rapid reduction of severely elevated blood pressure, and magnesium sulphate for eclampsia. Some of these agents, especially the calcium antagonists, show promise in that their use is associated with fewer side effects. Safety for the fetus, however, has not been adequately evaluated yet. Neither aspirin nor calcium supplements appear to improve the outcome in pregnancy. Currently, the dilemma whether to treat hypertension in pregnancy and pre-eclampsia-eclampsia syndrome with old, established, cost-effective drugs or the promising newer drugs provides an interesting academic challenge.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Pre-Eclampsia_MeSH S_drug_therapy_MeSH Pre-Eclampsia_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH 
****** 9337190
----K E
----T Prognostic value of bisoprolol-induced hemodynamic effects in heart failure during the Cardiac Insufficiency BIsoprolol Study (CIBIS).
----A BACKGROUND: To further evaluate the mechanism of beta-blocker-induced benefits in heart failure, the relationships between bisoprolol-induced hemodynamic effects and survival were studied during the Cardiac Insufficiency BIsoprolol Study (CIBIS). METHODS AND RESULTS: In 557 patients studied, bisoprolol significantly reduced heart rate (-16.3+/-15.3 versus -1.6+/-13.4 bpm, respectively; P<.001) compared with placebo at 2 months after inclusion in the study. Heart rate change over time had the highest predictive value for survival (P<.01). Left ventricular fractional shortening (LVFS) significantly increased in the bisoprolol group compared with the placebo group 5 months after inclusion (+0.04+/-0.06 versus -0.001+/-0.05, respectively; P<.001; n=160). LVFS change over time was also significantly correlated with further survival (P<.02 by Cox analysis). Using a nonparametric approach, we demonstrated a significant interaction between study treatment group and LVFS over time. Patients who demonstrated improvement of LVFS over time (82% and 51% of patients in the bisoprolol and the placebo groups, respectively; P<.02) were at lower risk, but the hazard did not further decrease with a further increase of fractional shortening, and there was no significant difference between study treatment groups. Finally, it could be demonstrated that each of the three factors (heart rate change over time, LVFS change over time, and bisoprolol treatment) made a specific contribution to mortality rate. CONCLUSIONS: Preservation of left ventricular function appears to play a key role in the bisoprolol-induced beneficial effects on prognosis in heart failure. Short-term beta-blocker-induced cardiac effects could provide a means to identify those patients who will experience improved survival over the long term.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Europe_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Models__Statistical_MeSH M_Placebos_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9337224
----K E
----T Incidence of and risk factors for atrial fibrillation in older adults.
----A BACKGROUND: This study aimed to describe the incidence of atrial fibrillation (AF) among older adults during 3 years of follow-up. METHODS AND RESULTS: In this cohort study, 5201 adults > or = 65 years old were examined annually on four occasions between June 1989 and May 1993. At baseline, participants answered questionnaires and underwent a detailed examination that included carotid ultrasound, pulmonary function tests, ECG, and echocardiography. Subjects with a pacemaker or AF at baseline (n=357) were excluded. New cases of AF were identified from three sources: (1) annual self-reports, (2) annual ECGs, and (3) hospital discharge diagnoses. Cox proportional-hazards models were used to assess baseline risk factors as predictors of incident AF. Among 4844 participants, 304 developed a first episode of AF during an average follow-up of 3.28 years, for an incidence of 19.2 per 1000 person-years. The onset was strongly associated with age, male sex, and the presence of clinical cardiovascular disease. For men 65 to 74 and 75 to 84 years old, the incidences were 17.6 and 42.7, respectively, and for women, 10.1 and 21.6 events per 1000 person-years. In stepwise models, the use of diuretics, a history of valvular heart disease, coronary disease, advancing age, higher levels of systolic blood pressure, height, glucose, and left atrial size were all associated with an increased risk of AF. The use of beta-blockers and high levels of alcohol use, cholesterol, and forced expiratory volume in 1 second were associated with a reduced risk of AF. CONCLUSIONS: The incidence of AF in older adults may be higher than estimated by previous population studies. Left atrial size appears to be an important risk factor, and the control of blood pressure and glucose may be important in preventing the development of AF.
----P Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_epidemiology_MeSH Atrial_Fibrillation_epidemiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH M_Cerebrovascular_Disorders_MeSH S_epidemiology_MeSH Cerebrovascular_Disorders_epidemiology_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hospital_Records_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH 
****** 9339958
----K I
----T The role of beta-blockers in left ventricular dysfunction and heart failure.
----A It was first reported by our group in 1975 that heart failure due to idiopathic dilated cardiomyopathy (IDC) could be improved by long term treatment with a beta-blocker, starting at a low dose and continuing with a stepwise up-titration. Since then, many studies have been performed in patients with heart failure of various aetiologies and the beneficial effects of long term beta-blockade have been confirmed. About 3000 patients have been included in randomised studies in which beta-blockade, given for more than 2 months, mostly elicited significant improvements in functional class, exercise capacity, cardiac function, quality of life and/or morbidity. When started at a very low dose (one-tenth to one-twentieth of the doses generally used in angina or hypertension), the treatment is well tolerated in most patients. In these studies, various types of beta-blockers were used, including beta1-selective blockers and nonselective blockers with additional properties (vasodilator and antioxidative) such as metoprolol, bisoprolol, bucindolol and carvedilol. Several large studies have also reported benefits on mortality and morbidity. In the Metoprolol in Dilated Cardiomyopathy (MDC) trial, metoprolol treatment in patients with IDC resulted in a 34% reduction of the primary combined endpoint, total number of deaths and need for cardiac transplantation. In the Cardiac Insufficiency Bisoprolol Study (CIBIS), in patients with idiopathic as well as ischaemic cardiomyopathy, there was a nonsignificant 20% reduction in mortality. In the US carvedilol studies (n = 1094), also in patients with ischaemic and idiopathic cardiomyopathy, carvedilol reduced mortality by 65%, which was highly significant. A nonsignificant reduction in mortality was observed in the Australia-New Zealand (ANZ) Heart Failure Study with carvedilol. In all these studies there was a reduction in hospitalisations, with all drugs being generally well tolerated. It can thus be concluded that the beneficial effects of beta-blockers on cardiac function and morbidity have been documented in a large number of studies in selected groups of patients. The treatment has been accepted in some countries by the regulatory authorities. Larger, placebo-controlled studies are needed to convincingly demonstrate a reduction in total mortality as observed in the pooling of the 4 US carvedilol studies. Such studies are in progress for various beta-blockers, which may lead to acceptance of their routine clinical use in patients with congestive heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_etiology_MeSH Cardiomyopathy__Congestive_etiology_MeSH S_mortality_MeSH Cardiomyopathy__Congestive_mortality_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Human_MeSH M_Length_of_Stay_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 9342132
----K E
----T The effect of esmolol on ST-segment depression and arrhythmias after electroconvulsive therapy.
----A Electroconvulsive therapy (ECT) induces sympathetically mediated hemodynamic alterations that can be associated with myocardial ischemia and arrhythmia generation. Esmolol, a short-acting beta-blocker, blunts the hypertension and tachycardia seen with ECT. The purpose of this study is to determine whether esmolol use during ECT reduces the incidence of myocardial ischemia or arrhythmias after ECT. In a randomized, double-blind, placebo-controlled protocol, with each patient acting as his/her own control, the effects of esmolol on the incidence of myocardial ischemia and arrhythmias were studied using two-lead Holter monitoring for at least 2 h post-ECT. Nineteen patients underwent 71 ECT treatments (34 placebo, 37 esmolol), recording 746 h of Holter data. The esmolol group had significantly reduced heart rate and mean arterial pressure immediately after ECT. There was no difference in the incidence of ECG defined ischemia post-ECT between groups, with 7 of 19 (36.8%) patients in the esmolol group showing ST-segment depression compared with 5 of 19 (26.3%) in the placebo group. There was no difference between groups in arrhythmia detection. This experiment demonstrates that (a) ECT is associated with a significant incidence of ST-segment depression, (b) esmolol blunts the sympathetic discharge during ECT, and (c) esmolol does not reduce the incidence of post-ECT ischemia or arrhythmia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH P_Electroconvulsive_Therapy_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH P_Premedication_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Tachycardia_MeSH S_physiopathology_MeSH Tachycardia_physiopathology_MeSH S_prevention_&_control_MeSH Tachycardia_prevention_&_control_MeSH 
****** 9342580
----K E
----T Pharmacokinetic and pharmacodynamic interaction of single doses of valsartan and atenolol.
----A OBJECTIVE: Valsartan (V), a specific inhibitor of the angiotensin II receptor subtype, AT1, has been developed for treatment of hypertension. Combination therapy with a beta-adrenoceptor blocking agent might be considered in cases with insufficient efficacy of V alone. Therefore, an interaction trial was performed to evaluate the effects of co-administration of V on the pharmacokinetics of atenolol (A), and vice versa, and to monitor the pharmacodynamic response of plasma angiotensin II (ANG II) concentrations and plasma renin activity (PRA), as well as of heart rate and blood pressure, under resting and exercise conditions. METHODS: Twelve healthy, normotensive, male volunteers aged 23-46 years were treated with single doses of either 160 mg V or 100 mg A alone, or with both drugs in combination (V + A) according to a three-period crossover design. Plasma concentrations of V and A were determined using HPLC with fluorimetric and UV detection, respectively, and concentration-time profiles were established over 24 h. Plasma ANG II concentrations and PRA were monitored using specific radioimmunoassays. Heart rate and blood pressure were measured at rest and during exercise on a cycle ergometer at a workload of 2.5 W/kg-1. RESULTS: For V, mean AUC and Cmax were slightly higher when A was co-administered, the ratios of log transformed values being 1.13 and 1.22 for AUC(0-inf) and Cmax, respectively. For A, mean AUC and Cmax were slightly lower when the drug was given in combination with V. The ratios of log-transformed values in this case were 0.90 and 0.92, respectively. The sharp increase in plasma ANG II concentrations and PRA, induced by administration of V, was significantly attenuated when the drug was combined with A. In the first 12 h after drug intake, heart rate and systolic blood pressure at rest were significantly decreased when V and A were co-administered compared with treatment with V alone. V given alone did not influence heart rate or systolic blood pressure during exercise, whereas A alone and V + A led to a significant reduction in those variables. Adverse experiences reported after A and V + A could be explained by the high degree of beta-adrenoceptor blockade resulting from the administration of A. CONCLUSIONS: Co-administration of single doses of V and A does not modify the pharmacokinetics of the two drugs to a clinically relevant degree. With respect to pharmacodynamics, a single dose of A attenuates the increase in plasma ANG II and PRA in response to a single dose of V, and V has no effect on the hemodynamic response to exercise. The combined treatment with single doses of 160 mg V and 100 mg A has some additive effects on resting blood pressure in healthy, normotensive subjects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin_II_MeSH S_blood_MeSH Angiotensin_II_blood_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Area_Under_Curve_MeSH M_Atenolol_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Interactions_MeSH M_Exercise_MeSH M_Half-Life_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metabolic_Clearance_Rate_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Tetrazoles_MeSH S_pharmacokinetics_MeSH Tetrazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Tetrazoles_pharmacology_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Valine_pharmacokinetics_MeSH S_pharmacology_MeSH Valine_pharmacology_MeSH 
****** 9347267
----K E
----T EUROASPIRE. A European Society of Cardiology survey of secondary prevention of coronary heart disease: principal results. EUROASPIRE Study Group. European Action on Secondary Prevention through Intervention to Reduce Events.
----A BACKGROUND: The three major European scientific societies in cardiovascular medicine--the European Society of Cardiology (ESC), the European Atherosclerosis Society and the European Society of Hypertension--published in October 1994 joint recommendations on prevention of coronary heart disease in clinical practice. Patients with established coronary heart disease, or other major atherosclerotic disease, were deemed to be the top priority for prevention. A European survey (EUROASPIRE) was therefore conducted under the auspices of the ESC to describe current clinical practice in relation to secondary prevention of coronary heart disease. AIMS: The aims of EUROASPIRE were (i) to determine whether the major risk factors for coronary heart disease are recorded in patients medical records; (ii) to measure the modifiable risk factors and describe their current management following hospitalization, and (ii) to determine whether first degree blood relatives have been screened. METHODS: The survey was conducted in selected geographical areas and hospitals in nine European countries. Consecutive patients (< or = 70 years) were identified retrospectively with the following diagnoses: coronary artery bypass grafting, percutaneous transluminal coronary angioplasty, acute myocardial infarction and acute myocardial ischaemia without infarction. Data collection was based on a retrospective review of hospital medical records and a prospective interview and examination of the patients. RESULTS: 4863 medical records were reviewed of whom 25% were women, and 3569 patients were interviewed (adjusted response rate 85%) with an average age of 61 years. Nineteen percent of patients smoked cigarettes, 25% were overweight (BMI > or = 30 kg.m-2), 53% had raised blood pressure (systolic BP > or = 140 and/or diastolic BP > or = 90 mmHg), 44% had raised total plasma cholesterol (total cholesterol > or = 5.5 mmol.l-1) and 18% were diabetic. Reported medication at interview was: antiplatelet drugs 81%, beta-blockers, 54% (58% in post-infarction patients). ACE inhibitors 30% (38% in post infarction patients) and lipid lowering drugs 32%. Of the patients receiving blood pressure lowering drugs (not always prescribed for the treatment of hypertension) 50% had a systolic BP > 140 mmHg and 21% > 160 mmHg, and of those receiving lipid lowering drugs, 49% had plasma total cholesterol > 5.5 mmol.l-1 and 13% > 6.5 mmol.l-1. Thirty-seven percent of patients had a family history of premature coronary heart disease in a first-degree blood relative, but only 21% of patients reported being advised to have their relatives screened for coronary risk factors. CONCLUSIONS: This European survey has demonstrated a high prevalence of modifiable risk factors in coronary heart disease patients. There is considerable potential for cardiologists and physicians to further reduce coronary heart disease morbidity and mortality and improve patients chances of survival.
----P Journal_Article 
----M M_Aged_MeSH M_Cardiology_MeSH S_methods_MeSH Cardiology_methods_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_genetics_MeSH Coronary_Disease_genetics_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Europe_MeSH S_epidemiology_MeSH Europe_epidemiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH P_Health_Surveys_MeSH M_Human_MeSH M_Male_MeSH M_Medical_Records_MeSH M_Middle_Aged_MeSH M_Morbidity_MeSH M_Pedigree_MeSH M_Questionnaires_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Societies__Medical_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 9352865
----K E
----T Transjugular intrahepatic portosystemic stent shunt versus sclerotherapy plus propranolol for variceal rebleeding.
----A BACKGROUND & AIMS: In patients with cirrhosis of the liver, after the first variceal bleeding episode, transjugular intrahepatic portosystemic stent shunting (TIPS) and endoscopic sclerotherapy plus propranolol (ES) were compared regarding prevention of variceal rebleeding and mortality. METHODS: Eighty-three patients with cirrhosis of the liver were randomized to undergo TIPS (n = 42) or ES (n = 41). RESULTS: Median observation time was in 1.6 years in the TIPS group and 1.45 years in the ES group. Cumulative rates of rebleeding were 23% in the TIPS group and 57% in the ES group (P = 0.0001). Hepatic encephalopathy was observed in 29% of the patients in the TIPS group and in 13% of those in the ES group (P = 0.041). Cumulative rates of survival were 69% in the TIPS group and 67% in the ES group (P = 0.62). Mortality rates in both groups were positively correlated with a higher Child's classification. CONCLUSIONS: Although TIPS significantly reduced the rate of rebleeding, survival rates were not improved. Because TIPS is associated with an increased risk of encephalopathy and high rates of shunt dysfunction, which requires reintervention, the procedure cannot be recommended for elective treatment after the first variceal bleeding episode, but it is an effective therapy in patients in whom endoscopic sclerotherapy fails to control bleeding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hepatic_Encephalopathy_MeSH S_etiology_MeSH Hepatic_Encephalopathy_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH S_adverse_effects_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_adverse_effects_MeSH S_mortality_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_mortality_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Recurrence_MeSH P_Sclerotherapy_MeSH 
****** 9352866
----K E
----T Effects of isosorbide-5-mononitrate compared with propranolol on first bleeding and long-term survival in cirrhosis.
----A BACKGROUND & AIMS: Isosorbide-5-mononitrate (Is-5-Mn) exerts beneficial hemodynamic effects in portal hypertension, yet the long-term clinical value is uncertain. The aim of this study was to determine the long-term effects of Is-5-Mn vs. propranolol (Pro) on first bleeding, complications, and death in cirrhosis. METHODS: One hundred eighteen patients included in a previously published randomized trial comparing Is-5-Mn (20 mg three times daily) with Pro were followed up for up to 7 years (range, 2-91 months). Fifty-seven patients received Is-5-Mn and 61 received Pro. RESULTS: Thirty episodes of first upper bleeding occurred; 16 were in the Is-5-Mn group. Actuarial probability of bleeding did not differ between the two groups. Endoscopic variceal red signs were the only independent predictors of early bleeding. Of the 52 patients who died, 28 were in the Is-5-Mn group. The likelihood of death was greater among patients assigned to Is-5-Mn than to Pro, but only in patients older than 50 years (72% vs. 48% at 6 years; P = 0.006). Child-Pugh score, bleeding, age, and assignment to Is-5-Mn were independent predictors of death. The likelihood of death without bleeding was also higher (P = 0.05) in the Is-5-Mn group. CONCLUSIONS: Is-5-Mn is as effective as Pro in preventing early bleeding but is associated with higher long-term mortality.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_Cirrhosis_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9352867
----K E
----T Endoscopic assessment of variceal volume and wall tension in cirrhotic patients: effects of pharmacological therapy.
----A BACKGROUND & AIMS: Variceal rupture is believed to occur when variceal wall tension is excessive. The combined use of endosonography, allowing the objective measurement of variceal radius, and endoscopic measurement of transmural variceal pressure may enable assessment of this important parameter. The aim of this study was to assess the effects on variceal hemodynamics of drugs acting through different mechanisms: decreasing portocollateral blood flow (propranolol) or resistance (isosorbide-5-mononitrate [ISMN]). METHODS: Repeated measurements of variceal radius, volume (by endosonography), and transmural pressure (using endoscopic gauge) were performed in 27 cirrhotic patients at baseline and 40 minutes after double-blind administration of placebo (n = 9), propranolol (n = 9), or ISMN (n = 9). RESULTS: Placebo had no effect. Propranolol significantly reduced variceal volume (-32% +/- 26%; P = 0.01), radius (-12% +/- 9%; P < 0.005), and pressure (-26% +/- 10%; P < 0.0001). The resulting decrease in wall tension (-34% +/- 13%; P < 0.0005) exceeded that in transmural pressure (P < 0.01). ISMN reduced transmural variceal pressure (-26% +/- 21%; P < 0.005), but not radius (-3% +/-14%; NS) and volume (-9% +/- 31%; NS). CONCLUSIONS: The combination of endosonography and endoscopic measurement of transmural variceal pressure allows quantitative estimation of variceal wall tension. Propranolol and ISMN reduce similarly transmural variceal pressure. Propranolol, but not ISMN, reduces variceal volume and radius. Therefore, despite similar decreases in variceal wall tension, propranolol may offer a greater therapeutic effect than ISMN in portal hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH M_Endosonography_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_ultrasonography_MeSH Esophageal_and_Gastric_Varices_ultrasonography_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_Cirrhosis_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_ultrasonography_MeSH Liver_Cirrhosis_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9352888
----K I
----T Beta-adrenergic blockers and nitrovasodilators for the treatment of portal hypertension: the good, the bad, the ugly.
----A 
----P Clinical_Trial Comment Editorial Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9352970
----K E
----T Safety and results of dobutamine stress echocardiography in women versus men and in patients older and younger than 75 years of age.
----A The purpose of this retrospective study was to examine 732 consecutive patients who underwent dobutamine stress echocardiography (DSE) in order to compare the safety and result profiles of this test between women versus men and in patients > or = 75 and < 75 years of age. Our study included 416 women (57%) and 316 men (43%; mean age 62 +/- 12 years [range 16 to 93]). Patients were divided into 3 age groups: (1) group I (n = 179): < 55 years (mean 47 +/- 6), (2) group II (n = 447): 55 to 74 years (mean 64 +/- 5), and (3) group III (n = 106): > or = 75 years (mean 80 +/- 4). DSE was more likely to have negative results in women than in men (prevalence of positivity = 20% vs 31%, p = 0.001), but DSE had a similar safety profile in both genders. Women required lower doses of dobutamine and atropine to reach an end point. There was a similar incidence of test positivity in older and younger patients (23% in group I, 24% in group II, and 30% in group III, p = NS). DSE was generally a safe test in patients > or = 75 years, but there was a different safety profile in the elderly group compared with younger patients--specifically, more frequent asymptomatic hypotension (7% in group I, 13% in group II, and 25% in group III, p = 0.0002) and ventricular arrhythmias (26% in group I, 30% in group II, and 41% in group III, p = 0.04), but less frequent chest pain (32% in group I, 23% in group II, and 17% in group III, p = 0.009). Multivariate analysis suggested that the baseline usage of beta blockers was also a major determinant of the safety and ischemia profile during DSE. In conclusion, there were significant gender- and/or age-specific differences in the safety and test result profile of DSE. These differences should be considered when performing or interpreting DSE, particularly in women and in patients aged > or = 75 years.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atropine_MeSH S_diagnostic_use_MeSH Atropine_diagnostic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH M_Dobutamine_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Echocardiography_MeSH S_adverse_effects_MeSH Echocardiography_adverse_effects_MeSH S_methods_MeSH Echocardiography_methods_MeSH M_Female_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Retrospective_Studies_MeSH M_Sex_Factors_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Fibrillation_MeSH S_chemically_induced_MeSH Ventricular_Fibrillation_chemically_induced_MeSH 
****** 9354317
----K E
----T Effects of tedisamil, atenolol and their combination on heart and rate-dependent QT interval in healthy volunteers.
----A AIMS: Tedisamil is a new blocker of K+ currents in cardiac tissues, exerts bradycardic effects and has shown clinical efficacy in angina pectoris. Theoretically, when coadministered with a beta-adrenoceptor blocker the tedisamil combination could induce dangerous bradycardia and QT interval prolongation. Therefore, the aim of this study was to evaluate the effects of tedisamil and atenolol alone and in combination, on heart rate and QT interval duration at rest and during exercise tests. METHODS: The effects of tedisamil (100 mg twice daily) and atenolol (50 mg twice daily) on heart rate and QT interval duration were analysed in a three-period crossover study in healthy male volunteers. RESULTS: This study showed that tedisamil exerted a significant (P<0.05) bradycardic action at rest (-10 beats min(-1); 95% CI: -6 to -15 beats min(-1)) similar to atenolol (-14 beats min(-1); -11 to -17) and drug combination (-9 beats min(-1); -6 to -12). During exercise, at the highest comparable workload, heart rate did not decrease significantly with tedisamil but decreased significantly with atenolol (-42 beats min(-1); -37 to -47) and combination (-47 beats min(-1); -41 to 52). Atenolol did not modify QT interval duration. Tedisamil alone and in combination with atenolol increased QT interval duration by 12% (95% CI: 7 to 17%) and 12% (8 to 16) respectively at RR=1000 ms, but not at RR<700 ms (combination). Tedisamil alone and in combination induced a reverse rate-dependent QT interval prolongation. CONCLUSIONS: These results indicate that the combination of tedisamil and atenolol is not associated with excessive bradycardia or excessive QT interval prolongation in healthy subjects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Anti-Arrhythmia_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH M_Area_Under_Curve_MeSH M_Atenolol_MeSH S_pharmacokinetics_MeSH Atenolol_pharmacokinetics_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Bicyclo_Compounds__Heterocyclic_MeSH S_adverse_effects_MeSH Bicyclo_Compounds__Heterocyclic_adverse_effects_MeSH S_pharmacokinetics_MeSH Bicyclo_Compounds__Heterocyclic_pharmacokinetics_MeSH S_pharmacology_MeSH Bicyclo_Compounds__Heterocyclic_pharmacology_MeSH M_Comparative_Study_MeSH M_Cyclopropanes_MeSH S_adverse_effects_MeSH Cyclopropanes_adverse_effects_MeSH S_pharmacokinetics_MeSH Cyclopropanes_pharmacokinetics_MeSH S_pharmacology_MeSH Cyclopropanes_pharmacology_MeSH M_Diarrhea_MeSH S_chemically_induced_MeSH Diarrhea_chemically_induced_MeSH M_Drug_Combinations_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH M_Half-Life_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metabolic_Clearance_Rate_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9356089
----K E
----T Myocardial ischemia and adverse cardiac outcomes in cardiac patients undergoing noncardiac surgery with sevoflurane and isoflurane. Sevoflurane Ischemia Study Group.
----A Sevoflurane is associated with less tachycardia and coronary vasodilation than isoflurane and thus might be associated with less myocardial ischemia. This multicenter study examined the incidence of myocardial ischemia and adverse cardiac outcomes in adults (40-87 yr) with cardiac disease having elective noncardiac surgery. Patients were randomized to receive either sevoflurane (S) (n = 106) or isoflurane (I) (n = 108) in conjunction with sodium thiopental, vecuronium, fentanyl, and 50%-70% N2O. Intraoperative hemodynamics were maintained within 20% of awake baseline with standard drugs. A Holter monitor was applied 3-24 h before surgery and maintained until 48 h after surgery. Electrocardiograms and blood samples for analysis of the MB isoenzyme fraction of creatine phosphokinase were obtained preoperatively and daily for 48 h postoperatively. Anesthetic exposure (1.79 +/- 0.15 [mean +/- SE] minimum alveolar concentration-hour) and duration of surgery (219 +/- 13 min) did not differ between groups. The incidence of ischemia in the pre-, intra- and postoperative periods, adverse cardiac outcomes (18% occurrence), intraoperative hemodynamic variations (+/-20% change from ward baseline), and administration of adjunct cardiovascular medications were similar between groups. In cardiac patients having noncardiac surgery, sevoflurane was comparable to isoflurane with respect to the incidence of intra- and postoperative myocardial ischemia and in the frequency of adverse cardiac outcomes. IMPLICATIONS: Surgical patients with heart disease are at risk of heart complications, some of which could be induced by an anesthetic. We compared the incidence of cardiac complications between patients receiving sevoflurane and isoflurane. We found that the frequency of additional heart problems in cardiac patients receiving sevoflurane was not different from that associated with isoflurane.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anesthetics__Inhalation_MeSH S_adverse_effects_MeSH Anesthetics__Inhalation_adverse_effects_MeSH M_Coronary_Disease_MeSH S_chemically_induced_MeSH Coronary_Disease_chemically_induced_MeSH M_Ethers_MeSH S_adverse_effects_MeSH Ethers_adverse_effects_MeSH M_Female_MeSH M_Heart_Diseases_MeSH S_chemically_induced_MeSH Heart_Diseases_chemically_induced_MeSH M_Human_MeSH M_Intraoperative_Complications_MeSH M_Isoflurane_MeSH S_adverse_effects_MeSH Isoflurane_adverse_effects_MeSH M_Male_MeSH P_Methyl_Ethers_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_chemically_induced_MeSH Myocardial_Ischemia_chemically_induced_MeSH M_Postoperative_Complications_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Surgical_Procedures__Operative_MeSH S_methods_MeSH Surgical_Procedures__Operative_methods_MeSH 
****** 9381523
----K E
----T Acute reversal of cyclosporine nephrotoxicity by neutral endopeptidase inhibition in stable renal transplant recipients.
----A BACKGROUND: Atrial natriuretic peptide and cyclosporine have opposing effects on renal hemodynamics and excretory function. METHODS: Twelve male stable cyclosporine-treated renal transplant recipients received a single 100-mg i.v. dose of the neutral endopeptidase EC 24.11 inhibitor candoxatrilat in a double-blind, placebo-controlled cross-over study. Each study day consisted of 2 hr of baseline and 7 hr of postdose evaluation. RESULTS: After administration of candoxatrilat, plasma atrial natriuretic factor rose from 12.8+/-1.6 (mean +/- SEM) to 44.1+/-6.8 pmol/L (P<0.001) in association with a threefold increase in urine cGMP excretion (573+/-195 pmol/min baseline to 1823+/-545 pmol/ min; P<0.001), marked natriuresis (207+/-34 micromol/min baseline to 416+/-62 micromol/min; P<0.001), fractional sodium excretion (3.3+/-0.5% baseline to 5.6+/-0.7%; P<0.01), and diuresis (3.4+/-0.5 ml/min baseline to 7.4+/-1 ml/min; P<0.001). All parameters remained elevated above baseline for the remaining 7-hr study period. In response to candoxatrilat, the glomerular filtration rate rose by 19% (P=0.01), renal plasma flow by 7% (P=0.04), renal blood flow by 13% (P=0.03) in association with an increase in filtration fraction from 24+/-2% to 28+/-2% (P=0.002) and small fall in renal vascular resistance from 0.38+/-0.04 to 0.30+/-0.04 mmHg x min x 1.73 m2 x ml(-1) (P=0.02). There was a fall in plasma angiotensin II without a change in plasma renin concentration or plasma aldosterone. Median urinary albumin excretion increased after candoxatrilat administration from 48 (3-131) to 114 (32-641) microg/min (P<0.01). CONCLUSIONS: Acute neutral endopeptidase inhibition with candoxatrilat appears to reverse the adverse renal hemodynamic and renal excretory effects of cyclosporine in stable renal transplant recipients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Cyclic_GMP_MeSH S_blood_MeSH Cyclic_GMP_blood_MeSH M_Cyclohexanecarboxylic_Acids_MeSH S_therapeutic_use_MeSH Cyclohexanecarboxylic_Acids_therapeutic_use_MeSH M_Cyclosporine_MeSH S_adverse_effects_MeSH Cyclosporine_adverse_effects_MeSH M_Diuresis_MeSH S_drug_effects_MeSH Diuresis_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Human_MeSH M_Immunosuppressive_Agents_MeSH S_adverse_effects_MeSH Immunosuppressive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH M_Kidney_Transplantation_MeSH S_immunology_MeSH Kidney_Transplantation_immunology_MeSH S_pathology_MeSH Kidney_Transplantation_pathology_MeSH S_physiology_MeSH Kidney_Transplantation_physiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neprilysin_MeSH S_antagonists_&_inhibitors_MeSH Neprilysin_antagonists_&_inhibitors_MeSH M_Protease_Inhibitors_MeSH S_therapeutic_use_MeSH Protease_Inhibitors_therapeutic_use_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Renal_Circulation_MeSH S_drug_effects_MeSH Renal_Circulation_drug_effects_MeSH M_Sodium_MeSH S_urine_MeSH Sodium_urine_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 9382659
----K I
----T Secondary prevention for ischemic heart disease. Relative numbers needed to treat with different therapies.
----A Secondary prevention of ischemic heart disease refers to the process of preventing further morbidity and reducing mortality rates in patients with clinical manifestations of the disease. Twenty-five large randomized, clinical trials addressing mortality rates and cardiovascular morbidity in patients with established ischemic heart disease are reviewed. Broadly defined, these were trials of aspirin and antiplatelet agents, anticoagulants, beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, lowering of cholesterol levels, exercise rehabilitation, and diet or vitamins. In trials using warfarin sodium, timolol maleate, propranolol hydrochloride, captopril, ramipril, and simvastatin and 2 diet studies, statistically significant improvements in total mortality rates were seen. Most other studies showed non-significant reductions in total mortality rates, with statistically significant reductions in 1 or more measures of cardiovascular morbidity. The methods necessary for the reader to calculate the number (of patients) needed to treat for other studies are also reviewed. The uses and limitations of the number needed to treat as a method to compare studies of different interventions in similar populations are discussed.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diet_MeSH M_Exercise_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH S_rehabilitation_MeSH Myocardial_Ischemia_rehabilitation_MeSH M_Randomized_Controlled_Trials_MeSH M_Sample_Size_MeSH M_Vitamins_MeSH S_therapeutic_use_MeSH Vitamins_therapeutic_use_MeSH 
****** 9359554
----K E
----T Effects of cardioselective beta blockers on ventilation and gas exchange in patients with heart disease during ramp treadmill testing.
----A The effects of cardioselective beta blockade on ventilation and gas exchange were investigated in 12 male subjects with coronary artery disease during ramp treadmill testing. Patients were able to maintain much of their functional capacity as measured by oxygen consumption in the beta-blocked condition, and also maintained minute ventilation by increasing respiratory rate despite a decrease in tidal volume.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Exercise_Test_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pulmonary_Gas_Exchange_MeSH S_drug_effects_MeSH Pulmonary_Gas_Exchange_drug_effects_MeSH M_Pulmonary_Ventilation_MeSH S_drug_effects_MeSH Pulmonary_Ventilation_drug_effects_MeSH 
****** 9441156
----K 1
----T [Dynamic cardiomyoplasty]
----A Between 1965 and 1995 the incidence of heart failure has been constantly rising and the mortality from this disease has increased fivefold. The introduction of ACE-inhibitors and of adrenergic beta-blockers have resulted in major symptomatic improvements in patients with mild to moderate heart failure. For end-stage disease, heart transplantation offers by now the only therapeutic option and yields excellent results. The permanent implantation of left heart assist-devices is just gaining increasing importance. Yet, both methods also have inherent drawbacks and may not be available to all patients, so that new methods are constantly evaluated. Cardiomyoplasty was introduced into clinical practice in 1985 by Alain Carpentier and since then more than 700 patients have been operated worldwide. After dissection of the latissimus dorsi muscle it is wrapped around the heart in a clockwise fashion (Figure 1). Two sensing electrodes are placed on the anterior aspect of the right ventricle and two stimulation electrodes between the proximal branches of the thoracodorsal nerve (Medtronic SP 5548). The electrodes are then connected with a burststimulator (Cardiomyostimulator, Medtronic 4710) (Figure 2). During the first 2 weeks following the operation the muscle is not stimulated in order to allow for the healing process. Thereafter, a stimulation protocol with a programmed, staged increase of the stimulation frequency is started, to induce transformation of the skeletal muscle into a "fatigue resistant" tissue. After 3 months the muscle is stimulated with every second heart beat (2:1 mode) with full burstimpulses containing 6 single impulses per burst for a duration of 185 ms (Figure 3). Cardiomyoplasty was conceived for patients in NYHA III and severely impaired myocardial function, in whom drug treatment does not produce the expected benefits. The criteria for patient selection are strictly followed, since it has been shown in the past, that the preoperative condition of the patient is of specific importance for the postoperative outcome. Contraindications are NYHA IV, advanced right ventricular dysfunction, secondary pulmonary hypertension (> 600 dyn x s x cm-5), LV end-diastolic diameter > 70 mm und AV-valve incompetence > Grad II. Between July 1985 und October 1996 647 patients received a cardiomyoplasty with the Medtronic Cardiomyoplasty System and the results from 438 patients were analyzed from the "Worldwide Cardiomyoplasty Study Group". One and 2 years following the operation NYHA-class had improved by one class in 41.9% and 53.3%, respectively, and by 2 classes in 38.1% and 30.5%, respectively. In 16% and 15% no improvement was found (Figure 4). Prospective investigation of the quality of life by a score revealed a considerable improvement in the level of daily activities and social interaction. In contrast, two years after the operation, only a small, but significant increase in LV-EF from 22.9 +/- 8.1% to 25.8 +/- 9.7% (p < 0.05) was shown. Heart rate, maximal O2-consumption, total exercise time, cardiac index, stroke volume and stroke work index did not change. According to the results of a recent FDA-study, in-hospital mortality was 12% between 1991 and 1993, and was reduced during a second phase starting 1994 to < 3%. One, 2 and 3-year survival of 349 patients who were in NYHA-III prior to the operation was 69%, 56% und 47%, respectively. 43 patients who were operated in NYHA IV exhibited considerably worse survival with only 48% after 1 year and 30% after 2 years, respectively. In a subgroup of 103 patients with a statistically low operative risk, 1, 2 and 3-year survival was 77%, 71% und 61%, respectively (Figure 5). As a mechanism of action the skeletal muscle wrap exerts some active improvement of systolic wall motion of the heart/skeletal muscle complex. However, probably more important is an acute and chronically persisting shift of the pressure-volume relation to the left. This process results in a "reverse remodel
----P Journal_Article Review Review__Tutorial 
----M M_Cardiomyoplasty_MeSH S_instrumentation_MeSH Cardiomyoplasty_instrumentation_MeSH M_English_Abstract_MeSH M_Equipment_Design_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_surgery_MeSH Heart_Failure__Congestive_surgery_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Postoperative_Complications_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH M_Quality_of_Life_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 9377617
----K I
----T Coadministration of tamsulosin and three antihypertensive agents in patients with benign prostatic hyperplasia: pharmacodynamic effect.
----A Tamsulosin, an alpha 1A-adrenoceptor antagonist, has recently been approved to treat patients with symptomatic benign prostatic hyperplasia (BPH). Tamsulosin is highly selective for prostatic receptors with minimal affinity for vascular receptors. Therefore, it should have little effect on blood pressure and should not potentiate other agents' antihypertensive activity. To test this hypothesis, we conducted three randomized, double-masked, placebo-controlled studies to evaluate how coadministration of tamsulosin would affect the pharmacodynamic profiles of nifedipine, enalapril, and atenolol. Each study enrolled 12 hypertensive men aged 45 years or older whose blood pressure was being controlled with maintenance doses of nifedipine (study 1), enalapril (study 2), or atenolol (study 3). All 36 subjects were treated with placebo for 5 days and then randomly assigned to either placebo (control group) or tamsulosin therapy (0.4 mg/d for 7 days followed by 0.8 mg/d for 7 days) in addition to continuing their maintenance antihypertensive therapy. Blood pressure and pulse rate were monitored over a 24-hour period on study days 4, 11, and 19. Coadministration of tamsulosin in these small studies had no clinically significant effects on the pharmacodynamic action of nifedipine, enalapril, or atenolol; it produced no clinically significant differences in pulse rate and blood pressure, did not alter electrocardiographic or Holter monitoring results, and did not cause increased side effects. Coadministration of tamsulosin with the three antihypertensive agents studied had a favorable safety profile. Our results in these small studies indicate that the dose of nifedipine, enalapril, or atenolol did not require adjustment in patients given tamsulosin, which may give tamsulosin an advantage over other alpha-blocking agents used to treat patients with BPH. Now that tamsulosin has been approved in the United States, further clinical use may confirm these findings.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypotension__Orthostatic_MeSH S_chemically_induced_MeSH Hypotension__Orthostatic_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prostatic_Hyperplasia_MeSH S_drug_therapy_MeSH Prostatic_Hyperplasia_drug_therapy_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9377859
----K 1
----T [Effect of beta blockade on the erythrocyte transport of Na+: evaluation during stimulation by cold pressure test in patients with essential hypertension]
----A Several studies have shown in essential hypertension alterations of the transmembrane red blood cells sodium fluxes, as an involvement, especially in the early phases, also of the adrenergic system. In this study we evaluated the behaviour of red blood cells fluxes of sodium before, during and after the cold pressor test, a method used also to evoke an adrenergic stimulation, in twenty hypertensive subjects, 14 males and 6 females, with an average age of 43.2 +/- 5.7 years, with normal weight and without cardiovascular complications and metabolic diseases. The behaviour of the Na+ total efflux (Na+ TE), of the Na+/K+ pump, of the Na+K+ cotransport (Na+/K+ CT), of the Na+/Li+ counter transport (Na+/Li+ Cnt), of the Na+ passive permeability (Na+ PP), of the intracellular Na+ (I Na+) and of the plasmatic noradrenaline (NE) was evaluated basally, at the third minute during cold pressor test (CPT) and 20 minutes after the end of the test. The test, which the same method, was repeated after a 30 day treatment with propranolol at the dose of 240 mg/day in three daily administrations. The beta-blockade caused, besides the reduction of both the systolic and diastolic pressure values, a significant increase in the Na+/K+ CT (from 248 +/- 41 to 314 +/- 71 mmol/l/cells/h, p < 0.001) and a decrease in the Na+ PP (from 0.039 +/- 0.004 to 0.023 +/- 0.007 hr-1, p < 0.00001), probably directed towards the reduction of the accumulation of intracellular Na+, that could compete, among the other mechanisms, with the anti-hypertensive action of the beta-blockers. The CPT caused, before the beta-blockade, a significant depression of the Na+/K+ pump (from 2057 +/- 149 to 1610 +/- 101 mmol/l/cells/h, p < 0.00001) and of the Na+ TE (from 2640 +/- 397 to 2032 +/- 179 mmol/l/cells/h, p < 0.00001) inversely correlated to the levels of NE (r = -0.60, p < 0.003), with a consequent increase in I Na+ (from 6.2 +/- 0.6 to 7.5 +/- 1.5 mmol/l/cells, p < 0.001), showing how the adrenergic activation in hypertensive subjects is able to interfere with the systems of transmembrane transport with an inhibitory attitude, that is expressed by an increase in the levels of I Na+. The beta-blockade was able to outweigh the depression of the Na+/K+ pump (from 1843 +/- 584 to 1728 +/- 640 mmol/l/cells/h, p: ns) and the reduction of the Na+ TE, preventing the accumulation of I Na+ (from 6.3 +/- 1.6 to 6.6 +/- 1.3 mmol/l/cells, p: ns). Such data show an increased susceptibility of the Na+ transport systems to the adrenergic stimuli in hypertensive subjects with a tendency to favor the accumulation of I Na+ and that the beta-blockade is able to antagonize the effects, with a maintenance of the intracellular levels of Na+.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Cold_MeSH M_English_Abstract_MeSH M_Erythrocytes_MeSH S_metabolism_MeSH Erythrocytes_metabolism_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Monosaccharide_Transport_Proteins_MeSH S_drug_effects_MeSH Monosaccharide_Transport_Proteins_drug_effects_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Pressure_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Sodium_MeSH S_blood_MeSH Sodium_blood_MeSH 
****** 9362385
----K E
----T TIPSS trials: design determines outcome.
----A 
----P Journal_Article 
----M M_Clinical_Trials_MeSH M_Endoscopy_MeSH M_Esophageal_Diseases_MeSH S_prevention_&_control_MeSH Esophageal_Diseases_prevention_&_control_MeSH S_therapy_MeSH Esophageal_Diseases_therapy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Hemorrhage_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH S_therapy_MeSH Hemorrhage_therapy_MeSH M_Human_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Research_Design_MeSH M_Sclerotherapy_MeSH M_Treatment_Outcome_MeSH 
****** 9361646
----K I
----T Report of the Canadian Hypertension Society Consensus Conference: 3. Pharmacologic treatment of hypertensive disorders in pregnancy.
----A OBJECTIVE: To provide Canadian physicians with evidence-based guidelines for the pharmacologic treatment of hypertensive disorders in pregnancy. OPTIONS: No medication, or treatment with antihypertensive or anticonvulsant drugs. OUTCOMES: Prevention of maternal complications, and prevention of perinatal complications and death. EVIDENCE: Pertinent articles published from 1962 to September 1996 retrieved from the Pregnancy and Childbirth Module of the Cochrane Database of Systematic Reviews and from MEDLINE; additional articles retrieved through a manual search of bibliographies; and expert opinion. Recommendations were graded according to levels of evidence. VALUES: Maternal and fetal well-being were equally valued, with the belief that treatment side effects should be minimized. BENEFITS, HARMS AND COSTS: Reduction in the rate of adverse perinatal outcomes, including death. Potential side effects of antihypertensive drugs include placental hypoperfusion, intrauterine growth retardation and long-term effects on the infant. RECOMMENDATIONS: A systolic blood pressure greater than 169 mm Hg or a diastolic pressure greater than 109 mm Hg in a pregnant woman should be considered an emergency and pharmacologic treatment with hydralazine, labetalol or nifedipine started. Otherwise, the thresholds at which to start antihypertensive treatment are a systolic pressure of 140 mm Hg or a diastolic pressure of 90 mm Hg in women with gestational hypertension without proteinuria or pre-existing hypertension before 28 weeks' gestation, those with gestational hypertension and proteinuria or symptoms at any time during the pregnancy, those with pre-existing hypertension and underlying conditions or target-organ damage, and those with pre-existing hypertension and superimposed gestational hypertension. The thresholds in other circumstances are a systolic pressure of 150 mm Hg or a diastolic pressure of 95 mm Hg. For nonsevere hypertension, methyldopa is the first-line drug; labetalol, pindolol, oxprenolol and nifedipine are second-line drugs. Fetal distress attributed to placental hypoperfusion is rare, and long-term effects on the infant are unknown. Magnesium sulfate is recommended for the prevention and treatment of seizures. VALIDATION: The guidelines are more precise but compatible with those from the US and Australia.
----P Consensus_Development_Conference Guideline Journal_Article Practice_Guideline Review 
----M M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Canada_MeSH M_Diastole_MeSH M_Evidence-Based_Medicine_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_diagnosis_MeSH Pregnancy_Complications__Cardiovascular_diagnosis_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Pregnancy_Outcome_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 9361662
----K E
----T Underutilization of beta-blockers in older patients with prior myocardial infarction or coronary artery disease in an academic, hospital-based geriatrics practice.
----A OBJECTIVE: To investigate the prevalence of beta-blocker use in older persons with prior myocardial infarction (MI) or coronary artery disease (CAD) without contraindications to beta-blockers in an academic hospital-based geriatrics practice. DESIGN: A retrospective analysis of charts from all older patients seen during January 1996 through March 1997 at an academic, hospital-based geriatrics practice was performed to investigate the prevalence of beta-blocker use in older patients with prior MI or CAD without contraindications to beta blockers. SETTING: An academic, hospital-based, primary care geriatrics practice staffed by fellows in a geriatrics training program and full-time faculty geriatricians. PATIENTS: One hundred thirty-nine women and 84 men, mean age 82 +/- 8 years (range 67 to 96), were included in the study. MEASUREMENTS AND MAIN RESULTS: Of 233 patients with CAD, 53 patients (23%) were receiving beta-blockers. Of 180 patients with CAD not receiving beta-blockers, 34 patients (19%) had contraindications to beta-blockers. Of 199 patients with CAD without contraindications to beta-blockers, 53 patients (27%) were receiving beta blockers. Of 162 patients with prior MI, 38 patients (23%) were receiving beta-blockers. Of 124 patients with prior MI not receiving beta-blockers, 19 patients (15%) had contraindications to beta-blockers. Of 143 patients with prior MI without contraindications to beta-blockers, 38 patients (27%) were receiving beta-blockers. CONCLUSIONS: There is marked underutilization of beta-blockers in treating older patients with prior MI or CAD in an academic, hospital-based geriatrics practice.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Geriatrics_MeSH S_statistics_&_numerical_data_MeSH Geriatrics_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_New_York_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Primary_Health_Care_MeSH S_statistics_&_numerical_data_MeSH Primary_Health_Care_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH 
****** 9411335
----K 1
----T [Effect of betaxolol on blood pressure and heart rate in mild to moderate hypertension]
----A The efficacy and safety of daily 20 mg betaxolol monotherapy was investigated in mild-moderate essential hypertension in a four week long, open label, single blind trial (with a placebo run-in). Twenty one patients of both sexes were enrolled. The systolic blood pressure in the supine position decreased from 158 to 142 mmHg, the diastolic blood pressure from 101 to 89 mmHg. The mean systolic values of the 24 hours ambulatory blood pressure monitoring decreased from 136 to 126 mmHg, the mean diastolic values from 87 to 80 mmHg. All decreases in blood pressure were significant. The reduction of the heart rate (80/min vs 63/min) was also significant. The decrease in blood pressure during daytime was significant, during night it was moderate. The blood pressure- and heart rate reducing effect of betaxolol was detectable however in the second half of the night, before wake-up. No side effect was recorded.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Betaxolol_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Severity_of_Illness_Index_MeSH M_Single-Blind_Method_MeSH 
****** 9383182
----K E
----T Differences between the effects of metoprolol and prazosin on the forearm vasculature in primary hypertension.
----A OBJECTIVES: To study the forearm vascular resistance in patients at rest and during ischaemia and cardiovascular responses to noradrenaline infusions during treatment with a beta1-adrenoceptor antagonist, metoprolol, and with an alpha1-adrenoceptor antagonist, prazosin. PATIENTS: Eighteen previously untreated primary hypertension patients were selected for therapy either with 50-250 mg/day metoprolol (n = 11) or with 3-20 mg/day prazosin (n = 8). METHODS: The minimal vascular resistance after ischaemic work was calculated from the forearm blood flow determined by venous occlusion plethysmography before treatment and after two and 16 months of treatment Arterial and venous plasma noradrenaline levels were determined and systemic pressor responses and forearm vasoconstriction were studied during intravenous infusion of noradrenaline. RESULTS: The resting mean arterial pressure was reduced differently by metoprolol and prazosin (by 20% versus by 8%; P < 0.001 for difference). The minimal vascular resistance decreased similarly after 16 months of metoprolol (17% decrease; P < 0.05) and of prazosin (24% decrease; P < 0.05) treatments. Arterial noradrenaline levels increased after 16 months of metoprolol treatment and after 2 and 16 months of prazosin treatment. The forearm noradrenaline spillover was reduced after 16 months on prazosin, but remained unchanged during metoprolol treatment. Pressor responses to intravenous noradrenaline were affected little by either treatment, whereas reflexogenic bradycardia was attenuated by prazosin treatment. CONCLUSION: The findings suggest that metoprolol and prazosin treatments reduce the minimal vascular resistance similarly, despite different reductions in blood pressure. Prazosin treatment might also reduce the forearm sympathetic nerve activity. Reductions in minimal forearm vascular resistance during antihypertensive therapy need not be related only to the lowering of the blood pressure per se.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Catecholamines_MeSH S_blood_MeSH Catecholamines_blood_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Ischemia_MeSH S_physiopathology_MeSH Ischemia_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Norepinephrine_MeSH S_pharmacology_MeSH Norepinephrine_pharmacology_MeSH M_Prazosin_MeSH S_pharmacology_MeSH Prazosin_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 9383607
----K E
----T Mode and risk indicators for death during 5 year follow-up of survivors of acute myocardial infarction. An evaluation with particular emphasis on congestive heart failure and age.
----A AIM: To describe the mortality rate and the place and mode of death during a 5-year follow-up of patients admitted to hospital with congestive heart failure following an acute myocardial infarction (AMI). METHODS: All the patients admitted to a single hospital following an AMI, regardless of age and whether or not they were admitted to a coronary care unit, were followed up prospectively for 5 years. RESULTS: A total of 882 AMI patients were included. The hospital mortality was 14%. Among patients who were discharged from hospital, the age range was 24-101 (median 70) years, 70% were men, 35% had experienced an anterior AMI and 31% had suffered an inferior AMI. Congestive heart failure was observed in 51% of the patients. Among patients discharged from hospital (n = 740), those with severe congestive heart failure had a mortality of 67% compared with 51% for those with moderate heart failure and 31% for those with no heart failure (P < 0.001). When simultaneously considering age, sex, history of cardiovascular disease, various complications in hospital and medication at discharge, the development of congestive heart failure was found to be an independent predictor of death. The mode and place of death after initial discharge from hospital was similar in patients with and in those without congestive heart failure. Among patients with congestive heart failure who were discharged from hospital, the following factors were associated with an increased risk of death: older age (P < 0.001), no prescription of beta-blockers at discharge (P < 0.01) and a previous history of infarction (P < 0.05). CONCLUSION: The prognosis during 5 years of follow-up after AMI was directly related to the severity of congestive heart failure based on a clinical assessment. The mode and place of death did not differ between patients with and without heart failure. Treatment with beta-blockers was associated with improved survival. Age had a major impact on the prognosis.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Case-Control_Studies_MeSH M_Cause_of_Death_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH M_Time_Factors_MeSH 
****** 9391283
----K E
----T Left ventricular atrioventricular plane displacement: an echocardiographic technique for rapid assessment of prognosis in heart failure.
----A OBJECTIVE: To assess the prognostic value of atrioventricular plane displacement in heart failure patients. DESIGN: Patients were followed prospectively for one year after atrioventricular plane displacement determination. SETTING: Malmo University Hospital, with a primary catchment area of 250,000 inhabitants. PATIENTS: 181 patients with a clinical diagnosis of heart failure; age 75.7 (SD 5.2) years, duration of heart failure 2.7 (5.7) years; 100 men, 81 women. MAIN OUTCOME MEASURES: Mortality in relation to atrioventricular plane displacement. RESULTS: Total mortality was 22.7% (41/181), and was highly significantly (P = 0.001) related to atrioventricular plane displacement. Mortality within prospectively defined categories of displacement was: > or = 10.0 mm, 0% (0/19); 8.2 to 9.9 mm, 10.3% (3/29); 6.4 to 8.1 mm, 19.4% (12/62); and < 6.4 mm, 36.6% (26/71). The groups were similar in age, sex, angiotensin converting enzyme inhibitor and beta blocker treatment, and cause and duration of heart failure. CONCLUSIONS: Mortality in heart failure is strongly related to atrioventricular plane displacement.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH S_ultrasonography_MeSH Ventricular_Dysfunction__Left_ultrasonography_MeSH 
****** 9391772
----K E
----T NSAIDs and increased blood pressure. What is the clinical significance?
----A Several randomised studies have demonstrated that various nonsteroidal anti-inflammatory drugs (NSAIDs) elevate blood pressure in normotensive and hypertensive individuals; however, these data have been contradicted by numerous negative studies. Two meta-analyses have demonstrated that, after pooling data drawn from published reports of randomised trials of younger adults, NSAID use produces a clinically significant increment in mean blood pressure of 5 mm Hg, most marked in patients with controlled hypertension. Stratification by NSAID type revealed that piroxicam, naproxen and indomethacin had the greatest, and sulindac the smallest, pressor effect. These data were supported by 2 large community studies involving elderly patients. Recent NSAID users had a 1.7-fold higher risk of requiring the initiation of antihypertensive therapy compared with nonusers; NSAID users also had a 40% increased risk of receiving a diagnosis of hypertension compared with nonusers. It is vital to determine the nature of the association in the elderly, 12 to 15% of whom are concurrently receiving an NSAID and an antihypertensive agent. Importantly, a 5 to 6 mm Hg increase in diastolic blood pressure maintained over a few years may be associated with a 67% increase in total stroke risk and a 15% increase in coronary heart disease events. While the mechanism(s) remain speculative, salt and water retention through several factors operating in parallel, coupled with increased total peripheral vascular resistance, via increased renal endothelin-1 synthesis, are potentially important. Clinicians should strive to avoid excessive use of NSAID treatment and consider well-tolerated therapeutic alternatives, including simple analgesics and physical therapy. For patients who require concomitant NSAID and antihypertensive treatment, physicians should be aware that indomethacin, naproxen and piroxicam may be associated with a greater pressor effect than many other NSAIDs, and that antagonism of beta-blockers may be greater than that of vasodilators (including ACE inhibitors and calcium antagonists) and diuretics. Finally, the progress of each patient should be monitored by careful blood pressure measurement, particularly during the period of initiation of NSAID therapy.
----P Journal_Article Review Review__Academic 
----M M_Adult_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_adverse_effects_MeSH Anti-Inflammatory_Agents__Non-Steroidal_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_chemically_induced_MeSH Hypertension_chemically_induced_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9395279
----K I
----T Cardiovascular prognosis in relation to apolipoproteins and other lipid parameters in patients with stable angina pectoris treated with verapamil or metoprolol: results from the Angina Prognosis Study in Stockholm (APSIS).
----A Relationships between apolipoproteins and other lipid parameters and cardiovascular (CV) prognosis were evaluated in the Angina Prognosis Study In Stockholm (APSIS). Out of 809 patients with stable angina pectoris, lipid variables were obtained in 786 patients at baseline, and after one month's double-blind treatment with metoprolol or verapamil, to evaluate treatment effects on these lipid variables. During a median follow-up time of 3.3 years (2663 patient years), 37 patients suffered a CV death, 30 suffered a non-fatal myocardial infarction (MI) and 100 underwent a revascularization. Apolipoprotein (apo) A-I, high-density lipoprotein cholesterol and triglycerides were predictors of CV death or non-fatal MI in univariate analyses, but only apo A-I remained as an independent predictor in multivariate analyses. All lipid variables except low density lipoprotein cholesterol were related to the risk of revascularization in univariate analyses, but only apo A-I and apo B were independent predictors of such events. Triglycerides were weakly, but not independently, associated with prognosis. Verapamil and metoprolol had differential short-term effects on lipids, with a shift towards a more atherogenic profile in metoprolol treated patients. However, there was no significant impact of the treatment given, or of these treatment effects on the risk of CV events. Results of the present study suggest that apolipoprotein levels were better predictors of CV events than other lipid parameters in patients with stable angina pectoris.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_blood_MeSH Angina_Pectoris_blood_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH M_Apolipoproteins_MeSH S_blood_MeSH Apolipoproteins_blood_MeSH S_drug_effects_MeSH Apolipoproteins_drug_effects_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH S_drug_effects_MeSH Lipoproteins__HDL_Cholesterol_drug_effects_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH S_drug_effects_MeSH Lipoproteins__LDL_Cholesterol_drug_effects_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9397289
----K E
----T Structure and function of small arteries of essential hypertensive patients following chronic treatment with once-a-day nifedipine.
----A In view of the important impact of small-artery structural and functional abnormalities on complications of hypertension and recent data suggesting that some antihypertensive agents may correct some of these abnormalities, a study of resistance artery structure and function in 20 well-controlled essential hypertensive patients who had received for a prolonged period of time monotherapy with the once-a-day extended release formulation of the calcium channel antagonist nifedipine (nidefipine GITS) or with the beta-blocker atenolol is reviewed. Resistance-size small arteries (standardized lumen diameter of 247 +/- 8 microns) were studied after dissection from a gluteal subcutaneous biopsy. Small arteries were investigated on a wire myograph and as pressurized vessels. On the myograph, the media width-to-lumen diameter ratio of arteries was 5.37 +/- 0.09% in normotensive subjects, 5.38 +/- 0.18% in patients treated with nifedipine GITS, 6.81 +/- 0.18% in patients treated with atenolol and 7.08 +/- 0.12% in untreated hypertensives (p < 0.001, untreated or atenolol-treated patients vs. normotensives or nifedipine-GITS-treated hypertensives), and similar results were found in pressurized arteries. Contractility and endothelium-dependent relaxation were impaired in small arteries from untreated or atenolol-treated patients in comparison to those from normotensive subjects or nifedipine-GITS-treated patients. In conclusion, hypertensive patients with well-controlled blood pressure under treatment for more than 1 year with nifedipine GITS exhibit normal structure and function of small arteries, whereas similar patients whose blood pressure is as well controlled by the beta-blocker atenolol present abnormally thick small arteries with impaired contractility and endothelium-dependent relaxation. It will be important to determine whether small arteries of other vascular beds are also improved by nifedipine GITS treatment of elevated blood pressure and whether this results in reduced morbidity and mortality in hypertensive patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Arterioles_MeSH S_drug_effects_MeSH Arterioles_drug_effects_MeSH S_physiopathology_MeSH Arterioles_physiopathology_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle__Smooth__Vascular_MeSH S_physiopathology_MeSH Muscle__Smooth__Vascular_physiopathology_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9400905
----K E
----T Effects of antihypertensive agents on circadian blood pressure in hypertensive patients with previous brain infarction.
----A To evaluate the effects of antihypertensive agents on the circadian blood pressure (BP) of patients with previous brain infarction, the ambulatory BP was measured non-invasively for 24 h before and after administration of antihypertensive agents. One hundred milligrams of acebutolol twice daily (n = 15) is effective in lowering the BP during the daytime, but has little effect during the night and the morning. Twenty milligrams of slow-release nifedipine twice daily (n = 14) produced a consistent reduction in the BP over the entire 24-h period and effectively blunted the rise in BP in the morning. Captopril (12.5 mg) twice daily (n = 15) produced a mild reduction in BP with little change in the circadian pattern. The slow-release nifedipine group had the greatest decrease in mean systolic and diastolic BP. The heart rate significantly increased after administration of slow-release nifedipine and decreased after administration of acebutolol. To reduce stroke recurrence, we should consider the effects of antihypertensive agents on circadian BP in hypertensive patients with previous brain infarction.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Acebutolol_MeSH S_administration_&_dosage_MeSH Acebutolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Captopril_MeSH S_administration_&_dosage_MeSH Captopril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cerebral_Infarction_MeSH S_complications_MeSH Cerebral_Infarction_complications_MeSH S_prevention_&_control_MeSH Cerebral_Infarction_prevention_&_control_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Treatment_Outcome_MeSH 
****** 9402450
----K E
----T Addition of felodipine to metoprolol vs replacement of metoprolol by felodipine in patients with angina pectoris despite adequate beta-blockade. Results of the Felodipine ER and Metoprolol CR in Angina (FEMINA) Study. Working Group on Cardiovascular Research, The Netherlands (WCN).
----A AIMS: The study aimed to compare the addition of felodipine to metoprolol, and of the replacement of metoprolol by felodipine, with continuation of metoprolol, in patients with angina pectoris despite optimal beta-blockade. METHODS AND RESULTS: The study was double-blind, parallel, randomized and controlled, and comprised 363 patients from 27 outpatient cardiology clinics in the Netherlands. The patients had angina and positive bicycle exercise tests despite optimal beta-blockade (resting heart rate < 65 beats.min-1). Randomization was to three treatment groups: continuation of metoprolol (control), addition of felodipine to metoprolol, and replacement of metoprolol by felodipine. Exercise tests were repeated after 2 and 5 weeks. The main outcome measure was: exercise result after 5 weeks, compared with baseline, between-group comparison of changes vs control. There were no significant differences in exercise duration and onset of chest pain vs control. The addition of felodipine increased time until 1 mm ST depression (43 s, 95% confidence interval 20-65 s), and decreased both ST depression at highest comparable work load (0.46 mm, 95% confidence interval 0.19-0.72), and maximal ST depression (0.49 mm, 95% confidence interval 0.23-0.74). Exercise results after replacement of metoprolol by felodipine were not different from control, apart from a significant increase in rate pressure product. Significantly more patients experienced adverse events in the felodipine monotherapy group. CONCLUSION: Combination of metoprolol and felodipine is to be preferred to felodipine monotherapy in patients who have signs and symptoms of myocardial ischaemia despite optimal beta-blockade.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9403359
----K E
----T The way to serotonergic use and abuse in migraine.
----A 5-HT is currently indicated to play a role in migraine (M). Previously evidenced 5-HT supersensitivity which characterizes M is insufficient to compensate for a possible deficit in 5-HT bioavailability. Inducing a further up-regulation of 5-HT receptor can yield improvement of M syndrome. Chronic treatments of methysergide and propranolol, drugs exerting antagonist action at 5-HT receptors, induced a significant amelioration in 256M sufferers. On the contrary, chronic treatments of ergotamine and sumatriptan, both provided with a 5-HT1 agonist activity, induced a worsening of M in 134 M sufferers. The M worsening was paralleled by an increase in consumption of analgesic drugs. Discussion concerns the effects of the chronically given 5-HT agonists and antagonists as well as the possible receptor mechanism underlying "craving for serotonin" in severe M. The increase of 5-HT supersensitivity evidenced at the end of M attacks is also discussed and its role in determining the interruption of the attack is here suggested.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Behavior_MeSH S_drug_effects_MeSH Behavior_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Ergotamine_MeSH S_pharmacology_MeSH Ergotamine_pharmacology_MeSH S_therapeutic_use_MeSH Ergotamine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Methysergide_MeSH S_pharmacology_MeSH Methysergide_pharmacology_MeSH S_therapeutic_use_MeSH Methysergide_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_metabolism_MeSH Migraine_metabolism_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Serotonin_Agonists_MeSH S_pharmacology_MeSH Serotonin_Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Serotonin_Antagonists_MeSH S_pharmacology_MeSH Serotonin_Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Serotonin_Antagonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_pharmacology_MeSH Sumatriptan_pharmacology_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasoconstrictor_Agents_MeSH S_pharmacology_MeSH Vasoconstrictor_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 9404261
----K E
----T Junctional ectopic tachycardia in six paediatric patients.
----A The presenting features and treatment responses of six children with junctional ectopic tachycardia are evaluated. Two of the patients were siblings and both presented in early childhood with cardiopulmonary failure. The elder sibling died, the surviving sibling was controlled on a combination of amiodarone, digoxin, and sotalol. The remaining four patients presented in later childhood with tachycardia induced cardiomyopathy. Two of the patients were diagnosed incidentally and have normalised their myocardial function on sotalol therapy. The other two presented in congestive cardiac failure. Radiofrequency His bundle ablation and insertion of a permanent pacemaker to control the arrhythmia was undertaken in the elder of the two patients. The remaining patient has had marginal recovery of myocardial function on a combination of amiodarone and sotalol treatment. Improvement in myocardial function may take several months and is dependent on control of the tachycardia in some patients. Sotalol, when used as single or combination treatment, was partially successful in four cases in reducing heart rate. None of the patients reverted to sinus rhythm.
----P Journal_Article 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Cardiac_Pacing__Artificial_MeSH M_Catheter_Ablation_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH P_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Infant_MeSH M_Male_MeSH M_Retrospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Ectopic_Junctional_MeSH S_diagnosis_MeSH Tachycardia__Ectopic_Junctional_diagnosis_MeSH S_drug_therapy_MeSH Tachycardia__Ectopic_Junctional_drug_therapy_MeSH S_surgery_MeSH Tachycardia__Ectopic_Junctional_surgery_MeSH 
****** 9408290
----K E
----T The values of detection of free radical mediated reactions in patients.
----A The peroxidative processes and individual antioxidant protection were measured in patients with different cardiovascular diseases. We concluded that monitoring of this system we were able to detect not only the actual changes of lipid peroxidation and antioxidant defence mechanisms, but additionally the therapeutic efficacy of the treatment.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Antioxidants_MeSH S_analysis_MeSH Antioxidants_analysis_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Catalase_MeSH S_blood_MeSH Catalase_blood_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Free_Radicals_MeSH S_analysis_MeSH Free_Radicals_analysis_MeSH S_metabolism_MeSH Free_Radicals_metabolism_MeSH M_Glutathione_MeSH S_blood_MeSH Glutathione_blood_MeSH M_Glutathione_Peroxidase_MeSH S_blood_MeSH Glutathione_Peroxidase_blood_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipid_Peroxidation_MeSH M_Malondialdehyde_MeSH S_blood_MeSH Malondialdehyde_blood_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Myocardial_Ischemia_MeSH S_blood_MeSH Myocardial_Ischemia_blood_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Reactive_Oxygen_Species_MeSH S_metabolism_MeSH Reactive_Oxygen_Species_metabolism_MeSH M_Superoxide_Dismutase_MeSH S_blood_MeSH Superoxide_Dismutase_blood_MeSH M_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH 
****** 9408806
----K E
----T How long should pindolol be associated with paroxetine to improve the antidepressant response?
----A A double-blind study was undertaken to investigate the period of treatment with the beta-adrenoreceptor/5-hydroxytryptamine 1A (5-HT1A) antagonist pindolol required to enhance the antidepressant effects of paroxetine. After 1 week of a placebo run-in period, 63 untreated major depressive inpatients were randomly assigned to three different groups. Group 1 received paroxetine (20 mg/day) plus placebo (4 weeks). Group 2 received paroxetine (20 mg/day) plus pindolol (7.5 mg/day) for 1 week and placebo for 3 weeks. Group 3 received both active treatments for the entire duration of the study (4 weeks). Clinical response was defined as a reduction of the score in the Hamilton Rating Scale for Depression (HAM-D) to 8 or below. Also, to preliminarily examine whether beta-adrenoreceptor blockade was involved in the action of pindolol, another group of 10 inpatients was treated in an open-label manner with paroxetine (20 mg/day) plus 50 mg/day of the beta-adrenergic antagonist metoprolol, devoid of significant affinity for 5-HT1A receptors. At endpoint, the incidence of treatment-emergent side effects did not significantly differ among the three groups. After 1 and 2 weeks of treatment, the two groups treated with paroxetine plus pindolol displayed a significantly greater response rate than the group treated with paroxetine plus placebo. At study completion, only the patients treated with pindolol for the entire period showed a significantly greater response rate (p = 0.05). HAM-D score were also significantly lower at endpoint in patients treated with the combination for 4 weeks (p = 0.00003). The group of patients treated with paroxetine and metoprolol exhibited a side-effect profile comparable to that of paroxetine alone. Response rates were also comparable. These findings support the efficacy of pindolol, but not of metoprolol, in accelerating the antidepressant effect of paroxetine and suggest that the administration of pindolol for the entire period of the acute treatment may increase the efficacy of paroxetine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Depressive_Disorder_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Headache_MeSH S_chemically_induced_MeSH Headache_chemically_induced_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Paroxetine_MeSH S_adverse_effects_MeSH Paroxetine_adverse_effects_MeSH S_therapeutic_use_MeSH Paroxetine_therapeutic_use_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9416986
----K E
----T Comparative effects of nebivolol and atenolol on blood pressure and insulin sensitivity in hypertensive subjects with type II diabetes.
----A The aim of this double-blind, parallel group study was to compare the effects of nebivolol and atenolol on blood pressure (BP) and insulin sensitivity in hypertensive patients with type II, non-insulin dependent diabetes mellitus (NIDDM). After a 4-week run-in period on placebo, 30 patients (14 males and 16 females) aged 43 to 69 years, with stable NIDDM and mild to moderate hypertension (DBP > or =95 and <116 mm Hg) were randomised to receive either nebivolol 5 mg or atenolol 50 mg, both administered once daily for 6 months. At the end of the placebo and the active treatment periods, supine and standing BP was measured, 24-h urinary C-peptide, HbA1c, plasma glucose and lipid levels were evaluated and an euglycaemic hyperinsulinaemic clamp was performed to evaluate insulin sensitivity: glucose infusion rate during the last 60 min of clamp and total glucose requirements were evaluated. Nebivolol 5 mg once daily was of an equivalent efficacy as atenolol 50 mg once daily at reducing supine and standing systolic and diastolic BP values. Neither beta-blocker adversely affected carbohydrate metabolism in terms of insulin sensitivity, whole body glucose utilization, HbA1c and 24-h urinary C-peptide excretion. No significant changes in cholesterol (total, high density and low density lipoprotein) and triglycerides plasma levels were observed with both beta-blockers. These findings indicate that, in hypertensive patients with NIDDM, ie, in subjects who have established insulin resistance, treatment with nebivolol and atenolol neither further deteriorated insulin sensitivity nor adversely affected the lipid profile.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Insulin_Resistance_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH 
****** 9416987
----K E
----T A low dose atenolol/bendrofluazide combination in patients with mild to moderate hypertension.
----A 
----P Clinical_Trial Letter Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH 
****** 9428940
----K E
----T Creatine kinase MB during myocardial infarction: relationship to preexisting coronary heart disease and medication.
----A Creatine kinase (CK) and its isoenzyme CK-MB are important tools for the diagnosis of acute myocardial infarction. The content of CK-MB relative to total CK in myocardial cells is variable; it is low in normal myocardium and increased several-fold in hypoxic myocardium. We tested the hypothesis that CK-MB mass (CK-MBm) could be related to cardiovascular history, preinfarctional medication and clinical course during myocardial infarction. In a prospective study CK and CK-MBm were measured 0, 6, 12, 18, 24, 36, 48 and 72 h after the admission to the coronary care unit. Peak values and areas under the curve (AUC) were determined and normalized for total CK activity (CK-MBm/CK). Of 185 patients with acute chest pain, 70 patients had 71 acute myocardial infarctions and were enrolled in the study. A history of chronic angina pectoris or hypertension had no influence on CK-MBm/CK levels. In contrast, treatment with beta-blockers before infarction resulted in a lower relative CK-MBm peak value (CK-MBm/CK 6.0 (median value), range 3.1-15.3, versus 7.0, range 0.5-17.3: p < 0.05). Other drugs had no influence. Patients with persistent pain on admission tended to have higher relative CK-MBm values (peak CK-MBm/CK: 6.8, range 0.5-17.3, versus 5.3, range 1.4-7.9, p = 0.08; AUC CK-MBm/CK: 0.05, range 0.01-0.10, versus 0.03, range 0.01-0.06, p < 0.05). Three vessel disease on coronary angiography was associated with higher peak CK-MBm/CK values during the acute phase of myocardial infarction than those with 1-2 vessel disease (Peak CK-MBm/CK: 7.9, range 5.5-17.3, versus 6.4, range 3.1-10.2, p < 0.05; AUC CK-MBm/CK: 0.06, range 0.02-0.11, versus 0.04, range 0.02-0.07, p < 0.05). We conclude that relative CK-MBm/CK levels reflect to a certain degree the extent of the coronary disease and that preinfarctional beta-blockade may result in lower CK-MBm levels.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Creatine_Kinase_MeSH S_blood_MeSH Creatine_Kinase_blood_MeSH M_Female_MeSH M_Human_MeSH M_Isoenzymes_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_enzymology_MeSH Myocardial_Infarction_enzymology_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Time_Factors_MeSH 
****** 9431839
----K E
----T The interaction between propranolol and the novel antimigraine agent zolmitriptan (311C90).
----A AIMS: Zolmitriptan (Zomig, formerly known as 311C90), a selective 5HT1B/1D agonist is under development as an acute oral treatment for migraine. Despite the use of prophylactic medication, such as propranolol, breakthrough attacks often occur in patients. Consequently we investigated the effects of propranolol on the pharmacokinetics of, and cardiovascular responses to, zolmitriptan. METHODS: A double-blind, randomized, crossover study of the effects of pre-treatment with propranolol 160 mg daily for 7 days or placebo on the pharmacokinetics and effects on blood pressure of a single 10 mg dose of zolmitriptan in 12 healthy volunteers. RESULTS: Propranolol increased mean zolmitriptan Cmax and AUC by 56% and 37% respectively; mean t1/2 was prolonged from 3.1 to 4.0 h. Mean Cmax and AUC of the pharmacologically active N-desmethyl metabolite were reduced by 24% and 11% respectively and the metabolite:parent AUC ratio (AUCm/AUCp) fell from 0.46 to 0.26. Mean Cmax and AUC for the inactive indole acetic acid metabolite were both reduced by 13% and AUCm/AUCp from 1.04 to 0.59. A small pressor effect of short duration was observed following zolmitriptan with mean peak rises of 13 and 11 mmHg in systolic and diastolic pressures respectively; propranolol had no effect on the pressor response. CONCLUSIONS: The results suggest that propranolol inhibits biotransformation of zolmitriptan but with no change in the small pressor response to zolmitriptan. It is therefore unlikely that the pharmacokinetic changes will lead to clinically important changes in pharmacological effects and dosage adjustment of zolmitriptan is not required in patients taking propranolol for migraine prophylaxis.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Area_Under_Curve_MeSH M_Biotransformation_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Half-Life_MeSH M_Human_MeSH M_Male_MeSH M_Oxazoles_MeSH S_pharmacokinetics_MeSH Oxazoles_pharmacokinetics_MeSH S_pharmacology_MeSH Oxazoles_pharmacology_MeSH P_Oxazolidinones_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Serotonin_Agonists_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_pharmacology_MeSH Serotonin_Agonists_pharmacology_MeSH 
****** 9438743
----K E
----T Run-in periods in randomized trials: implications for the application of results in clinical practice.
----A Prerandomization run-in periods are being used to select or exclude patients in an increasing number of clinical trials, but the implications of run-in periods for interpreting the results of clinical trials and applying these results in clinical practice have not been systematically examined. We analyzed illustrative examples of reports of clinical trials in which run-in periods were used to exclude noncompliant subjects, placebo responders, or subjects who could not tolerate or did not respond to active drug. The Physicians' Health Study exemplifies the use of a prerandomization run-in period to exclude subjects who are nonadherent, while recent trials of tacrine for Alzheimer disease and carvedilol for congestive heart failure typify the use of run-in periods to exclude patients who do not tolerate or do not respond to the study drug. The reported results of these studies are valid. However, because the reported results apply to subgroups of patients who cannot be defined readily based on demographic or clinical characteristics, the applicability of the results in clinical practice is diluted. Compared with results that would have been observed without the run-in period, the reported results overestimate the benefits and underestimate the risks of treatment, underestimate the number needed to treat, and yield a smaller P value. The Cardiac Arrhythmia Suppression Trial exemplifies the use of an active-drug run-in period that enhances clinical applicability by selecting a group of study subjects who closely resembled patients undergoing active clinical management for this problem. Run-in periods can dilute or enhance the clinical applicability of the results of a clinical trial, depending on the patient group to whom the results will be applied. Reports of clinical trials using run-in periods should indicate how this aspect of their design affects the application of the results to clinical practice.
----P Journal_Article 
----M M_Clinical_Protocols_MeSH M_Data_Interpretation__Statistical_MeSH M_Patient_Selection_MeSH P_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH M_Statistics_MeSH 
****** 9440450
----K E
----T Expansion rates of small abdominal aortic aneurysms.
----A BACKGROUND: The present study was carried out in order to examine those factors that influence the rate of expansion of small abdominal aortic aneurysms. METHODS: A retrospective study was undertaken of 112 patients who attended the St George Vascular Laboratory between 1987 and 1997. These patients had abdominal aortic aneurysms that were considered to be too small to warrant surgical repair at the time of presentation. Sequential ultrasound examinations were used to measure maximal anteroposterior aneurysm diameter. From these data, annual growth rates were calculated. Growth rate per annum was then compared with gender, age, initial aortic aneurysm diameter, presence of hypertensive disease, cardiac disease, family history of aneurysmal disease, diabetes mellitus, smoking, beta-adrenergic blockade and lipid lowering drugs. RESULTS: Univariate analysis showed that three factors were significantly related to growth rate: the initial size of the aortic aneurysm, the presence of cardiac disease and the presence of beta-adrenergic blockade. CONCLUSIONS: The presence of beta-adrenergic blockade appeared to have an independent effect on aneurysm growth rate, and suggests a possible role for beta-adrenergic blockade as a therapeutic strategy in controlling expansion rates of small abdominal aortic aneurysms. A controlled double-blind clinical trial is required to demonstrate this conclusively.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aorta__Abdominal_MeSH S_pathology_MeSH Aorta__Abdominal_pathology_MeSH M_Aortic_Aneurysm__Abdominal_MeSH S_drug_therapy_MeSH Aortic_Aneurysm__Abdominal_drug_therapy_MeSH S_pathology_MeSH Aortic_Aneurysm__Abdominal_pathology_MeSH S_surgery_MeSH Aortic_Aneurysm__Abdominal_surgery_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH 
****** 9443770
----K E
----T Bisoprolol and captopril effects on insulin receptor tyrosine kinase activity in essential hypertension.
----A Angiotension converting enzyme (ACE) inhibitors and beta-blockers have been reported to possess disparate effects on insulin sensitivity. The aim of this study was to study the effects of the selective beta-1 blocker bisoprolol and of the ACE inhibitor captopril on cellular insulin action in hypertensive individuals. After washout, 12 mild to moderate essential hypertensives were randomized in a double-blind manner to 5 mg bisoprolol daily or 25 mg captopril twice daily for 8 weeks. Erythrocyte insulin binding and insulin-stimulated tyrosine kinase (TK) activity were measured before and after therapy. Both agents decreased diastolic blood pressure significantly (bisoprolol 96.5+/-0.9 to 87.8+/-3.1 mm Hg; captopril 96.5+/-0.9 to 91.5+/-1.8 mm Hg; P < .05). Fasting plasma glucose, insulin, and insulin/glucose indices remained unchanged after both therapies, as did lipid profiles. Maximal insulin-stimulated TK activity, assessed by phosphorylation of the exogenous substrate poly-Glu80Tyr20, was significantly higher (P < .05) after bisoprolol treatment, but not after captopril treatment, when compared to placebo (bisoprolol 8.5+/-1.8; captopril 7.3+/-1.5; placebo: 6.4+/-1.3 pmol 32P-ATP/fmol bound insulin). However, captopril, but not bisoprolol, increased the sensitivity of the receptor TK activity, as measured by the half-maximal activity concentration (ED50). Specific insulin binding was not affected by these two agents. Thus, both captopril and bisoprolol may have favorable but different effects on TK activity and insulin action at the cellular level.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH M_Insulin_Resistance_MeSH M_Middle_Aged_MeSH M_Receptor__Insulin_MeSH S_drug_effects_MeSH Receptor__Insulin_drug_effects_MeSH S_metabolism_MeSH Receptor__Insulin_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 9442782
----K 5
----T Latanoprost. Two years' experience of its use in the United Kingdom. Latanoprost Study Group.
----A OBJECTIVE: The aim of the study was to assess the efficacy and safety of latanoprost in the long-term treatment of glaucoma. DESIGN: The study was designed as a randomized, 6-month double-masked parallel group, multicenter study comparing latanoprost with timolol followed by an 18-month open-label, multicenter study in which all patients were treated with latanoprost. PARTICIPANTS: In total, 277 patients were treated with latanoprost for up to 24 months. INTERVENTION: For the first 6 months of treatment, latanoprost (0.005%) administered once daily was compared with timolol (0.5%) administered twice daily. Patients then received latanoprost (once daily) for an 18-month follow-up period regardless of their initial treatment. MAIN OUTCOME MEASURES: Intraocular pressure (IOP) was measured over the 24-month treatment period, and any ocular-systemic symptoms or adverse events were evaluated. RESULTS: Latanoprost significantly reduced (P < 0.001) IOP by approximately 8 mmHg from pretreatment values, and this reduction was maintained over the 24-month treatment period with no sign of upward drift. Latanoprost is apparently free of any systemic side effect. The most significant ocular side effect with latanoprost was an increase in iris pigmentation, which occurred in 51 patients. CONCLUSIONS: Latanoprost, administered once daily, is effective and well tolerated for the long-term treatment of patients with open-angle glaucoma or ocular hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Eye_Color_MeSH S_drug_effects_MeSH Eye_Color_drug_effects_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH S_physiology_MeSH Intraocular_Pressure_physiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Ophthalmic_Solutions_MeSH M_Pigmentation_Disorders_MeSH S_chemically_induced_MeSH Pigmentation_Disorders_chemically_induced_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 9443168
----K I
----T A postmarketing study of flunarizine in migraine and vertigo.
----A This prospective, open multi-centre study on flunarizine focused on the risk/benefit ratio of the use of flunarizine in the prophylaxis of migraine and in the treatment of vertigo, due to disorder of the vestibular system. The assessment of risks focused on the incidence of new events of depression and/or extrapyramidal syndrome during flunarizine treatment. For migraine, flunarizine was compared to propranolol in 686 patients; for vertigo, flunarizine was compared to betahistine in 198 patients. The incidence of depression during follow-up in this study was significantly higher in the flunarizine group than in the propranolol group in the condition of migraine. There were no observations of an extrapyramidal syndrome. There was a suggestion that flunarizine has more benefits than propranolol in the condition of migraine, and that betahistine has more benefit than flunarizine in the condition of vertigo. Differences in dosages could possible explain these differences.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Data_Collection_MeSH M_Depressive_Disorder_MeSH S_complications_MeSH Depressive_Disorder_complications_MeSH S_psychology_MeSH Depressive_Disorder_psychology_MeSH M_Female_MeSH M_Flunarizine_MeSH S_adverse_effects_MeSH Flunarizine_adverse_effects_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_psychology_MeSH Migraine_psychology_MeSH M_Netherlands_MeSH M_Product_Surveillance__Postmarketing_MeSH M_Prospective_Studies_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Vertigo_MeSH S_drug_therapy_MeSH Vertigo_drug_therapy_MeSH S_psychology_MeSH Vertigo_psychology_MeSH 
****** 9444298
----K I
----T Combination neurohormonal blockade with ACE inhibitors, angiotensin II antagonists and beta-blockers in patients with congestive heart failure: design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study.
----A BACKGROUND: The Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study is a trial of combination neurohormonal blockade using an angiotensin II antagonist (candesartan), an angiotensin-converting enzyme inhibitor (enalapril) and a beta-blocker (metoprolol) in patients with congestive heart failure (CHF). OBJECTIVES: Primary objectives of stage I are to determine the efficacy (via the 6 min walk test) and safety of candesartan alone, and in combination with enalapril, versus enalapril alone. Secondary objectives are to determine the effect of the above combinations on neurohormones, ventricular function, quality of life and symptoms. Stage II objectives are similar, evaluating the effect of the addition of metoprolol or placebo to the above medication(s). DESIGN: Randomized, two-stage trial consisting of a three-way comparison (stage I), followed by a 3 x 2 partial factorial design (stage II). SETTING: Sixty out-patient clinics in five countries. PATIENTS: Patients with symptoms of CHF (New York Heart Association functional classes II to IV), ejection fraction less than 40% and 6 min walk distance of 500 m or less. INTERVENTIONS: In stage I, 770 patients are randomized to receive candesartan alone, enalapril alone, or candesartan plus enalapril. After five months (end of stage I), patients are assessed for eligibility to be randomized in stage II. Those who are not candidates for randomization to beta-blocker or placebo are followed on their stage I medications until the end of the study. In stage II, patients are randomized to receive metoprolol or placebo for a further six months in addition to their stage I medications. Endpoints are measured at baseline, end of stage I (week 20) and end of stage II (week 46). STUDY STATUS: The study has recently completed follow-up in both stages. The findings from this study will be used to design a large scale mortality study that will help further define the role of neurohormonal blockade in patients with CHF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Pilot_Projects_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 9444452
----K E
----T Variations in compliance among hypertensive patients by drug class: implications for health care costs.
----A Health care decision-makers require more information on differences in compliance rates associated with alternative classes of antihypertensive drugs and the implications of these differences for health care utilization and costs. We examined medical claims data from the Pennsylvania Medicaid Management Information System to investigate compliance rates for four major antihypertensive drug classes (angiotensin-converting enzyme [ACE] inhibitors, beta-blockers, calcium antagonists, and diuretics) and the health care costs associated with noncompliance. Multivariate analysis was used to relate antihypertensive drug class with compliance and variations in compliance with health care costs. The highest estimated rates of compliance were associated with ACE inhibitors and calcium antagonists, and these rates were significantly greater than with beta-blockers and diuretics. Moreover, poor compliance was associated with higher health care costs. Efforts to increase compliance with antihypertensive drug therapy are needed to improve patient outcomes and reduce health care costs.
----P Clinical_Trial Journal_Article 
----M M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cost_Savings_MeSH M_Female_MeSH M_Health_Care_Costs_MeSH S_statistics_&_numerical_data_MeSH Health_Care_Costs_statistics_&_numerical_data_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Patient_Compliance_MeSH M_Pennsylvania_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9447850
----K I
----T Prophylactic atenolol reduces postoperative myocardial ischemia. McSPI Research Group.
----A BACKGROUND: Perioperative myocardial ischemia occurs in 20-40% of patients at risk for cardiac complications and is associated with a ninefold increase in risk for perioperative cardiac death, myocardial infarction, or unstable angina, and a twofold long-term risk. Perioperative atenolol administration reduces the risk of death for as long as 2 yr after surgery. This randomized, placebo-controlled, double-blinded trial tested the hypothesis that perioperative atenolol administration reduces the incidence and severity of perioperative myocardial ischemia, potentially explaining the observed reduction in the risk for death. METHODS: Two-hundred patients with, or at risk for, coronary artery disease were randomized to two study groups (atenolol and placebo). Monitoring included a preoperative history and physical examination and daily assessment of any adverse events. Twelve-lead electrocardiography (ECG), three-lead Holter ECG, and creatinine phosphokinase with myocardial banding (CPK with MB) data were collected 24 h before until 7 days after surgery. Atenolol (0, 5, or 10 mg) or placebo was administered intravenously before induction of anesthesia and every 12 h after operation until the patient could take oral medications. Atenolol (0, 50, or 100 mg) was administered orally once a day as specified by blood pressure and heart rate. RESULTS: During the postoperative period, the incidence of myocardial ischemia was significantly reduced in the atenolol group: days 0-2 (atenolol 17 of 99 patients; placebo, 34 of 101 patients; P = 0.008) and days 0-7 (atenolol, 24 of 99 patients; placebo, 39 of 101 patients; P = 0.029). Patients with episodes of myocardial ischemia were more likely to die in the next 2 yr (P = 0.025). CONCLUSIONS: Perioperative administration of atenolol for 1 week to patients at high risk for coronary artery disease significantly reduces the incidence of postoperative myocardial ischemia. Reductions in perioperative myocardial ischemia are associated with reductions in the risk for death at 2 yr.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9463170
----K 1
----T [Use of verapamil vs. beta blockers in patients with myocardial infarct. Retrospective evaluation of the yearly case load of a coronary care unit]
----A BACKGROUND, MATERIALS AND METHODS: To compare the relative use of verapamil and beta-blockers, which have shown comparable efficacy in reducing mortality and reinfarction rates in selected patients with myocardial infarction (MI), we retrospectively evaluated the ongoing treatment at the time of the pre-discharge evaluation in 221 consecutive patients (167 males and 54 females; mean age: 62.3 +/- 10.8 years) discharged alive in 1994 from our Hospital with the diagnosis of Q-wave MI. RESULTS: The examination of the computerized files of our central database, showed that verapamil was administered (as a monotherapy or in association) to 4% of the patients, compared to 34% of beta-blockers. The choice between the two drugs appeared not to be influenced by age (62 +/- 11 vs 57 +/- 8 years), anterior (70% vs 57%) or inferior (30% vs 40%) MI location or echocardiographic left ventricular ejection fraction (50.2 +/- 10% vs 52.3 +/- 11%), which were comparable in both groups. On the other hand, beta-blockers were used significantly more often (52% vs 10%; p < 0.05) in the presence of hypertension, while verapamil was preferred (although statistical significance was not reached) in patients with contraindications to beta-blockers, such as chronic obstructive lung disease or peripheral artery disease (20% vs 9% and 10% vs 4%; p = ns, respectively). CONCLUSIONS: In conclusion, our study gives, for the first time, an estimate of the real use of verapamil in patients with MI, confirming, in keeping with the indications in the literature, that its administration is limited and essentially reserved to patients with contraindications to beta-blockers. A wider use of verapamil (and even more of beta-blockers) would be however hoped for, due to the relevant number of patients (62% of our population) treated with drugs, such as diltiazem, dihydropyridines or nitrates, for which a conclusive demonstration of efficacy on major clinical end-points are lacking.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Care_Units_MeSH M_Echocardiography_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Italy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Retrospective_Studies_MeSH M_Stroke_Volume_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9453014
----K E
----T A cross-over medication trial for patients with autosomal-dominant hypertension with brachydactyly.
----A We examined a family with autosomal-dominant hypertension and brachydactyly from northeastern Turkey. The hypertension was defined as severe, resulting in stroke before age 50 years, featuring normal renin, aldosterone, and catecholamine responses, and did not appear to be salt-sensitive. The responsible gene resides on chromosome 12p. To determine which medications were most effective, we performed a prospective clinical trial. We studied 13 affected individuals in a randomized double-blind, cross-over trial including a beta-blocker (BBL), alpha-blocker (ABL), calcium channel blocker (CCB), converting enzyme inhibitor (CEI), and hydrochlorothiazide (HCT) and placebo (PLA). We then added moxonidine (MOX) and continued the trial for an additional period in a single-blind fashion. Each drug was given for four weeks with an option to double the dose after two weeks; each washout period comprised two weeks. Blood, 24-hour urine, and saliva were studied at the outset, and blood and urine samples were obtained at the end of each phase. Blood pressure (BP) and heart rate measurements were with the patient ambulatory at 24 hours. All regimens required doubled doses at two weeks. Beta blocker, CCB, CEI, and ABL lowered BP (6 to 10 mm Hg) and BP load compared to PLA, while HCT and MOX did not. Converting enzyme inhibitor and HCT increased plasma renin activity (PRA), while BBL lowered PRA. The 24-hour urine analysis indicated a high dietary salt intake with a low potassium and calcium intake. The salivary electrolytes showed similar sodium and potassium concentrations, while chloride values were significantly higher in affected than nonaffected subjects. Thus, this monogenic form of hypertension resembles nonsalt-sensitive essential hypertension in that BBL, CCB, CEI, and ABL were effective, while HCT was not. The BP reduction was similar to other single drug trials in essential hypertension. The high salivary chloride values suggest an additional intermediary phenotype that may be related to electrolyte transport. These results raise the possibility that an as yet unknown hypertensive mechanism is operative in these subjects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Limb_Deformities__Congenital_MeSH S_genetics_MeSH Limb_Deformities__Congenital_genetics_MeSH M_Male_MeSH M_Potassium_Channels_MeSH S_physiology_MeSH Potassium_Channels_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 9456279
----K I
----T Comparison of sotalol and metoprolol in the prevention of atrial fibrillation after coronary artery bypass surgery.
----A New-onset atrial fibrillation (AF) is frequent after coronary artery bypass grafting (CABG), and beta-blockers decrease its incidence. To examine whether a beta-blocker with class III properties is superior to a pure one, 191 consecutive patients undergoing CABG were randomized to receive oral sotalol, 120 mg daily (n = 93), or metoprolol, 75 mg daily (n = 98), postoperatively. The doses were adjusted if beta-blockade was inadequate or excessive. AF occurred in 16 (16%) of 98 sotalol patients and in 30 (32%) of 93 metoprolol patients (p < 0.01). Symptoms related to beta-blockade or proarrhythmia did not appear. After CABG, sinus heart rate increased in both groups (p < 0.001) but less in the sotalol patients (p < 0.001) throughout the postoperative period. Corrected QT duration (by the Bazett equation) was prolonged after the operation in both groups (p < 0.001), whereas uncorrected QT duration at similar heart-rate levels were prolonged only in sotalol patients (mean increase, 31 ms; 95% confidence interval, 2042 ms; p < 0.01). Uncorrected QT durations at similar heart-rate levels were longer during sotalol (compared with metoprolol) treatment (p < 0.05). Heart rates or QT durations did not differ between the patients with or without AF. In conclusion, sotalol significantly reduces the incidence of AF after CABG. Although a marked class III effect is demonstrated with relatively low doses (as prolonged ventricular repolarization) in direct comparison unbiased by any rate correction, its contribution as an enhanced antifibrillatory mechanism in the postoperative state remains unconfirmed.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_epidemiology_MeSH Atrial_Fibrillation_epidemiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH M_Electrocardiography_MeSH S_methods_MeSH Electrocardiography_methods_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH 
****** 9456288
----K E
----T Insulin sensitivity in a long-term crossover trial with celiprolol and other antihypertensive agents.
----A The effects of a vasodilating beta-blocker, celiprolol, on insulin sensitivity and cardiovascular risk factors were compared with those of another beta1-selective adrenoceptor blocker, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. A randomized 21-month crossover trial was carried out with 25 patients with dyslipidemia receiving antihypertensive monotherapy. The study consisted of a 3-month active run-in period and two treatment periods, during which the patients received celiprolol (200-400 mg daily) or the control drug for 12 and 6 months in a crossover manner. A hyperinsulinemic euglycemic clamp and an oral glucose tolerance test (OGTT) were performed every 6 months. According to the clamp tests, the insulin-sensitivity index increased on average by 32% (p < 0.0001) during celiprolol treatment compared with that with the other antihypertensive agents, including ACE inhibitors. In OGTT, area under the incremental glucose curve decreased by 36% (p = 0.002) during celiprolol treatment, whereas insulin secretion diminished on average by 26% (p = 0.006). The mean decrease in fasting serum triglycerides was 11% (NS), whereas the high-density lipoprotein to low-density lipoprotein (HDL/LDL) ratio increased by 15% (p = 0.012). The results suggest that celiprolol improves insulin sensitivity of hypertensive patients with dyslipidemia in long-term therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_blood_MeSH Hyperlipidemia_blood_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH P_Insulin_Resistance_MeSH S_physiology_MeSH Insulin_Resistance_physiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9457458
----K 4
----T Comparison of two fixed beta-blocker-pilocarpine combinations. The Carteolol-Pilocarpine Study Group.
----A PURPOSE: To compare the efficacy and safety of a newly developed ophthalmic solution containing carteolol 2% and pilocarpine (2% (CBS341A) with a timolol 0.5% and pilocarpine 2% fixed combination. PATIENTS AND METHODS: A randomized, double-masked, multicenter study was conducted in 209 patients with primary open-angle glaucoma or ocular hypertension, whose intraocular pressure (IOP) was higher than 21 mm Hg on bet-blocker twice a day alone. The test medications were administered twice daily for 4 months. IOP was measured at 9 and 11 a.m. at the beginning of the study (with beta-blocker alone) and after one and four months of treatment. Adverse effects were recorded. RESULTS: Both combinations caused a similar, statistically significant decrease in IOP. At four months, in the CBS341A group a 2.4 mm Hg (9%) reduction in IOP was achieved at 9 a.m. and 4.1 mm Hg (17.3%) at 11 a.m. compared with respectively 3 mm Hg (11%) and 4.5 mm Hg (19.5%) in the timolol-pilocarpine group. No statistical difference was observed between the two groups in safety and efficacy. CONCLUSIONS: The carteolol-pilocarpine combination appears as safe and as effective as the timolol-pilocarpine combination in the medical treatment of primary open-angle glaucoma or ocular hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carteolol_MeSH S_administration_&_dosage_MeSH Carteolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Carteolol_adverse_effects_MeSH S_therapeutic_use_MeSH Carteolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscarinic_Agonists_MeSH S_administration_&_dosage_MeSH Muscarinic_Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Muscarinic_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Muscarinic_Agonists_therapeutic_use_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Pilocarpine_MeSH S_administration_&_dosage_MeSH Pilocarpine_administration_&_dosage_MeSH S_adverse_effects_MeSH Pilocarpine_adverse_effects_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 9462584
----K E
----T Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure.
----A OBJECTIVES: We 1) evaluated whether interleukin-6 (IL-6) is produced in the peripheral circulation in patients with congestive heart failure (CHF), 2) estimated the factors for increased IL-6, and 3) clarified the prognostic role of high plasma levels of IL-6 in patients with CHF. BACKGROUND: Although plasma levels of IL-6 have been reported to increase in patients with CHF, and production of IL-6 in endothelial cells and vascular smooth muscle cells has been postulated from in vitro studies, the origin of the increase of IL-6 in CHF remains unknown. Moreover, the prognostic value of a high plasma level of IL-6, independent of classic neurohumoral factors, remains to be elucidated. METHODS: A comparison was made of the plasma levels of IL-6 between the femoral artery and the femoral vein in 13 normal subjects and in 80 patients with CHF. In another study, we measured plasma IL-6 in 100 patients with CHF and follow-up data. RESULTS: Plasma IL-6 levels increased significantly from the femoral artery to the femoral vein in normal subjects and in patients with CHF. Arteriovenous IL-6 spillover in the leg increased with the severity of CHF. Among the hemodynamic variables and the various neurohumoral factors, the plasma norepinephrine (NE) level showed an independent and significant positive relation with the plasma IL-6 level in patients with CHF. Moreover, treatment with beta-adrenergic blocking agents showed an independent and significant negative relation with plasma IL-6 levels. In 100 patients, plasma IL-6 (p < 0.0001), NE (p = 0.0004) and left ventricular ejection fraction (0.015) were significant independent prognostic predictors by Cox proportional hazards analysis. CONCLUSIONS: Our findings indicate that the IL-6 spillover in the peripheral circulation increases with the severity of CHF and that the increase in plasma IL-6 is mainly associated with the activation of the sympathetic nervous system. High plasma levels of IL-6 can provide prognostic information in patients with CHF, independent of left ventricular ejection fraction and plasma NE, suggesting an important role for IL-6 in the pathophysiology of CHF.
----P Journal_Article 
----M M_Adrenergic_alpha-Agonists_MeSH S_blood_MeSH Adrenergic_alpha-Agonists_blood_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Case-Control_Studies_MeSH M_Comparative_Study_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH M_Endothelium__Vascular_MeSH S_metabolism_MeSH Endothelium__Vascular_metabolism_MeSH M_Female_MeSH M_Femoral_Artery_MeSH M_Femoral_Vein_MeSH M_Follow-Up_Studies_MeSH M_Forecasting_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Interleukin-6_MeSH S_biosynthesis_MeSH Interleukin-6_biosynthesis_MeSH S_blood_MeSH Interleukin-6_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle__Smooth__Vascular_MeSH S_metabolism_MeSH Muscle__Smooth__Vascular_metabolism_MeSH M_Neurotransmitters_MeSH S_blood_MeSH Neurotransmitters_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympathetic_Nervous_System_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Sympathomimetics_MeSH S_blood_MeSH Sympathomimetics_blood_MeSH M_Tumor_Necrosis_Factor_MeSH S_analysis_MeSH Tumor_Necrosis_Factor_analysis_MeSH M_Vasoconstrictor_Agents_MeSH S_blood_MeSH Vasoconstrictor_Agents_blood_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 9468004
----K E
----T Pro-haemorrhagic effects of calcium antagonists: a comparison of isradipine and atenolol on ex vivo platelet function in hypertensive subjects.
----A It has been suggested that long term treatment with calcium antagonist drugs might inhibit platelet function and lead to an anti-atheromatous effect. However recent data have also suggested that such an effect might increase mortality due to an increased incidence of gastrointestinal bleeding. We identified 43 subjects from general practice with uncomplicated mild to moderate hypertension to compare the effects of the calcium antagonist isradipine with that of the beta-blocker atenolol on platelet function, plasma beta-thromboglobulin levels, fibrinolysis, and serum lipids in a randomised double-blind parallel group study. After careful evaluation to exclude concomitant aspirin use, only 24 subjects were eligible to enter the study. While isradipine and atenolol produced comparable and clinically significant falls in blood pressure (167 +/- 2/102 +/- 1 to 153 +/- 3/91 +/- 2 mm Hg, and 165 +/- 2/101 +/- 1 to 156 +/- 4/91 +/- 2 mm Hg, respectively), neither drug produced a detectable effect on ex vivo platelet aggregation, platelet retention, or thromboxane generation with adrenaline, collagen, adenosine-di-phosphate, or platelet activating factor. However a decrease in plasma beta-thromboglobulin levels was observed which reached statistical significance (P < 0.05) after 12 weeks treatment in the isradipine but not the atenolol group. A 39% reduction with isradipine compared with 34% following atenolol treatment. Euglobulin clot lysis time was not altered by either drug. Serum cholesterol concentrations were also unaltered by drug treatment. Therapeutic doses of the calcium antagonist isradipine may produce a minor indirect effect on platelet function after several weeks of treatment. However, this is of doubtful clinical importance and may simply reflect an effect of lowered blood pressure on platelet function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Blood_Platelets_MeSH S_drug_effects_MeSH Blood_Platelets_drug_effects_MeSH S_physiology_MeSH Blood_Platelets_physiology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemorrhage_MeSH S_chemically_induced_MeSH Hemorrhage_chemically_induced_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isradipine_MeSH S_adverse_effects_MeSH Isradipine_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_beta-Thromboglobulin_MeSH S_analysis_MeSH beta-Thromboglobulin_analysis_MeSH 
****** 9468009
----K E
----T Nebivolol vs enalapril in the treatment of essential hypertension: a double-blind randomised trial.
----A The efficacy and acceptability of nebivolol 5 mg and enalapril 10 mg, each given once daily, were compared in essential hypertension in a multicentre, randomised, double-blind trial over 3 months. For the index pre-declared variable, sitting diastolic pressure at trough drug level, nebivolol achieved greater falls in pressure (-12.3 vs -9.9 mmHg; P = 0.009) and a higher response rate (70% vs 55%; P = 0.002). The trough-to-peak sitting diastolic ratios also favoured nebivolol (84% vs 60%, P = 0.002). Nebivolol, but not enalapril, slightly but significantly lowered heart rate. Both drugs were well-tolerated, although enalapril was accompanied by a significantly higher incidence of coughing.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH 
****** 9490238
----K E
----T Non-Q-wave versus Q-wave myocardial infarction after thrombolytic therapy: angiographic and prognostic insights from the global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries-I angiographic substudy. GUSTO-I Angiographic Investigators.
----A BACKGROUND: Although the stratification of patients with myocardial infarction into ECG subsets based on the presence or absence of new Q waves has important clinical and prognostic utility, systematic evaluation of the impact of thrombolytic therapy on the subsequent development and prognosis of non-Q-wave infarction has been limited to date. METHODS AND RESULTS: We examined 12-lead ECG, coronary anatomy, left ventricular function, and mortality among 2046 patients with ST-segment elevation infarction from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries angiographic subset to gain further insight into the pathophysiology and prognosis of Q- versus non-Q-wave infarction in the thrombolytic era. Non-Q-wave infarction developed in 409 patients (20%) after thrombolytic therapy. Compared with Q-wave patients, non-Q-wave patients were more likely to present with lesser ST-segment elevation in a nonanterior location. The infarct-related artery in non-Q-wave patients was more likely to be nonanterior (67% versus 58%, P=.012) and distally located (33% versus 39%, P=.021). Early (90-minute, 77% versus 65%, P=.001) and complete (54% versus 44%, P<.001) infarct-related artery patency was greater among the non-Q-wave group. Non-Q-wave patients had better global (ejection fraction, 66% versus 57%; P<.0001) and regional left ventricular function (10 versus 24 abnormal chords, P=.0001). In-hospital, 30-day, 1-year, and 2-year (6.3% versus 10.1%, P=.02) mortality rates were lower among non-Q-wave patients. CONCLUSIONS: The excellent prognosis among the subgroup of patients who develop non-Q-wave infarction after thrombolysis is related to early, complete, and sustained infarct-related artery patency with resultant limitation of left ventricular infarction and dysfunction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Coronary_Angiography_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Catheterization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Prognosis_MeSH M_Streptokinase_MeSH S_therapeutic_use_MeSH Streptokinase_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH P_Thrombolytic_Therapy_MeSH M_Tissue_Plasminogen_Activator_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9483388
----K E
----T Pregnancy-induced hypertension, antihypertensive drugs and the development of fetal behavioural states.
----A In 21 pregnancies complicated by pregnancy-induced hypertension (PIH) which was treated by antihypertensive drugs (labetalol, nifedipine), fetal behavioural recordings (quiet state, C1F; active state, C2F; no coincidence, NOC) and Doppler measurements of blood flow velocity in the umbilical artery (UA) (resistance index, RI) were made on two occasions (27-32 and 33-36 weeks of gestation). Data were compared to those of a control group of normally grown fetuses (n = 96); in 15 cases we were able to match fetuses from the study group for age (+/- 1 week) and weight (+/- 150 g) at birth with fetales from a control group. It was the aim of this study to investigate if there are disturbances in the development of fetal behavioural states and if possible disturbances are due to poor fetal growth or to antihypertensive therapy. Our results show that in PIH treated by antihypertensive drugs, there are disturbances in the development of fetal behavioural states with higher percentages of NOC and C1F, lower percentages of C2F, and higher UA RI values. These disturbances are mainly due to coexisting placental impairment and poor fetal growth rather than to nifedipine or labetalol therapy, although these drugs may cause some redistribution of states.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Embryo_MeSH S_drug_effects_MeSH Embryo_drug_effects_MeSH S_physiology_MeSH Embryo_physiology_MeSH S_ultrasonography_MeSH Embryo_ultrasonography_MeSH M_Embryo_and_Fetal_Development_MeSH S_drug_effects_MeSH Embryo_and_Fetal_Development_drug_effects_MeSH S_physiology_MeSH Embryo_and_Fetal_Development_physiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_embryology_MeSH Hypertension_embryology_MeSH M_Labetalol_MeSH S_pharmacology_MeSH Labetalol_pharmacology_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Male_MeSH M_Nifedipine_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Pregnancy_Outcome_MeSH M_Reference_Values_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultrasonography__Prenatal_MeSH 
****** 9484356
----K E
----T Do antiarthritic drugs decrease the risk for cognitive decline? An analysis based on data from the MRC treatment trial of hypertension in older adults.
----A We ascertained nonsteroidal anti-inflammatory drug (NSAID) use in 2,651 participants in the UK MRC treatment trial of hypertension in older adults and measured change in cognitive function over the subsequent 54 months. There was a significant, although modest, association between change in the Paired Associate Learning Test score over time and NSAID use, which was modified by age. NSAID users showed less decline, with younger subjects seeming to benefit more than older. We found no relationship between NSAID use and time taken to complete the Trail Making Test and also no relationship between anti-indigestion drug use and either cognitive outcome. These analyses highlight the need for larger studies with prospective classification of NSAID use and adequate control of confounding, including exposure to other medications. A randomized controlled trial of NSAIDs, in those known to be at risk of cognitive decline or dementia, may be indicated in the future.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cognition_Disorders_MeSH S_epidemiology_MeSH Cognition_Disorders_epidemiology_MeSH S_prevention_&_control_MeSH Cognition_Disorders_prevention_&_control_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Paired-Associate_Learning_MeSH S_drug_effects_MeSH Paired-Associate_Learning_drug_effects_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9489131
----K E
----T Evaluation of glucose tolerance during treatment with celiprolol in patients with mild arterial hypertension without diabetes mellitus. The Genker General Practitioners.
----A A prospective evaluation of the metabolic effects of Celiprolol, a third generation Beta-Blocking agent was done by 10 general practitioners in 45 mildly hypertensive patients. (diastolic blood pressure > or = 95 mm/Hg and < or = 115 mm/Hg. In 43 patients with complete data, blood pressure and resting heart rate decreased significantly after treatment, but weight and metabolic parameters were unchanged. After 6 months therapy the 22 patients with an impaired glucose tolerance test (IGTT) had a significant decrease in plasma glucose and insulin values, and a tendency for increased HDL. These favorable metabolic effects of Celiprolol in mildly hypertensive patients with an abnormal GTT are different from the findings with other beta-blockers and justify further study.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 9493257
----K E
----T Clinical trials comparing two treatment policies: which aspects of the treatment policies make a difference?
----A We discuss pragmatic clinical trials with survival endpoints in which subjects commonly change treatment during follow-up. Suppose that an intention-to-treat (ITT) analysis shows a significant difference between the randomized groups. We may want to ask questions about the reason for such a difference in outcome between randomized groups: for example, was the difference due to different policies for change to a third more beneficial regime? We address such questions using the semi-parametric accelerated life models of Robins, which exploit the randomization assumption fully and avoid direct comparisons of possibly differently selected subgroups. No assumption is made about the relationship of treatment actually prescribed to prognosis. A sensitivity analysis, using a range of plausible values for the causal effect of a covariate, estimates the contrasts between randomized groups that would have been observed if the covariate had universally been 0. The main technical problem is in dealing with censoring, for the method requires different degrees of recensoring for different values of the causal effect, and this can lead to estimates of low precision. The methods are applied to a randomized comparison of two anti-hypertensive treatments in which approximately half the subjects changed treatment during follow-up. Various time-dependent covariates, representing patterns of side-effects and treatments, are used in the model. We find that the observed difference in cardiovascular deaths between the randomized groups cannot be explained in this way by their different covariate patterns.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Clinical_Protocols_MeSH M_Comparative_Study_MeSH P_Data_Interpretation__Statistical_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH P_Drug_Therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH P_Models__Statistical_MeSH M_Placebos_MeSH P_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9495662
----K E
----T The Captopril Prevention Project (CAPPP) in hypertension--baseline data and current status.
----A The Captopril Prevention Project (CAPPP) is an ongoing intervention study conducted in 11,019 hypertensive patients in Sweden and Finland. Patients have been randomized to receive either conventional antihypertensive therapy (diuretics and/or beta-blockers) or captopril-based treatment. A prospective, randomized, open, blinded-endpoint evaluation (PROBE) study design is used to compare these two therapeutic regimens as regards cardiovascular morbidity and mortality. The rationale for the CAPPP Study are the many observations of beneficial effects of ACE inhibition, as compared to diuretics and beta-blockers, on intermediary endpoints such as insulin sensitivity, serum lipoproteins, left ventricular hypertrophy and renal function. Captopril has also been shown to be markedly effective in the treatment of left ventricular dysfunction as well as congestive heart failure. The hypothesis is that these differences might result in improved risk reduction when ACE inhibitors are used in the treatment of hypertension. The present paper describes the baseline data and the changes in blood pressure during the first year in the total cohort. During the first year the average blood pressure was reduced by 11/8 mm Hg. A number of substudies have been conducted in the CAPPP Study. In one of these insulin sensitivity was compared in a subgroup of the patients using the euglycemic insulin clamp technique. In another substudy the ACE gene was sequenced and some new polymorphisms were discovered. Several other substudies are in progress or in the planning phase. The main results of the CAPPP Study should be available by mid-1998. Some of the intended anayses of the final results as well as other planned substudies are briefly described here.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Data_Interpretation__Statistical_MeSH M_Female_MeSH M_Finland_MeSH S_epidemiology_MeSH Finland_epidemiology_MeSH M_Genes__Structural_MeSH S_genetics_MeSH Genes__Structural_genetics_MeSH M_Glucose_Clamp_Technique_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH S_drug_effects_MeSH Lipoproteins_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_genetics_MeSH Myocardial_Infarction_genetics_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_genetics_MeSH Peptidyl-Dipeptidase_A_genetics_MeSH M_Polymorphism_(Genetics)_MeSH M_Prospective_Studies_MeSH M_Sweden_MeSH S_epidemiology_MeSH Sweden_epidemiology_MeSH 
****** 9501808
----K E
----T Epidemiology and potential for prevention of abdominal aortic aneurysm.
----A BACKGROUND: Ruptured abdominal aortic aneurysm (AAA) is a common cause of death which is preventable by elective repair of an asymptomatic AAA. METHODS: The literature was reviewed with emphasis on epidemiological studies and population-based screening surveys. RESULTS AND CONCLUSION: The prevalence of small AAA ranges between 3 and 8 per cent. The incidence of asymptomatic AAA seems to be increasing, although exact incidence estimates vary. The most important risk factors for AAA are male sex, age, family history and smoking. Hypertension is associated with a mildly increased risk, but diabetes is not associated with any increase. Primary prevention of AAA is not a realistic option. There is no evidence of an effective medical treatment to prevent growth of small AAAs, although trials with propranolol are under way. The only intervention to prevent death from aneurysm is elective repair of the asymptomatic lesion. Screening for asymptomatic AAA can reduce the incidence of rupture. However, further studies are needed to determine the cost effectiveness of screening compared with that of other health programmes.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH P_Aortic_Aneurysm__Abdominal_MeSH S_epidemiology_MeSH Aortic_Aneurysm__Abdominal_epidemiology_MeSH S_genetics_MeSH Aortic_Aneurysm__Abdominal_genetics_MeSH S_prevention_&_control_MeSH Aortic_Aneurysm__Abdominal_prevention_&_control_MeSH M_England_MeSH S_epidemiology_MeSH England_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Mass_Screening_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9504355
----K E
----T Nebivolol vs atenolol and placebo in essential hypertension: a double-blind randomised trial.
----A A double-blind, randomised, parallel-group trial was conducted in patients with essential hypertension in British general practices, of nebivolol 5 mg, atenolol 50 mg, and placebo each given once daily. Both active drugs, in comparison with placebo, caused highly significant and similar reductions in systolic and diastolic pressures without orthostatic effect, and small significant falls in heart rate. Both active drugs were well tolerated, nebivolol marginally more so. Nebivolol, a long-acting, cardioselective, vasodilating beta-blocker which acts partly via the l-arginine/nitric oxide mechanism, appears potentially valuable for the treatment of hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 9506320
----K E
----T Temporal trends in pharmacotherapy for congestive heart failure at an academic medical center: 1990-1995.
----A The objectives of this study were to assess current practice patterns in pharmacotherapy for congestive heart failure at an academic medical center and to analyze temporal trends in management of congestive heart failure from 1990 to 1995. Records of all patients discharged from the hospital in 1990 or 1995 with a primary diagnosis of congestive heart failure who also underwent echocardiography were found by a search of the hospital's medical records database. All charts were reviewed, and relevant clinical data, including all discharge medications, were recorded. On the basis of echocardiograms, patients were classified as having preserved or impaired left ventricular systolic function (estimated ejection fraction > or =45% versus <45%). The use of digoxin, diuretics, angiotensin-converting enzyme (ACE) inhibitors, calcium and beta-blockers, nitrates, and hydralazine in 1990 and 1995 were compared in subgroups according to left ventricular function. A total of 297 patients were identified who fulfilled study criteria and for whom all pertinent data were available (1990, n = 109; 1995, n = 188). The median age was 74 years; 37.3% of the patients were men, and 45.1% were white. Among patients with impaired systolic function, the proportion receiving either an ACE inhibitor or the combination of nitrates and hydralazine increased from 80.9% in 1990 to 95.4% in 1995 (p = 0.009). In addition, among patients treated with an ACE inhibitor, the proportion receiving an optimal dose increased from 24.3% in 1990 to 61.5% in 1995 (p < 0.001). The use of beta-blockers also increased significantly during this time period (2.1% versus 15.7%; p = 0.031 ). Among patients with preserved ventricular function, the use of ACE inhibitors and beta-blockers increased from 1990 to 1995 (both p < 0.05). The use of other medications did not change for either subgroup. Current use of appropriate vasodilator therapy at an academic medical center is very high and is in accordance with published guidelines for the management of congestive heart failure. The use of vasodilators and beta-blockers has increased significantly since 1990 among patients with congestive heart failure with either impaired or preserved left ventricular contractility.
----P Journal_Article 
----M M_Academic_Medical_Centers_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Drug_Therapy_MeSH S_trends_MeSH Drug_Therapy_trends_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Physician's_Practice_Patterns_MeSH S_trends_MeSH Physician's_Practice_Patterns_trends_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH M_Ventricular_Function__Left_MeSH 
****** 9505927
----K I
----T Beta blockers in heart failure: a comparison of a vasodilating beta blocker with metoprolol.
----A OBJECTIVE: To determine whether a third generation vasodilating beta blocker (celiprolol) has long term clinical advantages over metoprolol in patients with chronic heart failure. DESIGN: A double blind placebo controlled randomised trial. SETTING: University teaching Hospital. PATIENTS: 50 patients with stable chronic heart failure (NYHA class II-IV) due to idiopathic dilated, ischaemic, or hypertensive cardiomyopathy, with left ventricular ejection fraction < 0.45. INTERVENTIONS: Celiprolol 200 mg daily (n = 21), metoprolol 50 mg twice daily (n = 19), or placebo (n = 10) for three months with a four week dose titration period. After the double blind period, patients entered an open label study (with placebo group receiving beta blockers) and were assessed after one year. MAIN OUTCOME MEASURES: Clinical response, efficacy, and tolerance were assessed by the Minnesota heart failure symptom questionnaire six minute walk test, Doppler echocardiography (systolic and diastolic function), radionuclide ventriculography, and atrial and brain natriuretic peptides measured at baseline and after three months. RESULTS: In the metoprolol group at 12 weeks v baseline there was a 47% reduction in symptom score (p < 0.001), improvement of NYHA class (mean (SEM), 2.6 (0.12) to 1.9 (0.13), p = 0.001), exercise distance (1246 (54) to 1402 (52) feet, p < 0.001), and left ventricular ejection fraction (26.9(3.1)% to 31(3.0)%, p = 0.016), and a fall in heart rate (resting, 79 (3) to 62 (3) beats/min, p < 0.001). In the celiprolol group there was a 38% reduction in symptom score (p = 0.02), less improvement in exercise distance (1191 (55) to 1256 (61) feet, p = 0.05), and no significant changes in NYHA class, left ventricular ejection fraction, or heart rate. Mortality at one year was 11% in metoprolol and 19% in the celiprolol group, and symptomatic improvement was maintained in the survivors. CONCLUSIONS: Both drugs were well tolerated but the vasodilator properties of celiprolol do not seem to provide any obvious additional benefit in the long term treatment of heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9508155
----K E
----T Effect of treatment of isolated systolic hypertension on left ventricular mass.
----A CONTEXT: Left ventricular (LV) hypertrophy is a common problem among elderly patients with isolated systolic hypertension (ISH), but the effect of treatment of ISH on LV mass is not known. OBJECTIVE: To assess the ability of antihypertensive drug treatment to reduce LV mass in ISH. DESIGN: Echocardiographic Substudy of the Systolic Hypertension in the Elderly Program (SHEP). PATIENTS: A total of 104 participants at the St Louis SHEP site who had interpretable baseline echocardiograms, 94 of whom had 3-year follow-up echocardiograms. INTERVENTION: The SHEP participants were randomized to placebo or active treatment with chlorthalidone (12.5-25 mg/d), with atenolol (25-50 mg/d) added if necessary to maintain goal blood pressure. MAIN OUTCOME MEASURE: Change in LV mass assessed by echocardiography. RESULTS: Minimum follow-up was 3 years. In the active treatment group, 91% and 80% of subjects were receiving treatment with chlorthalidone alone by the end of years 1 and 3, respectively. The LV mass index was 93 g/m2 in the active treatment group and 100 g/m2 in the placebo group (P<.001). The LV mass index declined by 13% (95% confidence interval, - 3% to - 23%) in the active treatment group compared with a 6% increase (95% confidence interval, - 3% to + 16%) in the placebo group over 3 years (P=.01). CONCLUSION: Treatment of ISH with a diuretic-based regimen reduces LV mass.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Ventricles_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH 
****** 9512833
----K E
----T Treating hypertension. Are the right drugs given to the right patients?
----A OBJECTIVE: To evaluate whether physicians are prescribing antihypertensive drugs appropriately and according to the recommendations of the Canadian Hypertension Society. DESIGN: Retrospective cohort study. SETTING: Family medicine teaching clinic in Montreal. PARTICIPANTS: A cohort of 183 patients followed between 1993 and 1995. Of 350 patients registered at the clinic, 167 were excluded because diagnosis of hypertension was not supported by chart review, their charts contained insufficient information, they were pregnant or younger than 18 years, or they had secondary hypertension and complex medical conditions. MAIN OUTCOME MEASURES: The dependent variable was the antihypertensive medication. Independent variables were age and sex of patients, duration of hypertension, total number of visits and number of visits for hypertension, number of physicians consulted at the clinic, associated medical conditions, diagnosis of target organ damage, blood pressure readings, and associated medications. RESULTS: Diuretics were prescribed most frequently (45.9%). Angiotensin-converting enzyme (ACE) inhibitors ranked second (28.4%), followed by calcium channel blockers (26.2%) and beta-blockers (18.0%). Age, sex, duration of hypertension, and blood pressure readings were not associated with medications. Prescription of beta-blockers was strongly associated with previous myocardial infarction, but not with diagnosis of angina pectoris. Patients with contraindications to beta-blockers were less likely to receive them and more likely to receive calcium channel blockers. Only 32% of diabetic patients received ACE inhibitors. CONCLUSION: Results suggest that some prescriptions for antihypertensive medications are inappropriate, but that physicians are following some of the Canadian Hypertension Society's recommendations. A better understanding of physicians' prescribing behaviours could help target continuing education interventions to improve prescribing for hypertension.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Canada_MeSH M_Cohort_Studies_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Education__Medical__Continuing_MeSH M_Evaluation_Studies_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Physician's_Practice_Patterns_MeSH M_Polypharmacy_MeSH M_Practice_Guidelines_MeSH M_Prescriptions__Drug_MeSH M_Retrospective_Studies_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9519501
----K E
----T Monotherapy with nifedipine GITS compared with atenolol in stable angina pectoris. The Working Group on Cardiovascular Research (WCN).
----A This double-blind, randomised multicentre study compares nifedipine gastrointestinal therapeutic system (GITS) with atenolol in 129 male patients, with exercise-induced angina pectoris. At 4 weeks, there was no significant difference between nifedipine GITS 60 mg o.d. and atenolol 100 mg o.d., in respect of improved time to onset of 0.1 mV ST-segment depression, time to onset of pain, and total exercise time. Atenolol, but not nifedipine, significantly reduced heart rate and systolic blood pressure at rest and during exercise. There were significantly more vasodilator-related side effects with nifedipine. Nifedipine GITS and atenolol as once-daily monotherapy are equally effective and safe, but have different effects on exercise parameters.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Delivery_Systems_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH 
****** 9524008
----K E
----T Effects on heart rate variability of isosorbide-5-mononitrate and metoprolol in patients with recent onset of angina pectoris.
----A BACKGROUND: Beta-blockers reduce sympathetic tone, increase vagal tone and improve prognosis in ischaemic heart disease. Nitroglycerin, being a vasodilator, may theoretically have an opposite effect and worsen the prognosis. The purpose of the present study was to analyse heart rate variability (HRV), which reflects autonomic tone, in angina patients on isosorbide-5-mononitrate (IS-5-MN) and/or metoprolol. METHODS AND RESULTS: Thirty-two patients (32-81 years old), with recently developed angina (median duration: 3 months), showing no other disease and on no drugs, were Holter-monitored 24-48 h at baseline and after 4-5 days on IS-5-MN (mean daily dose: 33 mg), on metoprolol (mean daily dose: 184 mg) and on the combined treatment. Recordings were analysed on the Marquette Series 8000 Holter scanner. Both IS-5-MN and metoprolol significantly reduced myocardial ischaemia (ST integral) and ventricular tachycardias. Metoprolol induced significant changes in the following parameters (baseline versus metoprolol): high-frequency peak 9 +/- 4 versus 11 +/- 4 ms (p < 0.001), low-to-high frequency ratio 2.5 +/- 0.6 versus 1.9 +/- 0.6 (p < 0.0001), root mean square of RR interval difference 23 +/- 7 versus 31 +/- 9 ms (p < 0.0001), RR intervals differing more than 50 ms from the preceding one 4.8 +/- 3.9 versus 10.0 +/- 7.0% (p < 0.0001), mean of all 5-min standard deviations 50 +/- 12 versus 56 +/- 11 ms (p < 0.001) and mean RR interval 819 +/- 90 versus 1,019 +/- 120 ms (p < 0.00001). The combined treatment caused approximately the same HRV changes as metoprolol alone. IS-5-MN had no significant effect on any HRV parameter, neither alone nor in combination with metoprolol. CONCLUSION: A clinically effective dose of metoprolol had potentially positive effects on HRV with increase in vagal and decrease in sympathetic tone while IS-5-MN had no effect on HRV, neither positive nor negative, neither alone nor in combination with metoprolol.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9527092
----K I
----T Effect of metoprolol in reducing myocardial ischemic threshold during exercise and during daily activity.
----A In a study of 48 patients with coronary artery disease and evidence of ischemia during exercise and daily life, metoprolol reduced the threshold of myocardial ischemia in a dose-dependent manner. This effect of beta blockers is probably due to increased coronary tone.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M P_Activities_of_Daily_Living_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Blood_Pressure_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Electrocardiography__Ambulatory_MeSH P_Exercise_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9531697
----K E
----T [Twiddler-Syndrome in a subpectoral implanted unipolar cardioverter-defibrillator]
----A Twiddler's syndrome is a rare complication in patients with pacemakers. We report this very rare syndrome in a patient with pectoral implanted unipolar cardioverter defibrillator. This syndrome was detected because the patient presented in the 3 month routine visit an exitblock with an increased pacing impedance. The defibrillation threshold remained unchanged. The chest x-ray revealed an inferolaterally migrated generator with a multiply rotated lead. The intraoperative exploration showed a generator which was rotated nine-fold around its longitudinal axis with a multiple twisted unipolar lead. The lead was substituted and the aggregate fixed with a suture to the underlying muscle fascia. An atrophy of the pectoralis muscle was found in this patient which previously resulted from a long hospital stay. This atrophy was identified as a possible risk factor for the development of Twiddler's syndrome. This report illustrates that Twiddler's syndrome, a rare complication in patients with pectoral ICD, may become a significant problem in these patients as it is for pacemaker patients but with more serious possible consequences.
----P Case_Reports Journal_Article 
----M M_Aged_MeSH M_Atrophy_MeSH S_etiology_MeSH Atrophy_etiology_MeSH M_Defibrillators__Implantable_MeSH S_adverse_effects_MeSH Defibrillators__Implantable_adverse_effects_MeSH M_English_Abstract_MeSH M_Foreign_Bodies_MeSH S_etiology_MeSH Foreign_Bodies_etiology_MeSH M_Foreign-Body_Migration_MeSH S_etiology_MeSH Foreign-Body_Migration_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Pectoralis_Muscles_MeSH S_pathology_MeSH Pectoralis_Muscles_pathology_MeSH M_Risk_Factors_MeSH 
****** 9532813
----K 1
----T [Safety and feasibility of dobutamine-atropine stress echocardiography]
----A PURPOSE: To study the safety and feasibility of dobutamine-atropine stress echocardiography (DASE) in patients with known or suspected coronary artery disease. METHODS: There were 3,000 DASE that were studied in a prospective fashion. All symptoms and side effects were stored in a data base format. RESULTS: Major test-related complications observed included one case of myocardial infarction, four cases of sustained ventricular tachycardia and five cases of atropine intoxication. There was no death or ventricular fibrillation as a direct or indirect consequence of the test. The infusion protocol allowed to us to examine patients using beta blockers, and led to 95% feasibility. CONCLUSION: DASE is a safe and feasible method for the study of patients with suspected or known coronary artery disease.
----P Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Atropine_MeSH S_adverse_effects_MeSH Atropine_adverse_effects_MeSH S_diagnostic_use_MeSH Atropine_diagnostic_use_MeSH M_Cardiotonic_Agents_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Coronary_Disease_MeSH S_ultrasonography_MeSH Coronary_Disease_ultrasonography_MeSH M_Dobutamine_MeSH S_adverse_effects_MeSH Dobutamine_adverse_effects_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_English_Abstract_MeSH P_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH 
****** 9539469
----K E
----T Depressed heart rate variability is associated with events in patients with stable coronary artery disease and preserved left ventricular function. REGRESS Study Group.
----A BACKGROUND: Little is known about the value of heart rate variability in patients with symptomatic coronary artery disease with a preserved left ventricular function. We hypothesized that in these patients heart rate variability might be a helpful adjunct to conventional parameters to predict clinical events. METHODS: In a prospective 2-year follow-up study ambulatory electrocardiographic recordings were performed in 263 consecutive male patients (mean age 56+/-8 years) with stable angina pectoris and a mean left ventricular ejection fraction of 71%+/-12%. Clinical events consisted mainly of coronary events such as percutaneous transluminal angioplasty or coronary artery bypass graft operation. RESULTS: Low measures of standard deviation of normal R-R intervals, standard deviation of the mean R-R intervals of 5 minutes, and two spectral components of heart rate variability were found in patients who had had an event compared with patients with no event. Adjusted for severity of angina, the presence of a previous myocardial infarction, and the use of beta-blockers in a logistic regression model this relation remained statistically significant for SDNN. Healthy volunteers appeared to have the highest measures of heart rate variability. CONCLUSION: In patients with ischemic heart disease and normal or near normal ventricular function decreased heart rate variability is associated with adverse clinical events.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cineangiography_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Risk_Factors_MeSH M_Stroke_Volume_MeSH M_Ventricular_Function__Left_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 9540127
----K E
----T Hypertension-induced congestive heart failure.
----A Arterial hypertension used to be the most common cause of congestive left ventricular failure. With the availability and common use of antihypertensive treatment the incidence and prevalence of hypertension-induced left ventricular failure has gradually declined. Today congestive heart failure due to underlying coronary heart disease is by far more common than the hypertension-induced variety. The effect of treatment of left ventricular failure in recent years, in particular with angiotensin converting enzyme inhibitors and carvedilol, has been impressive.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Survival_Rate_MeSH 
****** 9542820
----K 1
----T [Is antihypertensive treatment a risk factor of coronary disease? Therapy-related triglyceride increase nor diabetes increase the risk]
----A In an observational study designed to determine whether metabolic changes during long-term antihypertensive drug treatment are associated with an increased risk of coronary heart disease (CHD), 686 middle-aged hypertensive men recruited from a random population screening sample were followed up for 15 years. Antihypertensive treatment predominantly consisted of beta-adrenoceptor blockers and/or thiazide diuretics. CHD and diabetes mellitus were checked for at annual examinations. Time-dependent Cox regression analysis was used to determine correlation between the incidence of CHD and entry characteristics, the monitored serum levels of cholesterol and triglyceride concentrations and the development of diabetes mellitus. Univariate analysis showed the presence of diabetes mellitus a entry to the study and increased baseline serum concentrations of cholesterol and of triglycerides each to be a significant predictor of CHD, the respective relative risks (RR) being 2.12, 1.21 and 1.21. However, analysis of monitored levels of metabolic variables during follow-up showed only an increased serum cholesterol concentration to be significantly and independently associated with CHD (RR 1.07). Although serum triglyceride concentrations increased slightly during follow-up, they were unrelated to the incidence of CHD; nor was onset of diabetes mellitus during follow-up significantly associated with an increased risk of CHD (RR 1.48. Thus, the study showed the presence of metabolic disturbances such as diabetes mellitus and hyperlipidaemia before the start of antihypertensive treatment to be of positive predictive value in middle-aged hypertensive men, and an increase in the monitored serum cholesterol level to be an independent predictor of CHD, whereas neither drug-related diabetes nor an increase in the monitored serum triglyceride concentration seemed to be associated with the occurrence of CHD.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diuretics__Thiazide_MeSH S_adverse_effects_MeSH Diuretics__Thiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_English_Abstract_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Risk_Factors_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 9544865
----K E
----T Effect of antihypertensive treatment on cardiac and subcutaneous artery structure: a comparison between calcium channel blocker and thiazide-based regimens.
----A The effects of two antihypertensive regimens (isradipine and hydrochlorothiazide-amiloride) on the ratio between media thickness and lumen diameter of subcutaneous arteries and on left ventricular mass in essential hypertension were compared. Fifty patients, aged 46.3+/-8 (mean+/-SD) years, with newly diagnosed or poorly controlled essential hypertension were randomized to treatment with either isradipine or hydrochlorothiazide-amiloride. Atenolol and hydralazine were added in both groups as secondary and tertiary drugs, respectively, when needed for normalization of diastolic blood pressure. A subcutaneous gluteal biopsy was taken surgically before medication and again after 9 months of successful antihypertensive treatment. Two small resistance arteries were isolated from each biopsy and mounted in a Mulvany-Halpem isometric small vessel myograph. The media thickness-to-lumen diameter ratio (percentage) of the vessels was measured under standardized conditions and meaned. Left ventricular mass (LVM) index was determined by echocardiography according to the Penn convention. Ten patients were treated with isradipine as monotherapy, whereas only one patient was well controlled on diuretics as monotherapy. Mean blood pressure was reduced equally with the two regimens, from 131+/-9 mm Hg to 101+/-10 mm Hg with the isradipine and from 128+/-9 mm Hg to 99+/-7 mm Hg with the thiazide/atenolol regimen. LVM decreased significantly in both groups by 130+/-75 g with the isradipine-based regimen and by 70+/-53 g with the hydrochlorothiazide/atenolol-based regimen. The reduction of LVM was significantly greater on the isradipine-based regimen than on the thiazide-based regimen (P < .01). There was a significant reduction of media thickness-to-lumen diameter ratio during treatment with the isradipine-based regimen from 10.9% to 8.8% (P < .01). The reduction in the thiazide regimen was from 9.7% to 8.5%, which was not significant (P = .07). The study demonstrated significant reduction of hypertensive changes in peripheral resistance artery structure during antihypertensive treatment with an isradipine-based regimen. The thiazide/betablocker-based regimen did not have a significant effect on the vessels. Significant reduction of LVM was achieved with both isradipine-based and thiazide/atenolol-based regimens. The reduction of LVM obtained with the isradipine-based regimen was significantly greater than that of the thiazide/atenolol-based regimen.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Amiloride_MeSH S_therapeutic_use_MeSH Amiloride_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH S_pathology_MeSH Arteries_pathology_MeSH M_Buttocks_MeSH S_blood_supply_MeSH Buttocks_blood_supply_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isradipine_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9544866
----K E
----T Little effect of ordinary antihypertensive therapy on nocturnal high blood pressure in patients with sleep disordered breathing.
----A The antihypertensive effects of four different antihypertensive medications (beta-blocking agent, atenolol 50 mg; calcium-antagonist, isradipine SRO [slow release] 2.5 mg; diuretic, hydrochlorothiazide [HCTZ] 25 mg; and angiotension converting enzyme-inhibitor, spirapril 6 mg) on obese patients with sleep disordered breathing and hypertension were compared by the ambulatory blood pressure measurement (ABPM). Eighteen patients were randomized in a double-blind, crossover fashion to receive each of the four different medications for 8 weeks. ABPM was performed at baseline and after an 8-week treatment with these medications. A 2- to 3-week washout period occurred both at baseline and between each of the four medications. Three patients were omitted from statistical analysis because of technical problems of ABPM. Atenolol, isradipine SRO, and spirapril decreased significantly (P < .01) the mean 24-h systolic blood pressure, whereas HCTZ did not. The mean 24-h diastolic blood pressure decreased significantly after all four medications: 12 (SD+/-14) mm Hg with atenolol, 7 (SD+/-10) mm Hg with isradipine SRO, 3 mm Hg (SD+/-14) with HCTZ, and 6 (SD+/-15) mm Hg with spirapril (P < .01). During nighttime none of the medications reduced the mean diastolic or systolic blood pressure significantly. According to the 24-h blood pressure curve the influence of these four medications during the whole measurement period was not similar. Atenolol and spirapril lost their antihypertensive effect during the early morning hours. The antihypertensive effect of HCTZ varied markedly from hour to hour. The trough-to-peak ratio of no medication was >0.50. Negative correlation was observed between the apnea time and the mean systolic 24-h (r = -0.604, P = NS) and the mean systolic nocturnal blood pressure change (r = -0.590, P = NS). Our study revealed that the daytime high blood pressure was quite easily controlled by the ordinary monotherapy in these patients with partial upper airway obstruction and hypertension. Instead none of the medications used decreased nocturnal high blood pressure markedly.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_analogs_&_derivatives_MeSH Enalapril_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isradipine_MeSH S_therapeutic_use_MeSH Isradipine_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Sleep_Apnea_Syndromes_MeSH S_complications_MeSH Sleep_Apnea_Syndromes_complications_MeSH M_Treatment_Failure_MeSH 
****** 9545143
----K E
----T Statins in the prevention of coronary heart disease.
----A Although epidemiologic studies proved that a causal relationship exists between elevated serum cholesterol levels and coronary heart disease, it is only recently that cholesterol-lowering strategies have shown significant reductions in total mortality. In the last few years, three landmark coronary artery disease-reduction trials with HMG-coenzyme A reductase inhibitors (statins) showed significant reductions in coronary heart disease and mortality. Statins have beneficial effects on coronary heart disease and overall mortality in primary and secondary prevention, including in women and the elderly. Angiographic studies reveal the potential mechanisms through which statins exert their clinical benefits.
----P Journal_Article Review Review__Tutorial 
----M M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Clinical_Trials_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Human_MeSH M_Simvastatin_MeSH S_therapeutic_use_MeSH Simvastatin_therapeutic_use_MeSH 
****** 9547441
----K E
----T Nebivolol in the treatment of cardiac failure: a double-blind controlled clinical trial.
----A BACKGROUND: Nebivolol is a highly cardioselective long-acting beta-blocker with vasodilating properties, which acts in part via the endothelial L-arginine/nitric oxide pathway. As an antihypertensive drug it is effective in once-daily dosage. Nebivolol has previously been shown to improve left ventricular function in patients with cardiac impairment. METHODS AND RESULTS: This paper reports a double-blind randomized trial comparing, in patients with heart failure, once-daily nebivolol 2.5 or 5.0 mg (initiated in all at 2.5 mg) with placebo on a constant background of digitalis plus diuretic. There was with nebivolol no overall deterioration of cardiac function or cardiac symptoms, and especially not of exercise capacity, in comparison with placebo. One patient on nebivolol 2.5 mg developed hypotension and pulmonary edema, and one patient on nebivolol 5 mg, bradycardia. All the remaining patients continued with unchanged diuretic and digitalis dosage. Nebivolol was accompanied by a trend toward clinical and functional improvement; rather better results were obtained with 2.5 than 5.0 mg. CONCLUSIONS: In view of increasing interest in beta-blockade in heart failure, nebivolol merits further study in this context. The capacity of nebivolol to enhance endothelial nitric oxide production appears potentially attractive.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9551875
----K E
----T Comparison of the angiotensin II receptor antagonist irbesartan with atenolol for treatment of hypertension.
----A In this multicenter, double-blind study, the antihypertensive efficacy and safety of irbesartan were compared with those of atenolol in patients with mild-to-moderate hypertension. Following a 4- to 5-week placebo lead-in period, 231 patients with seated diastolic blood pressure (SeDBP) 95-110 mmHg were randomized to irbesartan 75 mg or atenolol 50 mg once daily for 24 weeks. Doses were doubled at Week 6 for SeDBP > or = 90 mmHg. At Week 12, or anytime thereafter, doses were doubled for SeDBP > or = 90 mmHg if not done at Week 6, and hydrochlorothiazide and then nifedipine were added. Efficacy was determined by change from baseline in blood pressure and by therapeutic response rates. Safety was assessed by monitoring adverse events (AEs). Both treatments significantly lowered blood pressure from baseline. There were no significant differences between treatment groups with respect to blood pressure changes or therapeutic response. Atenolol significantly reduced seated heart rate compared with irbesartan at Week 12. The incidences of serious AEs and discontinuations due to AEs were approximately twice as high in the atenolol group compared with the irbesartan group. Thus, in comparison to atenolol, irbesartan < or = 150 mg provided at least equivalent blood pressure control while demonstrating an excellent safety and tolerability profile.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9551876
----K E
----T A 5-year comparison of doxazosin and atenolol in patients with mild-to-moderate hypertension: effects on blood pressure, serum lipids, and coronary heart disease risk.
----A The long-term efficacy and safety of once-daily treatment with doxazosin or atenolol were compared in a 5-year study in patients with mild-to-moderate hypertension. The study consisted of a 1-year, multicenter, double-blind, parallel-group phase, followed by a 4-year, open-label extension phase. Of the 228 patients enrolled, 100 patients (54/111 doxazosin and 46/117 atenolol) completed the 5-year study. Both treatments were similarly efficacious in controlling blood pressure. As assessed by the Framingham risk equation, which incorporates lipid parameter values, patients receiving doxazosin had significantly less chance of developing coronary heart disease (CHD) within 10 years compared with those patients receiving atenolol (p < 0.05). Doxazosin significantly (p=0.0005) reduced the mean CHD risk from baseline to final visit by 12.3%; whereas, atenolol produced essentially no change in mean risk (0.2% increase). In patients receiving doxazosin, statistically significant (p < 0.05) increases from baseline were observed in serum concentrations of high-density lipoprotein (HDL) cholesterol and the HDL/total cholesterol ratio during the first 2 and 3 years of treatment, respectively. In contrast, significant (p < 0.05) percent reductions from baseline in both these lipid parameters were seen in atenolol-treated patients during most of the 5-year trial. Between-group differences were statistically significant (p < 0.01) at all time points. Decreases in total cholesterol were similar between the two treatment groups. Triglycerides, however, significantly increased with atenolol treatment (p < 0.0001 vs baseline) while remaining essentially unchanged with doxazosin treatment. The safety profiles of doxazosin and atenolol were comparable. Thus, while demonstrating similar antihypertensive efficacy and safety during this 5-year study, once-daily treatment with doxazosin produced a significantly greater beneficial effect on both 10-year CHD risk and serum lipid parameters compared with atenolol.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH 
****** 9554680
----K E
----T Influence of long-term, low-dose, diuretic-based, antihypertensive therapy on glucose, lipid, uric acid, and potassium levels in older men and women with isolated systolic hypertension: The Systolic Hypertension in the Elderly Program. SHEP Cooperative Research Group.
----A BACKGROUND: Previous studies often of short duration have raised concerns that antihypertensive therapy with diuretics and beta-blockers adversely alters levels of other cardiovascular disease risk factors. METHODS: The Systolic Hypertension in the Elderly Program was a community-based, multicenter, randomized, double-blind, placebo-controlled clinical trial of treatment of isolated systolic hypertension in men and women aged 60 years and older. This retrospective analysis evaluated development of diabetes mellitus in all 4736 participants in the Systolic Hypertension in the Elderly Program, including changes in serum chemistry test results in a subgroup for 3 years. Patients were randomized to receive placebo or treatment with active drugs, with the dose increased in stepwise fashion if blood pressure control goals were not attained: step 1, 12.5 mg of chlorthalidone or 25.0 mg of chlorthalidone; and step 2, the addition of 25 mg of atenolol or 50 mg of atenolol or reserpine or matching placebo. RESULTS: After 3 years, the active treatment group had a 13/4 mm Hg greater reduction in systolic and diastolic blood pressure than the placebo group (both groups, P<.001). New cases of diabetes were reported by 8.6% of the participants in the active treatment group and 7.5% of the participants in the placebo group (P=.25). Small effects of active treatment compared with placebo were observed with fasting levels of glucose (+0.20 mmol/L [+3.6 mg/dL]; P<.01), total cholesterol (+0.09 mmol/L [+3.5 mg/dL]; P<.01), high-density lipoprotein cholesterol (-0.02 mmol/L [-0.77 mg/dL]; P<.01) and creatinine (+2.8 micromol/L [+0.03 mg/dL]; P<.001). Larger effects were seen with fasting levels of triglycerides (+0.9 mmol/L [+17 mg/dL]; P<.001), uric acid (+35 micromol/L [+.06 mg/dL]; P<.001), and potassium (-0.3 mmol/L; P<.001). No evidence was found for a subgroup at higher risk of risk factor changes with active treatment. CONCLUSIONS: Antihypertensive therapy with low-dose chlorthalidone (supplemented if necessary) for isolated systolic hypertension lowers blood pressure and its cardiovascular disease complications and has relatively mild effects on other cardiovascular disease risk factor levels.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_pharmacology_MeSH Chlorthalidone_pharmacology_MeSH M_Diuretics__Sulfamyl_MeSH S_administration_&_dosage_MeSH Diuretics__Sulfamyl_administration_&_dosage_MeSH S_pharmacology_MeSH Diuretics__Sulfamyl_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Uric_Acid_MeSH S_blood_MeSH Uric_Acid_blood_MeSH 
****** 9553680
----K 1
----T [Antihypertensive action of various talinolol dosages after four week's treatment in comparison with placebo]
----A The dose dependence of the antihypertensive effect of the beta 1 selective blocker talinolol (CAS 57460-41-0, Cordanum) was investigated in 97 essential hypertensive patients (mild to moderate) using the ambulatory blood pressure monitoring (ABPM) in a single-centre, double-blind, randomized parallel-group study. After 4 weeks of treatment a comparison was made between the once daily administered doses of 50, 100 and 200 mg as well as with placebo. The primary parameter was the mean diastolic blood pressure between 8.00 and 22.00 (dTMW). Furthermore, the duration of action of the once daily administration of 200 mg talinolol was compared with the twice daily application of 100 mg each. With regard to dTMW an increasing antihypertensive effect was determined for the dosage step from 50 mg to 100 mg talinolol/d. No further increase in the blood pressure lowering effect was observed with 200 mg talinolol/d. The highest frequency of therapy responders was found in the 100 mg group with 72.2%. Moreover it could be demonstrated, that within the dosage range of 1 x 100-200 mg Talinolol/d a significant and 24 h lasting reduction of blood pressure and pulse rate was achieved, including the early morning period. There were no differences between the blood pressure profile of the 200 mg group and the 2 x 100 mg group at the end of the 4 weeks treatment. All talinolol dosages investigated in this study were proved to be safe and well tolerated. The observed complaints classified as adverse drug reactions represented typical side effects of beta-blockers of mild to moderate intensity. It can be concluded from the results that the once daily intake of talinolol in the dosage range of 100-200 mg/d shows a reliable efficacy in the treatment of essential hypertension accompanied by a noncritical safety profile.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 9557374
----K 1
----T [A failed improvement in pulmonary function and exercise capacity with carvedilol in congestive heart failure despite an excellent effect on left ventricular function]
----A This study was aimed at investigating in chronic heart failure (CHF) the effects that beta-blockade with carvedilol may have on lung function, and their relationship with left ventricular (LV) performance and peak exercise oxygen uptake (VO2p). CHF causes disturbances in ventilation and pulmonary gas transfer (stress failure of alveolar-capillary membrane) that participate in limiting VO2p. Carvedilol improves LV function and not VO2p. Twenty-one NYHA functional class II-III patients were randomized (2 to 1) to carvedilol (25 mg bid., 14 patients) or placebo (7 patients) for 6 months. Rest forced expiratory volume (FEV1), vital capacity (VC), total lung capacity (TLC), carbon monoxide diffusing capacity (DLCO), its alveolar-capillary membrane component (DM), pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure, EDP), LV diastolic (EDD) and systolic (ESD) dimensions, stroke volume (SV), ejection fraction (EF), fiber shortening velocity (VCF) were measured at baseline and at 3 and 6 months. VO2p, peak ratio of dead space to tidal volume (VD/VTp), ventilatory equivalent for CO2 production (VE/VCO2), VO2 at anaerobic threshold (VO2at) were also determined. FEV1, VC, TLC, DLCO, DM were impaired in CHF compared to 14 volunteers, and did not vary with treatment. Carvedilol reduced EDP, EDD, ESD, and increased EF, SV, VCF, without affecting VO2p, VO2at, VD/VTp, VE/VCO2, at 3 and 6 months. Placebo was ineffective. In CHF, carvedilol exerts neutral effects on ventilation and pulmonary gas transfer and ameliorates LV function at rest. This proves that antifailure treatment may not be similarly effective on cardiac and pulmonary function; and does not contradict the possibility that persistence of lung impairment may contribute to lack of improvement in exercise performance with carvedilol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_English_Abstract_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH S_physiology_MeSH Exercise_Tolerance_physiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Lung_MeSH S_drug_effects_MeSH Lung_drug_effects_MeSH S_physiopathology_MeSH Lung_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Respiratory_Function_Tests_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 10178465
----K E
----T Treatment patterns for heart failure in a primary care environment.
----A Little published information regarding current pharmacotherapeutic treatment patterns for congestive heart failure (CHF) in nonacademic, ambulatory care settings is available. We sought to assess, in a nonacademic primary care environment, pharmacotherapeutic treatment patterns for CHF with respect to consistency with clinical trial evidence and published treatment guideline recommendations. Over an 18-month period, we examined CHF pharmacotherapy using a computerized, integrated clinical diagnoses and prescription database from an outpatient community healthcare center without academic affiliations. We identified adult patients meeting contact criteria and with diagnosis of CHF by International Classification of Diseases (ICD-9-CM) coding and assessed prescribed therapy as well as select comorbid conditions. Drugs of interest included those with known or suspected benefit or detriment and those with unproven benefit. An eligible group of 14,983 patients was identified, from which a cohort of 148 patients with CHF was selected. Forty-one percent of these 148 patients were prescribed an angiotensin converting enzyme (ACE) inhibitor, 34% digoxin, 12% diuretic, 12% hydralazine + nitrate, 20% inhaled beta-agonists, and 66% warfarin. Only 5% of patients were prescribed the combination of an ACE inhibitor, digoxin, and diuretic. Thirty-one percent had a comorbid diagnosis of atrial fibrillation, of whom 44% were prescribed digoxin, 22% diltiazem, 15% beta-blockers, 15% digoxin and diltiazem, 7% digoxin and a beta-blocker, and 33% warfarin. In general, recommended therapies for CHF appeared underutilized in this cohort, whereas those of unclear benefit and potential detriment appeared overutilized. Although these results may not be readily generalized to the entire healthcare system, they do suggest a need for additional analysis and potential intervention.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Drug_Utilization_Review_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_Review_statistics_&_numerical_data_MeSH M_Female_MeSH M_Guideline_Adherence_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_New_England_MeSH M_Physician's_Practice_Patterns_MeSH S_statistics_&_numerical_data_MeSH Physician's_Practice_Patterns_statistics_&_numerical_data_MeSH M_Practice_Guidelines_MeSH M_Primary_Health_Care_MeSH S_standards_MeSH Primary_Health_Care_standards_MeSH 
****** 9562008
----K E
----T Regression of radial artery wall hypertrophy and improvement of carotid artery compliance after long-term antihypertensive treatment in elderly patients.
----A OBJECTIVES: The present study was designed to assess whether a diuretic- or an angiotensin-converting enzyme inhibitor-based treatment can reduce arterial wall hypertrophy of a distal muscular medium-sized artery--the radial artery--and the stiffness of a proximal large elastic artery--the common carotid artery. BACKGROUND: Large-artery wall thickness and stiffness are increased during sustained essential hypertension and contribute to the increased risk of complications. Whether antihypertensive treatment can normalize the wall hypertrophy of conducting arteries has not yet been determined. METHODS: Seventy-seven elderly hypertensive patients were randomized to receive 9 months of double-blind treatment with perindopril (2 to 8 mg/day) or the diuretic combination of hydrochlorothiazide (12.5 to 50 mg/day) plus amiloride (1.25 to 5 mg/day) after a 1-month placebo washout period. If systolic blood pressure remained at >160 mm Hg after 5 months, chlorthalidone or atenolol was added, respectively. Arterial variables, including radial artery mass and common carotid artery compliance, were calculated from noninvasive measurements of internal diameter and wall thickness with the use of high resolution echo-tracking systems at baseline and after 5 and 9 months. RESULTS: During treatment, blood pressure and arterial variables changed to the same extent in both groups. After a 9-month treatment, systolic, diastolic and pulse pressures and radial artery wall thickness, mass and thickness/radius ratio decreased significantly (p < 0.01), whereas carotid compliance increased (p < 0.001). The decrease in radial artery thickness/radius ratio after a 9-month treatment was significantly related to the reduction in pulse pressure (p < 0.01), whereas the improvement in carotid compliance was related to the reduction in mean arterial pressure (p < 0.01). In healthy subjects and untreated hypertensive patients, radial artery diameter, wall thickness and thickness/radius ratio and carotid artery compliance did not change significantly during a 9-month observation period. CONCLUSIONS: These results indicate that in elderly hypertensive patients, both angiotensin-converting enzyme inhibitor- and diuretic combination-based treatments can reduce radial artery wall hypertrophy and improve carotid artery compliance.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Carotid_Artery__Common_MeSH S_pathology_MeSH Carotid_Artery__Common_pathology_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Elasticity_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH M_Radial_Artery_MeSH S_pathology_MeSH Radial_Artery_pathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tunica_Intima_MeSH S_pathology_MeSH Tunica_Intima_pathology_MeSH 
****** 9562649
----K E
----T Hemodynamic performances in patients treated with sotalol after electrical cardioversion of atrial fibrillation.
----A The negative inotropic effect of nearly all antiarrhythmic drugs, especially important in patients with impaired left ventricular function, represents a major drawback of medical therapy. The aim of this study is to evaluate the atrial and ventricular function and the exercise capacity in patients with mild heart failure treated with d,l-sotalol after electrical conversion of atrial fibrillation. The study included patients with persistent atrial fibrillation (for more than 2 weeks but less than 1 year) and mild heart failure (< or = class II NYHA). All patients had comparable basal echocardiographic findings, and received captopril. After successful cardioversion the patients were randomized in two groups: group 1 treated with sotalol (mean dose 240 mg q.d., max. 320 mg) and group 2--without sotalol. The drop-out criterion was the failure to maintain sinus rhythm. Finally, in the study remained 17 patients (10 men, 7 women, aged 41-60 years); group 1 included 10 patients and group 2-7 patients. They were assessed by quantitative echocardiography + Doppler and by standard ecg exercise test at less than 1 month but more than 2 weeks, and at 1, 3, and 6 months. When first evaluated (2 weeks-1 month), peak A wave velocity and atrial filling ratio were higher in group 2 than in group 1 (37 +/- 10 cm/s vs 20 +/- 5 cm/s and 23% +/- 7 vs 13% +/- 5, respectively) and group 1 had also a lower exercise tolerance (80 +/- 25 W vs 110 +/- 10 W). There were no significant differences between groups 1 and 2 in left atrial and left ventricular dimensions, ejection fraction and E wave deceleration time. After 1 month there were no significant differences in Doppler characteristics, echocardiographic parameters and exercise tolerance between the two groups. Group 1 remained at a lower heart rate and had a lower maximal double product (17250 mmHg/min vs 22100 mmHg/min) corresponding to a lower cardiac work. At 3 and 6 months there were no significant changes in all characteristics between the two groups. In conclusion, sotalol seems to be a well tolerated antiarrhythmic agent in patients with mild heart failure, after conversion of persistent atrial fibrillation. In this setting: 1. Sotalol could reversibly amplify the effect of atrial stunning after electrical cardioversion of atrial fibrillation, but this effect is brief. 2. Sotalol has no relevant negative inotropic effect, at least not in association with captopril. 3. Sotalol improves the effort capacity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH S_ultrasonography_MeSH Atrial_Fibrillation_ultrasonography_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler_MeSH S_drug_effects_MeSH Echocardiography__Doppler_drug_effects_MeSH P_Electric_Countershock_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Time_Factors_MeSH 
****** 9563219
----K E
----T Assessment of effects of propranolol on portal hemodynamics in cirrhosis by duplex ultrasonography.
----A OBJECTIVE: To study the effect of propranolol on portal hemodynamics in cirrhotics using duplex ultrasonography. METHODS: Portal venous flow was measured by duplex ultrasonography in 12 healthy volunteers and ten men with cirrhosis. The cirrhotics were evaluated prior to and after ingestion of propranolol (60 mg twice daily for seven days) or placebo in a randomized cross-over fashion. Variations in heart rate, blood pressure, portal vein diameter, and portal venous flow and velocity were evaluated. RESULTS: The mean (SD) portal venous flow in the volunteers was 746 (280) mL/min, portal flow velocity was 18.5 (3.6) cm/s and portal vein diameter was 9.2 (1.4) mm. In cirrhotics, propranolol decreased portal blood flow from 586 (220) to 413 (120) mL/min (p < 0.03), the overall reduction being 29.5%. This effect was due to decrease in portal flow velocity, from 12.5 (3.3) to 9.7 (2.3) cm/s (p < 0.03) without significant change in portal vein diameter. No changes were observed with placebo. CONCLUSIONS: Propranolol decreases portal flow velocity and thus portal venous flow in cirrhotics.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH S_ultrasonography_MeSH Hypertension__Portal_ultrasonography_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_Vein_MeSH S_drug_effects_MeSH Portal_Vein_drug_effects_MeSH S_ultrasonography_MeSH Portal_Vein_ultrasonography_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Random_Allocation_MeSH M_Reproducibility_of_Results_MeSH M_Ultrasonography__Doppler__Duplex_MeSH 
****** 9567598
----K E
----T Effect of antihypertensives on plasma potassium in end stage renal disease: a retrospective study.
----A The antihypertensive drug therapy and the peri-operative plasma potassium trend in end stage renal disease (ESRD) patients undergoing renal transplant were analysed. Out of consecutive 107 live related donor renal transplant, complete data available for 74 patients between June 1991 and March 1993, were entered in proforma and analysed. On the basis of antihypertensive or no antihypertensive drugs prescribed, patients were grouped in 6 categories. Group I patients taking no antihypertensives were taken as control. All patients were comparable for their age, sex, weight, immunosuppressive therapy, anaesthetic and fluid management during surgery. At the time of induction of anaesthesia, patients taking atenolol (plasma K+ levels being 5.34 +/- 0.75 mmol/l in group II and 5.44 +/- 0.63 mmol/l in group III) or captopril (serum K+ level being 5.05 +/- 0.94 mmol/l in group V) in combination with nifedipine and with or without clonidine had significant hyperkalaemia than the patient without antihypertensives (serum K+ level being 4.49 +/- 0.71 mmol/l). Patients, on these two antihypertensives, frequently needed active treatment of alarming hyperkalaemia (blood K+ more than 5 mmol/l and tall 'T' wave in lead II) and cardiac arrhythmias. In conclusion, ESRD patients taking atenolol or captopril are needed to be frequently monitored for blood potassium levels and it would be advisable to avoid these drugs to control hypertension in ESRD patients, especially, when scheduled for renal transplantation.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_blood_MeSH Kidney_Failure__Chronic_blood_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_surgery_MeSH Kidney_Failure__Chronic_surgery_MeSH M_Kidney_Transplantation_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Retrospective_Studies_MeSH 
****** 9570492
----K E
----T Serum levels of excitatory amino acids, serine, glycine, histidine, threonine, taurine, alanine and arginine in treatment-resistant depression: modulation by treatment with antidepressants and prediction of clinical responsivity.
----A Previous research has revealed that major depression is accompanied by disorders in excitatory amino acids, e.g. glutamate and aspartate, and alterations in serum levels of other amino acids, e.g. serine, glycine and taurine. The aim of the present study was to examine serum levels of aspartate, asparagine, glutamate, glutamine, serine, glycine, threonine, histidine, alanine, taurine and arginine in major depression patients with treatment-resistant depression (TRD). No significant differences in the serum concentrations of any of the above amino acids could be found between patients with and without TRD and normal controls. Non-responders to treatment with antidepressants during a period of 5 weeks were characterized by significantly lower serum levels of aspartate, asparagine, serine, threonine and taurine. A 5-week period of treatment with antidepressants significantly reduced the serum levels of aspartate, glutamate and taurine, and significantly increased the serum concentrations of glutamine. The results suggest that alterations in serum levels of aspartate, asparagine, serine, threonine and taurine may predict the subsequent response to treatment with antidepressants, and that the latter may modulate serum levels of excitatory amino acids and taurine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Alanine_MeSH S_blood_MeSH Alanine_blood_MeSH M_Antidepressive_Agents_MeSH S_adverse_effects_MeSH Antidepressive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Antidepressive_Agents__Tricyclic_MeSH S_adverse_effects_MeSH Antidepressive_Agents__Tricyclic_adverse_effects_MeSH S_therapeutic_use_MeSH Antidepressive_Agents__Tricyclic_therapeutic_use_MeSH M_Arginine_MeSH S_blood_MeSH Arginine_blood_MeSH M_Asparagine_MeSH S_blood_MeSH Asparagine_blood_MeSH M_Aspartic_Acid_MeSH S_blood_MeSH Aspartic_Acid_blood_MeSH M_Comparative_Study_MeSH M_Depression__Involutional_MeSH S_blood_MeSH Depression__Involutional_blood_MeSH S_drug_therapy_MeSH Depression__Involutional_drug_therapy_MeSH S_psychology_MeSH Depression__Involutional_psychology_MeSH M_Drug_Resistance_MeSH M_Drug_Therapy__Combination_MeSH M_Excitatory_Amino_Acids_MeSH S_blood_MeSH Excitatory_Amino_Acids_blood_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_adverse_effects_MeSH Fluoxetine_adverse_effects_MeSH S_therapeutic_use_MeSH Fluoxetine_therapeutic_use_MeSH M_Glycine_MeSH S_blood_MeSH Glycine_blood_MeSH M_Histidine_MeSH S_blood_MeSH Histidine_blood_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Personality_Inventory_MeSH M_Pindolol_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Prognosis_MeSH M_Serine_MeSH S_blood_MeSH Serine_blood_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_adverse_effects_MeSH Serotonin_Uptake_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Taurine_MeSH S_blood_MeSH Taurine_blood_MeSH M_Threonine_MeSH S_blood_MeSH Threonine_blood_MeSH M_Trazodone_MeSH S_adverse_effects_MeSH Trazodone_adverse_effects_MeSH S_therapeutic_use_MeSH Trazodone_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9571349
----K E
----T Outcome results of the Fosinopril Versus Amlodipine Cardiovascular Events Randomized Trial (FACET) in patients with hypertension and NIDDM.
----A OBJECTIVE: ACE inhibitors and calcium antagonists may favorably affect serum lipids and glucose metabolism. The primary aim of the Fosinopril Versus Amlodipine Cardiovascular Events Randomized Trial (FACET) was to compare the effects of fosinopril and amlodipine on serum lipids and diabetes control in NIDDM patients with hypertension. Prospectively defined cardiovascular events were assessed as secondary outcomes. RESEARCH DESIGN AND METHODS: Inclusion criteria included a diagnosis of NIDDM and hypertension (systolic blood pressure of > 140 mmHg or diastolic blood pressure of > 90 mmHg). Exclusion criteria included a history of coronary heart disease or stroke, serum creatinine > 1.5 mg/dl, albuminuria > 40 micrograms/min, and use of lipid-lowering drugs, aspirin, or antihypertensive agents other than beta-blockers or diuretics. A total of 380 hypertensive diabetics were randomly assigned to open-label fosinopril (20 mg/day) or amlodipine (10 mg/day) and followed for up to 3.5 years. If blood pressure was not controlled, the other study drug was added. RESULTS: Both treatments were effective in lowering blood pressure. At the end of follow-up, between the two groups there was no significant difference in total serum cholesterol, HDL cholesterol, HbA1c, fasting serum glucose, or plasma insulin. The patients receiving fosinopril had a significantly lower risk of the combined outcome of acute myocardial infarction, stroke, or hospitalized angina than those receiving amlodipine (14/189 vs. 27/191; hazards ratio = 0.49, 95% CI = 0.26-0.95). CONCLUSIONS: Fosinopril and amlodipine had similar effects on biochemical measures, but the patients randomized to fosinopril had a significantly lower risk of major vascular events, compared with the patients randomized to amlodipine.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_analysis_MeSH Fibrinogen_analysis_MeSH M_Follow-Up_Studies_MeSH M_Fosinopril_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_analysis_MeSH Hemoglobin_A__Glycosylated_analysis_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9571355
----K E
----T Effects of perindopril and carvedilol on endothelium-dependent vascular functions in patients with diabetes and hypertension.
----A OBJECTIVE: To compare the effects of the ACE inhibitor perindopril and the beta-blocker carvedilol on blood pressure and endothelial functions in NIDDM patients with hypertension. RESEARCH DESIGN AND METHODS: We conducted a double-blind randomized trial in 26 patients with NIDDM and mild hypertension. A 4-week run-in placebo period preceded the active 12-week treatment with perindopril (4-8 mg daily) or carvedilol (25-50 mg daily). Endothelial functions were assessed by evaluating the hemodynamic (mean blood pressure, leg blood flow) and rheological (platelet aggregation, blood viscosity, and blood filterability) responses to an intravenous bolus of 3 g L-arginine, the natural precursor of nitric oxide. RESULTS: Both perindopril and carvedilol significantly reduced mean blood pressure (P < 0.001) and increased leg blood flow (P < 0.05) to the same extent; blood filterability remained unchanged in both perindopril- and carvedilol-treated groups. Carvedilol reduced platelet aggregation and blood viscosity significantly (P < 0.05) but perindopril did not. Before treatment, the hemodynamic and rheologic responses to L-arginine were significantly lower in patients (P < 0.05-0.01) than in 20 nondiabetic nonhypertensive control subjects. After 12 weeks of treatment, both drugs normalized the hemodynamic responses to L-arginine. Platelet aggregation response to L-arginine was ameliorated by carvedilol and remained unchanged in the perindopril group. CONCLUSIONS: At the doses used, both drugs effectively reduce blood pressure and normalize the hemodynamic responses to L-arginine. The implications of the ameliorated endothelial function for the poor cardiovascular outlook of the NIDDM hypertensive patient need further assessment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arginine_MeSH S_diagnostic_use_MeSH Arginine_diagnostic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Viscosity_MeSH S_drug_effects_MeSH Blood_Viscosity_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiology_MeSH Endothelium__Vascular_physiology_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Leg_MeSH S_blood_supply_MeSH Leg_blood_supply_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH M_Platelet_Aggregation_MeSH S_drug_effects_MeSH Platelet_Aggregation_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Reference_Values_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Rheology_MeSH S_drug_effects_MeSH Rheology_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 9575602
----K E
----T The occurrence of Raynaud's phenomenon in a general population: the Framingham Study.
----A The prevalence and predisposing conditions for primary and secondary Raynaud's phenomenon (RP) were examined in The Framingham Study based on 16 years of follow-up of a cohort of 4182 men and women. The association with atypical chest pain and migraine headache was also investigated. Over the 16 years of follow-up there were 130 men and 171 women who developed primary RP. The prevalence in women (9.6%) was somewhat higher than in men (8.1%) and 81.4% of the RP was primary. Secondary RP was equally prevalent in men (18.6%) and women (19.7%). The most common causes of secondary RP were beta-blocker use (34.2%), carpal tunnel syndrome (10.5%) and rheumatoid arthritis (7.2%). Primary RP cases differed from noncases by having lower systolic blood pressure (p < or = 0.001) and diastolic blood pressure (p < 0.0001), and more coronary disease (p = 0.009), smoking (p < or = 0.01) and higher blood sugars (p < or = 0.009). Atypical chest pain was present more often than noted previously in The Framingham Study general population survey, and was equally prevalent in primary and secondary RP and in the two sexes. Associated migraine was more prevalent in women (14.4%) than men (5.0%). Vibrating tool use with associated RP occurred in 14.6%.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Arthritis__Rheumatoid_MeSH S_complications_MeSH Arthritis__Rheumatoid_complications_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH M_Carpal_Tunnel_Syndrome_MeSH S_complications_MeSH Carpal_Tunnel_Syndrome_complications_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Massachusetts_MeSH S_epidemiology_MeSH Massachusetts_epidemiology_MeSH M_Middle_Aged_MeSH M_Raynaud_Disease_MeSH S_epidemiology_MeSH Raynaud_Disease_epidemiology_MeSH S_etiology_MeSH Raynaud_Disease_etiology_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Vibration_MeSH S_adverse_effects_MeSH Vibration_adverse_effects_MeSH 
****** 9581729
----K E
----T Combined oral positive inotropic and beta-blocker therapy for treatment of refractory class IV heart failure.
----A OBJECTIVES: We sought to assess the effects of combined oral positive inotropic and beta-blocker therapy in patients with severe heart failure. BACKGROUND: Patients with severe, class IV heart failure who receive standard medical therapy exhibit a 1-year mortality rate >50%. Moreover, such patients generally do not tolerate beta-blockade, a promising new therapy for chronic heart failure. Positive inotropes, including phosphodiesterase inhibitors, are associated with increased mortality when administered over the long term in these patients. The addition of a beta-blocker to positive inotropic therapy might attenuate this adverse effect, although long-term oral inotropic therapy might serve as a bridge to beta-blockade. METHODS: Thirty patients with severe heart failure (left ventricular ejection fraction [LVEF] 17.2+/-1.2%, cardiac index 1.6+/-0.1 liter/min per m2) were treated with the combination of oral enoximone (a phosphodiesterase inhibitor) and oral metoprolol at two institutions. Enoximone was given at a dose of < or = 1 mg/kg body weight three times a day. After clinical stabilization, metoprolol was initiated at 6.25 mg twice a day and slowly titrated up to a target dose of 100 to 200 mg/day. RESULTS: Ninety-six percent of the patients tolerated enoximone, whereas 80% tolerated the addition of metoprolol. The mean duration of combination therapy was 9.4+/-1.8 months. The mean length of follow-up was 20.9+/-3.9 months. Of the 23 patients receiving the combination therapy, 48% were weaned off enoximone over the long term. The LVEF increased significantly, from 17.7+/-1.6% to 27.6+/-3.4% (p=0.01), whereas the New York Heart Association functional class improved from 4+/-0 to 2.8+/-0.1 (p=0.0001). The number of hospital admissions tended to decrease during therapy (p=0.06). The estimated probability of survival at 1 year was 81+/-9%. Heart transplantation was performed successfully in nine patients (30%). CONCLUSIONS: Combination therapy with a positive inotrope and a beta-blocker appears to be useful in the treatment of severe, class IV heart failure. It may be used as a palliative measure when transplantation is not an option or as a bridge to heart transplantation. Further study of this form of combined therapy is warranted.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_pharmacology_MeSH Cardiotonic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Enoximone_MeSH S_pharmacology_MeSH Enoximone_pharmacology_MeSH S_therapeutic_use_MeSH Enoximone_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Phosphodiesterase_Inhibitors_MeSH S_pharmacology_MeSH Phosphodiesterase_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Phosphodiesterase_Inhibitors_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9585392
----K I
----T Which drugs benefit diabetic patients for secondary prevention of myocardial infarction? DARTS/MEMO Collaboration.
----A Diabetic patients have increased mortality following myocardial infarction. We review the evidence for benefit in diabetic patients, of the major drug groups used as secondary prevention. Beta blockers: meta-analyses suggest a reduction in mortality of 35% with beta blockers. Diabetic patients should receive beta blockers post myocardial infarction. In many patients, the benefits of beta blockers will outweigh relative contraindications. Aspirin: meta-analyses of antiplatelet therapy in high-risk subjects have shown substantial benefits. Aspirin should be prescribed for secondary prevention. Lipid lowering with statins: subgroup analyses of the major secondary prevention trials show substantial benefits across a wide range of baseline cholesterol and LDL levels. These drugs should be prescribed as secondary prevention to patients with diabetes whose total cholesterol is > 4.0 mmol(-1). Angiotensin converting enzyme inhibitors (ACEIs): the few subgroup analyses that exist from ACEI trials suggest that diabetic and non-diabetic patients derive similar benefits. Diabetic subjects who have systolic dysfunction after myocardial infarction should receive ACEIs. Treatment combination: data exist to suggest that most of these drugs produce benefit independently. Conclusion: diabetic patients benefit from secondary prevention with drug treatment as much as, or more than, non-diabetic patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Simvastatin_MeSH S_therapeutic_use_MeSH Simvastatin_therapeutic_use_MeSH 
****** 9591892
----K E
----T Value of the addition of amlodipine to atenolol in patients with angina pectoris despite adequate beta blockade.
----A Anginal patients who remain symptomatic despite optimally dosed beta blockade may also be given dihydropyridine calcium antagonists. This treatment regimen was examined in a double-blind parallel, randomized, controlled study in 147 patients with angina and positive bicycle exercise tests despite optimal beta blockade with atenolol (heart rate at rest <60 beats/min). Patients were randomized to atenolol and/or placebo (control), and atenolol and/or amlodipine. The main outcome measurement was exercise tolerance after 8 weeks compared with baseline. After 8 weeks, no significant differences in time to 0.1-mV ST-segment depression, time to chest pain, and time to end of exercise were observed. The number of patients with chest pain during exercise decreased significantly in the amlodipine group (p = 0.04 vs controls). The subgroup of patients with an early (<6 minutes) onset of chest pain at baseline showed a significant increase in time to chest pain after amlodipine (p = 0.0001 vs controls). In the amlodipine group, ST depression and rate-pressure product at submaximum comparable workload decreased to 0.4 mm (0.56) (p = 0.03 vs controls) and 1.223 (2.652) beats/ min x mm Hg (p = 0.01 vs controls). The number of patients in each group with adverse events was not different. The addition of amlodipine to the treatment of patients with myocardial ischemia, despite optimal beta blockade, is well tolerated and may lead to improvement in symptomatic anginal patients, who have a rapid onset of exercise-induced ischemia.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9591893
----K E
----T Amlodipine versus diltiazem as additional antianginal treatment to atenolol. Centralised European Studies in Angina Research (CESAR) Investigators.
----A The antianginal efficacy and tolerability of amlodipine and diltiazem were compared in a double-blind randomized trial of 97 patients with angina resistant to atenolol alone. Both amlodipine and diltiazem significantly reduced the frequency of angina attacks (p <0.001) and glyceryl trinitrate consumption (p <0.05 to p <0.01). During Holter monitoring, both treatments reduced the overall frequency of ambulatory myocardial ischemia, although changes did not reach statistical significance. Exercise test parameters (total exercise time, time to angina, time to ST depression, and maximum ST depression) tended to improve with both treatments, but changes did not achieve statistical significance relative to baseline or to each other. Both drugs were generally well tolerated. Adverse events occurred in 15 patients in the amlodipine group (30%) and in 17 patients in the diltiazem group (36%), but patients taking diltiazem reported almost twice as many adverse events (30) patients taking amlodipine (18). Quality of life, as assessed by total Nottingham Health Profile Scores, was not significantly different between treatments. The addition of either once-daily amlodipine or twice-daily sustained release diltiazem improved symptoms in patients with angina resistant to atenolol alone, but diltiazem was associated with more frequent and more serious adverse events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9591916
----K E
----T Effects of carvedilol on right ventricular function in chronic heart failure.
----A This study investigated the effects of carvedilol on right ventricular (RV) volume and systolic function in chronic heart failure patients. Carvedilol treatment resulted in a significant improvement of RV ejection fraction and systolic performance, which paralleled the improvement of systolic function demonstrated in the left ventricle.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Right_MeSH S_physiology_MeSH Ventricular_Function__Right_physiology_MeSH 
****** 9593066
----K E
----T Effects of doxazosin and atenolol on atherothrombogenic risk profile in hypertensive middle-aged men.
----A The alpha-blockers prazosin and doxazosin reduce hypertriglyceridemia (HTG) and increase serum levels of high-density lipoprotein (HDL)-cholesterol, whereas beta-blockers such as atenolol have the opposite effect. As HTG is associated with reduced fibrinolysis and hypercoagulability, we investigated the effects of doxazosin and atenolol on serum lipids and hemostatic factors in hypertensive men with an atherothrombogenic risk profile. The study was randomized and open, but blinded to investigator of biochemical results. Forty-five men (mean age, 44.5 years) with central obesity [median body-mass index (BMI), 28 kg/m2] and moderate hypertension [median diastolic blood pressure (DBP), 104.5 mm Hg] were treated with atenolol (n = 22) or doxazosin (n = 23) for 22 weeks, after which changes in between-group differences from baseline were estimated. After intervention, significant between-group differences in favor of doxazosin were found: lower triglycerides (p = 0.008) and higher HDL cholesterol (p = 0.036); furthermore, improvement of fibrinolysis: lower plasminogen activator inhibitor-1 (PAI-1) activity (p = 0.012), higher tissue plasminogen activator (tPA) activity after venous occlusion (VO); and higher levels of serum D-dimer, both unstimulated (p = 0.0016) and after VO (p = 0.0032). In addition, lower levels of serum testosterone were found in the atenolol group (p = 0.0016). A profile with reduced HTG, increased HDL cholesterol, and improved fibrinolysis was obtained with doxazosin when compared with atenolol. Furthermore, the observed decrease in serum testosterone on atenolol treatment would rather favor long-term treatment with doxazosin in this study population.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Female_MeSH M_Fibrinolysis_MeSH S_drug_effects_MeSH Fibrinolysis_drug_effects_MeSH M_Gonadal_Steroid_Hormones_MeSH S_blood_MeSH Gonadal_Steroid_Hormones_blood_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_metabolism_MeSH Hyperlipidemia_metabolism_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_metabolism_MeSH Lipoproteins__HDL_Cholesterol_metabolism_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Plasminogen_Activators_MeSH S_metabolism_MeSH Plasminogen_Activators_metabolism_MeSH 
****** 9593558
----K E
----T Prospective study of calcium channel blocker use, cardiovascular disease, and total mortality among hypertensive women: the Nurses' Health Study.
----A BACKGROUND: In several observational studies, patients prescribed calcium channel blockers had higher risks of cardiovascular diseases and mortality than those prescribed other antihypertensive medications. We explored these associations in the Nurses' Health Study. METHODS AND RESULTS: A total of 14 617 women who reported hypertension and regular use of diuretics, beta-blockers, calcium channel blockers, ACE inhibitors, or a combination in 1988 were included in the analyses. Cardiovascular events and deaths were ascertained through May 1, 1994. We documented 234 cases of myocardial infarction. Calcium channel blocker monodrug users had an age-adjusted relative risk (RR) of myocardial infarction of 2.36 (95% CI, 1.43 to 3.91) compared with those prescribed thiazide diuretics. Women prescribed calcium channel blockers had a higher prevalence of ischemic heart disease. After adjustment for these and other coronary risk factors, the RR was 1.64 (95% CI, 0.97 to 2.77). Comparing the use of any calcium channel blocker (monodrug and multidrug users) with that of any other antihypertensive agent, the adjusted RR was 1.42 (95% CI, 1.01 to 2.01). An association between calcium channel blocker use and myocardial infarction was apparent among women who had ever smoked cigarettes (covariate-adjusted RR, 1.81; 95% CI, 1.20 to 2.72) but not among never-smokers (RR, 0.94; 95% CI, 0.48 to 1.84). CONCLUSIONS: In analyses adjusted only for age, we found a significant elevation in RR of total myocardial infarction among women who used calcium channel blockers compared with those who did not. After adjustment for comorbidity and other covariates, the RR was reduced. Whether the remaining observed elevated risk is real, or a result of residual confounding by indication, or chance, or a combination of the above cannot be evaluated with certainty on the basis of these observational data.
----P Journal_Article 
----M M_Adult_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Nursing_Staff_MeSH M_Prospective_Studies_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Analysis_MeSH 
****** 9595254
----K I
----T Toward improved antihypertensive therapy with calcium channel blockers.
----A Outcome trials are the scientific method of determining if an antihypertensive agent really works; and for a therapy to work well, it should reduce mortality. The FDA requires only that blood pressure be controlled safely, but current evidence-based medicine demands answers to the mortality/morbidity question. We need this outcome trial information on all the classes of antihypertensives, including calcium channel blockers. For example, we often rely on surrogate endpoints such as control of blood pressure or control of PVCs. If we treat hypertensives with PVCs using beta-blockers or calcium channel blockers, we may see both control of blood pressure and suppression of PVCs. However, as we learned from the CAST trial with flecainide and encainide, PVCs can be controlled, but mortality may increase. On the other hand, the Lewis trial demonstrated that captopril, an ACE inhibitor, reduced proteinuria, which is another surrogate endpoint in diabetic hypertensives with nephropathy, although blood pressure was controlled with diuretic and conventional therapy. Importantly, captopril also reduced morbidity and mortality without influencing blood pressure. Unfortunately, there are no outcome trials measuring mortality endpoints for most of the antihypertensive agents in use today, especially in patients with uncomplicated hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_African_Continental_Ancestry_Group_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Clinical_Trials_MeSH M_Cohort_Studies_MeSH M_Drug_Delivery_Systems_MeSH M_European_Continental_Ancestry_Group_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 9599555
----K E
----T [Do cardioselective beta-antagonists block the cardiac beta-receptor function also in the long run?]
----A As the human cardiomyocyte expresses both beta 1 and beta 2 adrenoceptors it is to be expected that the inhibition of one species of receptors can be counteracted by the other. This hypothesis was tested in 40 middle-aged men scheduled for coronary artery bypass surgery. Half the patients had been treated with cardioselective beta 1 antagonists for more than three months while the 20 control patients had never been beta-blocked. The haemodynamic status after induction of a standardized fentanyl/midazolam anaesthesia and the sensitivity of the cardiovascular beta-adrenoceptors to isoprenaline titration were similar in both groups. In conclusion, patients chronically treated with cardioselective beta 1-blockers compensate for the perturbation to such a degree that their cardiovascular function is indistinguishable from patients who have never received beta-blockers.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH M_English_Abstract_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Isoproterenol_MeSH S_administration_&_dosage_MeSH Isoproterenol_administration_&_dosage_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Receptors__Adrenergic__beta_MeSH S_drug_effects_MeSH Receptors__Adrenergic__beta_drug_effects_MeSH M_Time_Factors_MeSH 
****** 9605783
----K E
----T Elderly patients receive less aggressive medical and invasive management of unstable angina: potential impact of practice guidelines.
----A BACKGROUND: The Agency for Health Care Policy and Research (AHCPR) released a practice guideline on the diagnosis and management of unstable angina in 1994. OBJECTIVE: To examine practice variation across the age spectrum in the management of patients hospitalized with unstable angina 2 years before release of the AHCPR guideline. DESIGN: Retrospective cohort. SETTING: Urban academic hospital. PATIENTS: All nonreferral patients diagnosed as having unstable angina who were hospitalized directly from the emergency department to the intensive care or telemetry unit between October 1, 1991, and September 30, 1992. MEASUREMENTS: Percentage of eligible patients receiving medical treatment concordant with 8 important AHCPR guideline recommendations. RESULTS: Half of the 280 patients were older than 66 years; women were older than men on average (70 vs 64 years; P<.001). After excluding those with contraindications to therapy, patients in the oldest quartile (age, 75.20-93.37 years) were less likely than younger patients to receive aspirin (P<.009), beta-blockers (P<.04), and referral for cardiac catheterization (P<.001). Overall guideline concordance weighted for the number of eligible patients declined with increasing age (87.4%, 87.4%, 84.0%, and 74.9% for age quartiles 1 to 4, respectively; chi2, P<.001). Increasing age, the presence of congestive heart failure at presentation, a history of congestive heart failure, previous myocardial infarction, increasing comorbidity, and elevated creatinine concentration were associated with care that was less concordant with AHCPR guideline recommendations; only age and congestive heart failure at presentation remained significant in the multivariate analysis (odds ratios, 1.28 per decade [95% confidence interval, 1.02-1.61] and 3.16 [95% confidence interval, 1.57-6.36], respectively). CONCLUSIONS: Older patients were less likely to receive standard therapies for unstable angina before release of the 1994 AHCPR guideline. Patients presenting with congestive heart failure also received care that was more discordant with guideline recommendations. The AHCPR guideline allows identification of patients who receive nonstandard care and, if applied to those patients with the greatest likelihood to benefit, could lead to improved health care delivery.
----P Journal_Article 
----M P_Age_Factors_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_complications_MeSH Angina__Unstable_complications_MeSH S_diagnosis_MeSH Angina__Unstable_diagnosis_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH P_Patient_Selection_MeSH P_Physician's_Practice_Patterns_MeSH M_Practice_Guidelines_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Withholding_Treatment_MeSH 
****** 9607389
----K E
----T Insulin receptor number in arterial hypertension: response to treatment with fosinopril or atenolol.
----A Human insulin receptor (hINR) number and its response to medical treatment was evaluated in 14 male controls and 40 male hypertensive patients. Twenty patients treated with fosinopril (10 to 20 mg daily orally) comprised Group A and 20 treated with atenolol (25 to 50 mg daily orally) Group B. The hINR number (receptors x 10(3)/red cell) was greater in controls compared to untreated patients (8.22+/-2.4 v 5.53+/-1.27, P < .001). After 6 months of treatment the hINR number increased in Group A (5.73+/-1.47 v 7.5+/-2.06, P < .001) and remained unchanged (5.35+/-1.09 v 5.5+/-1.31, P = NS) in Group B. Thus, hINR number is decreased in hypertension and, in contrast to atenolol, fosinopril treatment is associated with an increase in hINR number, suggesting a favorable effect on glucose metabolism.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Fosinopril_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptor__Insulin_MeSH S_drug_effects_MeSH Receptor__Insulin_drug_effects_MeSH S_metabolism_MeSH Receptor__Insulin_metabolism_MeSH M_Reference_Values_MeSH M_Treatment_Outcome_MeSH 
****** 9607690
----K E
----T Can heart rate predict blood pressure response to anti-hypertensive drug therapy?
----A The use of heart rate in clinical practice is limited by its variability under measurement situations. The mean heart rate on ambulatory monitoring provides a more robust statistic for clinical use. We examined the relationship between mean heart rate on initial referral ambulatory blood pressure monitoring (ABPM) to the BP-lowering efficacy of the four main groups of anti-hypertensive medications, in a referral hypertensive population. Patients were retrospectively identified by review of the BP database, and data collected from the initial referral BP monitor off medication, and the subsequent ABPM after treatment with either beta-blockers, diuretics, calcium antagonists or angiotensin-converting enzyme (ACE) inhibitors. The change in mean arterial BP from the initial to the subsequent ABPM (ie, as a result of treatment) was correlated with the mean heart rate on the initial ABPM. A moderate association was found for initial daytime heart rate and BP response to beta-blockers (r = 0.24, P = 0.02), and ACE inhibitors (r = 0.14, P = 0.05). No such association was found for calcium antagonists or diuretics. When the groups were divided into those with a mean daytime heart rate <75 and > or =75 beats per min, BP reduction from beta-blocker and ACE inhibitor therapy was significantly greater in those patients with a higher daytime heart rate. We conclude that average daytime heart rate on pre-treatment ABPM can be useful as a predictor of BP response to beta-blockade or ACE inhibition.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Forecasting_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9617599
----K E
----T Moexipril. A review of its use in the management of essential hypertension.
----A Moexipril is a prodrug which is hydrolysed after oral administration to its active metabolite moexiprilat, an inhibitor of the angiotensin converting enzyme (ACE). Once daily administration of moexipril 7.5 or 15 mg effectively reduces blood pressure in patients with essential hypertension (including the elderly and postmenopausal women with this condition). In double-blind randomised comparative studies, moexipril 7.5 to 15 mg once daily showed similar efficacy to other antihypertensive agents, including captopril, hydrochlorothiazide, atenolol, metoprolol, sustained release verapamil and nitrendipine. Combined therapy with hydrochlorothiazide and moexipril had a significantly greater antihypertensive effect than either agent alone. Moexipril is well tolerated by the majority of patients and compares well in this respect with other antihypertensive agents. Its tolerability profile appears to be characteristic of ACE inhibitors as a class (the most common adverse events being headache, symptoms of upper respiratory tract infection and cough). Moexipril generally had no clinically significant effect on lipid, glucose or electrolyte metabolism or haematological parameters, and, in particular, it was not associated with any significant changes in lipid or glucose metabolism in postmenopausal women (with or without hormone replacement therapy). CONCLUSIONS: Once daily moexipril is a useful agent for the treatment of essential hypertension, which compares well with currently available options in terms of clinical efficacy and tolerability. In addition, clinical experience to date supports its use in postmenopausal women.
----P Journal_Article Review Review__Tutorial 
----M M_Age_Factors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isoquinolines_MeSH S_pharmacokinetics_MeSH Isoquinolines_pharmacokinetics_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Male_MeSH M_Prodrugs_MeSH S_pharmacokinetics_MeSH Prodrugs_pharmacokinetics_MeSH S_therapeutic_use_MeSH Prodrugs_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 9622282
----K I
----T Effects of a cardioselective beta-blocker on postprandial triglyceride-rich lipoproteins, low density lipoprotein particle size and glucose-insulin homeostasis in middle-aged men with modestly increased cardiovascular risk.
----A Beta-adrenergic receptor-blocking agents are commonly used for treatment of hypertension, angina pectoris and arrhythmias and as secondary prevention after myocardial infarction. The modest protection against myocardial infarction conferred by these compounds in primary-preventive studies has suggested that beneficial effects of beta-blockade are counteracted by known adverse influences on lipid and glucose metabolism. As most beta-blockers increase plasma triglycerides and decrease the high density lipoprotein (HDL) cholesterol concentration, a randomized, double-blind, cross-over study was conducted to evaluate whether a 12-week treatment with metoprolol (100 mg o.d.) or placebo affected the metabolism of postprandial triglyceride-rich lipoproteins in 15 middle-aged men with a modestly increased cardiovascular risk. Metoprolol treatment significantly increased the postprandial responses of very low density lipoprotein (VLDL) and VLDL remnants to a mixed meal-type of oral fat tolerance test. The effect was particularly prominent for larger (Svedberg flotation rate (Sf) > 400 and Sf 60-400) particle species (P < 0.001 in repeated measures ANOVA), whereas the smaller (Sf 20-60) particles were less affected (P < 0.05). The changes in the postprandial responses of the different VLDL species were mainly related to an effect on the fasting plasma concentrations, with limited or no influences on VLDL catabolism during the postprandial state. In contrast, metoprolol treatment did not significantly influence the postprandial responses of chylomicrons and chylomicron remnants. Notably, the enhanced fasting and postprandial triglyceridaemia during metoprolol treatment was neither accompanied by a rise in fasting or postprandial free fatty acid concentrations, nor by alterations of the glucose and insulin responses to a standard oral glucose challenge. The ensuing shift in the LDL particle size distribution towards smaller particles was limited (fraction small LDL: metoprolol 22.8 +/- 15.7% versus placebo 19.3 +/- 15.0%, P < 0.05). In conclusion, metoprolol treatment primarily enhances fasting and postprandial triglyceridaemia in middle-aged men by increasing the basal hepatic production of VLDL.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Apolipoproteins_B_MeSH S_blood_MeSH Apolipoproteins_B_blood_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Cardiovascular_Diseases_MeSH S_blood_MeSH Cardiovascular_Diseases_blood_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH M_Chylomicrons_MeSH S_blood_MeSH Chylomicrons_blood_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Fatty_Acids__Nonesterified_MeSH S_blood_MeSH Fatty_Acids__Nonesterified_blood_MeSH M_Follow-Up_Studies_MeSH M_Homeostasis_MeSH M_Human_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Lipoproteins__LDL_MeSH S_blood_MeSH Lipoproteins__LDL_blood_MeSH M_Lipoproteins__VLDL_MeSH S_blood_MeSH Lipoproteins__VLDL_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Postprandial_Period_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 9623012
----K E
----T Short-term effects of atenolol in patients with dilated cardiomyopathy.
----A Dilated cardiomyopathy is a common cause of heart failure with systolic dysfunction. Medications used to treat this condition are usually for symptomatic relief. We studied the effect of atenolol in heart failure caused by dilated cardiomyopathy in a double blinded randomized fashion. There were 17 males and 5 females. All patients underwent right and left heart catheterization, coronary angiography, endomyocardial biopsy, exercise testing and doppler echocardiography. By 3 months, atenolol significantly reduced resting and exercise heart rate and pulmonary capillary wedge pressure. There was no difference in exercise capacity. We conclude from this study that atenolol improve hemodynamic condition in patients with dilated cardiomyopathy without improving exercise capacity during this short observation period.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Chi-Square_Distribution_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pulmonary_Wedge_Pressure_MeSH S_drug_effects_MeSH Pulmonary_Wedge_Pressure_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9626844
----K E
----T Circadian blood pressure changes and myocardial ischemia in hypertensive patients with coronary artery disease.
----A OBJECTIVES: We sought to evaluate whether different circadian blood pressure (BP) changes could influence the occurrence of ischemic episodes in untreated and treated hypertensive patients with stable coronary artery disease (CAD). BACKGROUND: In hypertensive patients with CAD the occurrence of myocardial ischemia could be influenced by either high or low BP values. Ambulatory monitoring has shown that circadian BP profile is not uniform in hypertensive patients. METHODS: Twenty-one patients with a nighttime BP fall < 10% ("nondippers"), 35 with a nighttime BP fall between > 10% and < 20% ("dippers") and 14 with a nighttime BP fall > 20% ("overdippers") with CAD underwent simultaneous ambulatory BP and electrocardiographic monitoring before and during drug therapy with nitrates and atenolol or verapamil in a prospective, randomized, open, blinded end point design. RESULTS: Daytime BP was not significantly different among the groups both before and during therapy. Nighttime BP was different by definition. Treatment significantly reduced BP values in each group (p < 0.05). Daytime ischemic episodes did not differ among the groups either before or during therapy. Drug therapy significantly reduced daytime ischemia (p < 0.05). In untreated patients, nighttime ischemia was more frequent in nondippers than in dippers and overdippers (p < 0.05). Drug therapy significantly reduced nocturnal ischemia in nondippers (p < 0.05), had no significant effect in dippers and significantly increased nighttime ischemia in overdippers (p < 0.05). During treatment, nighttime ischemia was more frequent in overdippers than in dippers and nondippers (p < 0.05). The same results were achieved when ischemic episodes were defined with more restrictive criteria (ST segment depression > or = 2 mm). CONCLUSIONS: Circadian BP changes can influence the occurrence of myocardial ischemia in untreated and treated hypertensive patients with CAD. Nocturnal ischemia was found to be more frequent in nondippers among untreated patients and in overdippers among treated patients, potentially suggesting different therapeutic approaches based on circadian BP profile.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH M_Prospective_Studies_MeSH M_Statistics__Nonparametric_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9630111
----K E
----T Coronary artery disease in diabetic and nondiabetic patients with lower extremity arterial disease: A report from the Coronary Artery Surgery Study Registry.
----A OBJECTIVE: Patients with lower extremity arterial disease (LEAD) are at an increased risk of having coronary artery disease (CAD). Diabetics are at especially high risk for having LEAD with concomitant CAD. This study was undertaken (1) to define the clinical and arteriographic features associated with CAD among diabetics and nondiabetics with LEAD and (2) to determine the long-term survival and predictors of mortality of diabetics and nondiabetics with LEAD and CAD. RESEARCH DESIGN AND METHODS: Two hundred sixty-three diabetics and 1137 nondiabetics from the Coronary Artery Surgery Study who had evidence of LEAD, who were 50 years and older, and who had arteriographically proven CAD were monitored for a mean of 12.8 years. RESULTS: Among all the subjects with LEAD there was a high prevalence of current and past smoking, history of previous myocardial infarction, systemic hypertension, congestive heart failure, high degrees of angina pectoris and unstable angina pectoris, and use of beta-blockers. On arteriographic evaluation a high prevalence of three-vessel epicardial coronary disease and involvement of multiple coronary segments with > or =50% diameter narrowing was found. Multivariate analysis showed the number of coronary segments with >50% occlusion, the presence of cerebrovascular disease, the use of digitalis, and elevated systolic blood pressure were independently associated with diabetes. On follow-up diabetics had a significantly higher mortality rate (mostly cardiac) than nondiabetics: median survival, 8.1 years and 12.7 years, respectively. At 15 years the mortality rates were 77.1% and 62.0%, respectively. On multivariate analysis, age, number of coronary occlusions, number of significantly narrowed epicardial arteries, diminished myocardial contractility, hypertension, and smoking were significant predictors of mortality in the total group and in each subgroup. Coronary artery bypass grafting surgery was protective. The presence of diabetes was an independent risk factor for mortality. CONCLUSIONS: The presence of LEAD is associated with multivessel epicardial and multiple coronary segment occlusion. On long-term follow-up there is a high mortality rate. In patients with LEAD and diabetes, CAD is especially severe and prognosis is poor.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH M_Arterial_Occlusive_Diseases_MeSH S_complications_MeSH Arterial_Occlusive_Diseases_complications_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Leg_MeSH S_blood_supply_MeSH Leg_blood_supply_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Registries_MeSH M_Smoking_MeSH M_Survival_Rate_MeSH 
****** 9629401
----K I
----T Propranolol vs flunarizine vs flunarizine plus propranolol in migraine without aura prophylaxis. A double-blind trial.
----A Fourty-five migraine without aura patients underwent a parallel double-blind trial aiming the comparison of the effects of propranolol 60 mg/day to flunarizine 10 mg/day and to propranolol 60 mg/day plus flunarizine 10 mg/day simultaneously. There were 3 groups, each one with 15 patients. After a 20-day-baseline period, each group received one kind of treatment during 120 days. Migraine index on propranolol was 23.4*, on flunarizine 18.7* and on both drugs 14.4*, mean frequency of attacks on propranolol was 1.26**, on flunarizine 1.2** and on both drugs 1.13** (*p < 0.05, **p < 0.01 compared to baseline) and global evaluation was reduced with all forms of treatment. It was not found statistical differences between groups, nevertheless there was a trend in the group using two drugs reaching lower values in migraine index, frequency of attacks and global evaluation. In individuals using flunarizine (alone or associated with propranolol) the therapeutic effect was largely maintained up to 45 days after drug withdrawal.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_1-Propanol_MeSH S_therapeutic_use_MeSH 1-Propanol_therapeutic_use_MeSH M_Adolescent_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Flunarizine_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9629648
----K E
----T Clinical trial designs based on sequential conditional probability ratio tests and reverse stochastic curtailing.
----A We propose a group sequential method based on the sequential conditional probability ratio test and show that it has the conservatism desired in practice. We also propose calculating the discordant probability, that is, the probability that the sequential test concludes differently from a fixed-sample test at the planned end of the trial, recognizing that this probability could be substantial, even if the sequential test has the same size and power as the fixed-sample size test at the planned end of the study. In addition, we show that the proposed method can be used as a stochastic curtailing tool. Thus, the method accommodates unplanned interim analyses as well as those deemed necessary based on data trends, virtually without inflating the type I error, but it is less conservative than the usual stochastic curtailing. The method is implemented through an interactive computer program.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Biometry_MeSH S_methods_MeSH Biometry_methods_MeSH M_Clinical_Trials_MeSH S_methods_MeSH Clinical_Trials_methods_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Models__Statistical_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Probability_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH P_Research_Design_MeSH M_Stochastic_Processes_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9631978
----K E
----T Efficacy of low-dose combination of bisoprolol/hydrochlorothiazide compared with amlodipine and enalapril in men and women with essential hypertension.
----A The efficacy of the low-dose combination of bisoprolol/hydrochlorothiazide was compared with amlodipine and enalapril. The low-dose combination was found to be at least as effective as amlodipine and more effective than enalapril in both men and women.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_adverse_effects_MeSH Enalapril_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9631979
----K E
----T Beta-blocker therapy of severe congestive heart failure in infants with left to right shunts.
----A We report on the clinical and neurohumoral effects of adding low-dose propranolol to conventional therapy with digoxin and diuretics in 6 infants with severe congestive heart failure due to large left-to-right shunts. A significant decrease in heart failure scores and a decrease of the highly activated renin-angiotensin-1 aldosterone system by approximately 70% strongly suggests a beneficial effect of this new therapeutic approach.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Child__Preschool_MeSH M_Combined_Modality_Therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Defects__Congenital_MeSH S_drug_therapy_MeSH Heart_Defects__Congenital_drug_therapy_MeSH S_physiopathology_MeSH Heart_Defects__Congenital_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Infant_MeSH M_Male_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9633797
----K E
----T Comparison of effects of antihypertensive drugs on heart rate: changes from baseline by baseline group and over time. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A Baseline heart rate is becoming recognized as a predictor of cardiovascular risk. Various antihypertensive drugs have differing effects on heart rate. A randomized controlled clinical trial of 1292 ambulatory men with stage 1 or 2 hypertension was conducted in 15 Veterans Affairs medical centers. Patients were treated with hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem, prazosin, or placebo for up to 2 years. Heart rates were measured at baseline, the end of titration, 1 year, and 2 years. Data were also stratified by baseline heart rate. A subset of patients had heart rate also determined by electrocardiogram. All drugs except prazosin reduced heart rate from baseline; additional small decreases were obtained over time with hydrochlorothiazide and placebo. The decrease initially achieved with clonidine was attenuated over time. The overall reduction in heart rate was greatest for atenolol (-12.2 beats/min) and least for prazosin (+3.8 beats/min). Only atenolol effected a further reduction of heart rate for patients whose baseline rate was < or =65 beats/min. All drugs reduced heart rate when the baseline was > or =85 beats/min. Data derived by electrocardiogram yielded similar results. The drugs used in this study differ in their ability to reduce heart rate, sustain that reduction over time, and to change heart rate in groups with high or low rates at baseline. The importance of these comparative changes as independent cardiac risk factor variables remains to be determined.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Electrocardiography_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Time_Factors_MeSH 
****** 9633801
----K E
----T Hemodynamic differences between metoprolol and carvedilol in hypertensive patients.
----A Resting hemodynamics were measured before, at 2 and 24 h after the first dose, and after 4 weeks of monotherapy with either metoprolol or carvedilol in a randomized single-blind study. We analyzed results from 24 hypertensive patients (30-68 years of age) with adequate blood-pressure lowering on monotherapy. Acutely, both drugs lowered systolic blood pressure and heart rate. Whereas metoprolol reduced cardiac output and increased both systemic and femoral artery resistance, carvedilol did not alter cardiac output but led to reductions in the systemic and regional resistances. After 4 weeks of therapy, cardiac output remained reduced and vascular resistances increased in the metoprolol group, whereas in carvedilol patients cardiac output continued to be unchanged and the trend for vascular resistances to be decreased persisted. Acutely and chronically the differences in the hemodynamic effects of the two medications were statistically significant. The study results indicate that carvedilol's vasodilatory action is not subject to tolerance development. Chronic afterload reduction associated with the decrease in systemic vascular resistance may lead to additional savings in myocardial oxygen consumption, a beneficial feature particularly in those patients with concomitant ischemic heart disease. It may also have a favorable influence on concentric cardiac hypertrophy and changes in the walls of arteriolar resistance vessels.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 9633802
----K E
----T Cost-minimization and the number needed to treat in uncomplicated hypertension.
----A The goal of this study was to compare the direct costs associated with the prescription of thiazide diuretics, beta-receptor blockers (beta-blockers), angiotensin converting enzyme inhibitors (ACEI), a-receptor blockers (alpha-blockers), and calcium channel blockers (CCB) for the prevention of stroke, myocardial infarction (MI) and premature death in uncomplicated hypertension. We performed a cost-minimization analysis based on numbers-needed-to-treat (NNT) derived from the metaanalysis of 15 major clinical trials of hypertension treatment, and the average wholesale prices of both the most commonly prescribed and the least expensive drugs in each class. The inclusion criteria for clinical trials were that they be randomized, controlled trials of drug therapy of uncomplicated mild-to-moderate hypertension with stroke, MI, or death as endpoints. The wholesale drug costs and the total direct outpatient treatment costs to prevent a stroke, MI or death among middle-aged and elderly hypertensives were our outcome measures. The estimated wholesale drug acquisition cost to prevent one major event (MI or stroke or death) ranged from $4730 to $346,236 among middle-aged patients, and from $1595 to $116,754 in the elderly; generic diuretic or beta-blocker therapy was more economical than treatment with an ACEI, alpha-blocker, or CCB. The associated 5-year NNT was 86 for middle-aged patients and 29 for elderly patients. Diuretic therapy remained more cost-effective even under the unlikely assumption that the newer drugs were 50% more effective than diuretics at preventing these major events. The costs associated with potassium supplementation did not eliminate the advantage of diuretics. Treatment costs to prevent major hypertensive complications are much lower with diuretics and beta-blockers than with ACEI, CCB, or alpha-blockers, especially in middle-aged patients.
----P Journal_Article Meta-Analysis 
----M M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH P_Cost_Control_MeSH P_Drug_Costs_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Sensitivity_and_Specificity_MeSH 
****** 9634263
----K I
----T Are beta-blockers efficacious as first-line therapy for hypertension in the elderly? A systematic review.
----A OBJECTIVE: To assess antihypertensive efficacy of beta-blockers and their effects on cardiovascular morbidity and mortality and all-cause morbidity compared with diuretics in elderly patients with hypertension. DATA SOURCE: A MEDLINE search of English-language articles published between January 1966 and January 1998 using the terms hypertension (drug therapy) and elderly or aged or geriatric, and cerebrovascular or cardiovascular diseases, and morbidity or mortality. References from identified articles were also reviewed. DATA SELECTION: Randomized trials lasting at least 1 year, which used as first-line agents diuretics and/or beta-blockers, and reported morbidity and mortality outcomes in elderly patients with hypertension. DATA SYNTHESIS AND RESULTS: Ten trials involving a total of 16164 elderly patients (> or =60 years) were included. Two thirds of the patients assigned to diuretics were well controlled on monotherapy, whereas less than a third of the patients assigned to beta-blockers were well controlled on monotherapy. Diuretic therapy was superior to beta-blockade with regard to all end points and was effective in preventing cerebrovascular events (odds ratio [OR], 0.61; 95% confidence interval [CI], 0.51-0.72), fatal stroke (OR, 0.67; 95% CI, 0.49-0.90), coronary heart disease (OR, 0.74; 95% CI, 0.64-0.85), cardiovascular mortality (OR, 0.75; 95% CI, 0.64-0.87), and all-cause mortality (OR, 0.86; 95% CI, 0.77-0.96). In contrast, beta-blocker therapy only reduced the odds for cerebrovascular events (OR, 0.75; 95% CI, 0.57-0.98) but was ineffective in preventing coronary heart disease, cardiovascular mortality, and all-cause mortality (ORs, 1.01, 0.98, and 1.05, respectively). CONCLUSIONS: In contrast to diuretics, which remain the standard first-line therapy, beta-blockers, until proven otherwise, should no longer be considered appropriate first-line therapy of uncomplicated hypertension in the elderly hypertensive patient.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Models__Statistical_MeSH M_Morbidity_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9639377
----K I
----T Tachycardia-induced change of atrial refractory period in humans: rate dependency and effects of antiarrhythmic drugs.
----A BACKGROUND: Atrial fibrillation (AF) has been shown to shorten the atrial effective refractory period (ERP) and make the atrium more vulnerable to AF. This study investigated the effect of atrial rate and antiarrhythmic drugs on ERP shortening induced by tachycardia. METHODS AND RESULTS: Seventy adult patients without structural heart disease were included. For the first part of the study, right atrial ERP was measured with a drive cycle length of 500 ms before and after 10 minutes of rapid atrial pacing using five pacing cycle lengths (450, 400, 350, 300, and 250 ms) in 10 patients. For the second part of the study, the remaining 60 patients were included to study the effects of antiarrhythmic drugs on changes in atrial ERP induced by AF. Atrial ERP was measured with a drive cycle of 500 ms before and after an episode of pacing-induced AF. After the patients were randomized to receive one of six antiarrhythmic drugs (procainamide, propafenone, propranolol, dl-sotalol, amiodarone, and verapamil), atrial ERP was measured before and after another episode of pacing-induced AF. In the first part of the study, atrial ERP shortened significantly after 10 minutes of rapid atrial pacing, and the degree of shortening was correlated with pacing cycle length. The second part of the study showed that atrial ERP shortened after conversion of AF (172+/-15 versus 202+/-14 ms, P<0.0001) and that ERP shortening was attenuated after verapamil infusion (-4.6+/-1.2% versus -15.1+/-3.4%, P<0.001) but was unchanged after infusion of the other antiarrhythmic drugs. Furthermore, all of these antiarrhythmic drugs could decrease the incidence and duration of secondary AF. CONCLUSIONS: The atrial ERP shortening induced by tachycardia was a rate-dependent response. Verapamil, but not other antiarrhythmic drugs, could markedly attenuate this effect. However, verapamil and the other drugs could decrease the incidence and duration of secondary AF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Atrial_Fibrillation_MeSH S_diagnosis_MeSH Atrial_Fibrillation_diagnosis_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Electrocardiography_MeSH M_Electrophysiology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pacemaker__Artificial_MeSH M_Procainamide_MeSH S_administration_&_dosage_MeSH Procainamide_administration_&_dosage_MeSH M_Propafenone_MeSH S_administration_&_dosage_MeSH Propafenone_administration_&_dosage_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Supraventricular_MeSH S_diagnosis_MeSH Tachycardia__Supraventricular_diagnosis_MeSH S_drug_therapy_MeSH Tachycardia__Supraventricular_drug_therapy_MeSH S_physiopathology_MeSH Tachycardia__Supraventricular_physiopathology_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH 
****** 9643273
----K E
----T A comparison of the effects of mibefradil and atenolol on regression of left ventricular hypertrophy in hypertensive patients.
----A OBJECTIVE: This study was designed to compare the effect of mibefradil, a selective T-type calcium channel antagonist, with the beta-blocker atenolol on regression of left ventricular (LV) hypertrophy in hypertensive patients. METHODS: In this multicenter, double-blind, active-controlled, randomized, parallel-group comparison, 66 patients with mild-to-moderate hypertension (sitting diastolic blood pressure, SDBP, 95-114 mm Hg) and LV mass index > 102 g/m2 for males and > 88 g/m2 for females were randomized to an initial treatment with 50 mg of either mibefradil or atenolol for 4 weeks. Doses were increased to 100 mg/day if blood pressure was not normalized to < or = 90 mm Hg, and, if needed, 25 mg of hydrochlorothiazide was added. Treatment continued for a total of 24 weeks. LV hypertrophy was assessed by echocardiography, and trough SDBP and adverse events were recorded. RESULTS: Treatment with mibefradil or atenolol resulted in decreases from baseline in LV mass index of 11.1% (p < 0.001) and 9.1% (p < 0.001), respectively. The treatment difference (mibefradil vs. atenolol) was not statistically significant. Reductions in SDBP with mibefradil and atenolol were 14.3 and 10.7 mm Hg, respectively, again not statistically significant. Both drugs were well tolerated; however, overall there were more potentially drug-related adverse events reported with atenolol (48.5%) than with mibefradil (24.2%). CONCLUSIONS: The reductions in LV hypertrophy and blood pressure achieved with mibefradil were larger but statistically equivalent to those with atenolol, but a lower overall incidence of treatment-related adverse events was seen in the mibefradil-treated patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_adverse_effects_MeSH Benzimidazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Mibefradil_MeSH M_Tetrahydronaphthalenes_MeSH S_adverse_effects_MeSH Tetrahydronaphthalenes_adverse_effects_MeSH S_therapeutic_use_MeSH Tetrahydronaphthalenes_therapeutic_use_MeSH 
****** 9645829
----K I
----T Diuretic-based treatment and cardiovascular events in patients with mild renal dysfunction enrolled in the systolic hypertension in the elderly program.
----A BACKGROUND: It is expected that the treatment of hypertension in patients with renal disease decreases the risk of cardiovascular events, but the evidence in these patients is lacking. OBJECTIVE: To assess the effect of diuretic-based treatment on cardiovascular events in patients with isolated systolic hypertension and renal dysfunction. METHODS: A total of 4336 persons aged 60 years and older with systolic blood pressures of 160 mm Hg and higher and diastolic blood pressures of less than 90 mm Hg were randomly assigned to receive either placebo or chlorthalidone (12.5-25.0 mg/d), with the addition of atenolol (25-50 mg/d) or reserpine (0.05-0.10 mg/d) if needed, and observed for 5 years. The risk of first-occurring cardiovascular events, including stroke, transient ischemic attack, myocardial infarction, heart failure, coronary artery bypass surgery, angioplasty, aneurysm, endarterectomy, sudden death, or rapid death, was stratified according to baseline serum creatinine levels (35.4-84.0, 84.1-101.6, 101.7-119.3, and 119.4-212.2 micromol/L [0.4-0.9, 1.0-1.1, 1.2-1.3, and 1.4-2.4 mg/dL]). RESULTS: Systolic blood pressure reduction was not affected by baseline serum creatinine levels. Active treatment did not affect the risk of serum creatinine levels becoming elevated during follow-up. The risk of hypokalemia with active treatment decreased significantly with increasing baseline serum creatinine levels. In the 4 baseline serum creatinine groups, the relative risk (95% confidence interval) of cardiovascular events developing with active treatment was 0.73 (0.54-0.97), 0.63 (0.49-0.82), 0.62 (0.44-0.87), and 0.59 (0.38-0.91). The results were similar for the outcomes of stroke or coronary artery events and in analyses stratified by sex or age. CONCLUSION: Diuretic-based treatment of patients with isolated systolic hypertension prevents the development of cardiovascular events in older persons with mild renal dysfunction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Cardiovascular_Diseases_MeSH S_blood_MeSH Cardiovascular_Diseases_blood_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_blood_MeSH Kidney_Failure__Chronic_blood_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Severity_of_Illness_Index_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 9645897
----K E
----T Effect of beta-blocker therapy in patients with coronary artery disease in New York Heart Association classes II and III. The Bezafibrate Infarction Prevention (BIP) Study Group.
----A The aim of the study was to investigate the effect of beta-blocker treatment on a large cohort of patients with coronary artery disease in functional classes II and III according to the New York Heart Association (NYHA) classification. Among 11,575 patients with coronary artery disease screened for participation, but not included in the Bezafibrate Infarction Prevention (BIP) study, 3,225 (28%) were in NYHA classes II and III. In the latter group of patients we compared the prognosis of 1,109 (34%) treated with beta blockers with 2,116 counterparts not receiving beta-blocker therapy. After a mean follow-up of 4 years, all-cause and cardiac mortality rates were significantly lower among beta-blocker users, 9% and 5%, respectively, than among beta-blocker nonusers, 17% and 11%, respectively (p <0.01 for both). After multivariate adjustment, treatment with beta blockers was associated with a lower all-cause mortality risk (hazards ratio [HR] 0.62, 95% confidence interval [CI] 0.49 to 0.78), and a lower cardiac mortality risk (HR = 0.61, 95% CI 0.45 to 0.83) than was no treatment with a beta blocker. Lower total mortality risk was noted among patients in NYHA class II (HR 0.63, 95% CI 0.48 to 0.82) and in NYHA class III (HR 0.57, 95% CI 0.37 to 0.87) as well as in patients with (HR 0.62, 95% CI 0.48 to 0.81) or without (HR 0.70, 95% CI 0.45 to 1.09) a previous myocardial infarction. We conclude that beta-blocker therapy in coronary patients in NYHA classes II or III is safe and associated with a lower risk for all-cause and cardiac mortality.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_pathology_MeSH Coronary_Disease_pathology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Odds_Ratio_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 9657539
----K E
----T Regression of left ventricular wall thickness during ACE-inhibitor treatment of essential hypertension is associated with an increase in insulin mediated skeletal muscle blood flow.
----A Left ventricular hypertrophy (LVH) has been associated with insulin resistance, a condition with an impaired insulin-mediated vasodilation in skeletal muscle. ACE-inhibitors have been reported to be superior to most other antihypertensive drugs in inducing a regression of LVH. In a double-blind study with parallel groups, 50 patients with essential hypertension were randomized to treatment with either fosinopril (20 mg o.d.) or atenolol (50 mg o.d.) for 12-16 weeks. Left ventricle wall thickness (LVWT, defined as the sum of interventricular septum and posterior wall), diastolic function (represented by the ratio between the E-wave and the A-wave of mitral blood flow) and femoral artery blood flow (FBF) were evaluated using ultrasonic measurements. FBF was measured at normoinsulinemia and after 2 h of euglycemic hyperinsulinemia. Before treatment, the insulin-induced increase in FBF was inversely related to the LVWT (r = -0.52, p < 0.02). The reduction in ambulatory 24-h SBP/DBP was 13/9 mmHg for fosinopril and 15/14 for atenolol, ambulatory DBP being significantly more reduced by atenolol (p = 0.03 for difference in treatment effect). However, only fosinopril treatment resulted in a significant reduction in LVWT (from 20.5 mm to 19.4 mm, p < 0.05). The degree of reduction in LVWT was related to the increase in FBF in the fosinopril group (r = -0.45, p < 0.05). For fosinopril (but not for atenolol), there was a positive relationship between the change in E/A ratio and the change in femoral artery stroke volume (r = 0.80, p < 0.01). Conclusion: Impaired insulin-induced stimulation of leg blood flow was related to an increased LVWT. Furthermore, during fosinopril treatment, regression of LVWT was associated with enhanced skeletal muscle blood flow during hyperinsulinemia. This indicates that impaired peripheral blood flow (and thereby increased afterload) may be a possible mechanism explaining the previously found association between insulin resistance and cardiovascular hypertrophy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypoglycemic_Agents_MeSH S_pharmacology_MeSH Hypoglycemic_Agents_pharmacology_MeSH M_Insulin_MeSH S_pharmacology_MeSH Insulin_pharmacology_MeSH M_Insulin_Resistance_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle__Skeletal_MeSH S_blood_supply_MeSH Muscle__Skeletal_blood_supply_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9657623
----K E
----T Vagal cardiac activity in essential hypertension: the effects of metoprolol and ramipril.
----A Cardiovascular parasympathetic activity is attenuated in essential hypertension. Both beta-adrenoceptor antagonists and angiotensin converting enzyme inhibitors have been reported to increase vagal modulation of heart rate and baroreflex sensitivity, but the relations between the antihypertensive and vagal cardiac effects of these drugs have remained unclear in essential hypertension. In the present study we evaluated the effects of a 4-week crossover monotherapy with metoprolol and ramipril on spectrum analysis indices of heart rate variability in the supine rest and head-up tilted positions, baroreflex sensitivity (phenylephrine method), and 24-h ambulatory blood pressure (BP) in 12 formerly untreated stage 1-2 essential hypertensive patients. Compared to the pretreatment values, both drugs decreased BP similarly and significantly. However, the drugs showed different effects on cardiac vagal activity: metoprolol increased significantly mean R-R interval, R-R interval total, and high-frequency variability at supine rest and baroreflex sensitivity, but ramipril did not significantly affect these variables. The metoprolol-induced decrease in ambulatory BP correlated with the prolongation of the R-R interval and the increase of high-frequency variability at supine rest. The present data show that 4-week treatment with metoprolol increases tonic and reflex vagal cardiac activity, whereas ramipril does not affect vagal cardiac control in essential hypertension. Increase in vagal activity may contribute to the BP-lowering effect of metoprolol in hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Autonomic_Nervous_System_physiopathology_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Heart_MeSH S_innervation_MeSH Heart_innervation_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_pharmacology_MeSH Ramipril_pharmacology_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH 
****** 9660383
----K E
----T Risk factors for stroke and type of stroke in persons with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group.
----A BACKGROUND AND PURPOSE: We sought to determine risk factors for stroke and stroke type in persons with isolated systolic hypertension (ISH). METHODS: We performed proportional hazards analyses of data from the Systolic Hypertension in the Elderly Program, a double-blind, randomized, placebo-controlled trial of 4736 persons aged > or =60 years with ISH (systolic blood pressure, 160 to 219 mm Hg; diastolic blood pressure, <90 mm Hg). One treatment group received chlorthalidone (12.5 to 25 mg/d) with step-up to atenolol (25.0 to 50.0 mg/d) or reserpine (0.05 to 0.10 mg/d), if needed. The other treatment group received matching placebo. The main outcome measures were stroke, stroke or transient ischemic attack [TIA], and stroke types: ischemic (including lacunar, atherosclerotic, and embolic) and hemorrhagic. RESULTS: During an average follow-up of 4.5 years, 384 strokes or TIAs and 262 strokes (including 217 ischemic, 66 lacunar, 26 atherosclerotic, and 25 embolic strokes) were documented. In multivariate analyses, placebo treatment, older age, smoking, history of diabetes, higher systolic blood pressure, lower HDL cholesterol, and ECG abnormality were significantly associated (P<0.05) with increased incidence of stroke or TIA, stroke, or ischemic stroke. Greater lacunar stroke risk was significantly related to placebo treatment, older age, history of diabetes (relative risk [RR] = 3.03; 95% confidence interval [CI], 1.70 to 5.40), and smoking (RR = 3.04; 95% CI, 1.73 to 5.37). Greater atherosclerotic and embolic stroke risk were significantly related to presence of carotid bruit (RR = 5.75; 95% CI, 2.50 to 13.24) and older age (RR = 1.65 per 5 years; 95% CI, 1.25 to 2.18), respectively. CONCLUSIONS: In older persons with ISH, history of diabetes and smoking are important risk factors for lacunar stroke, whereas carotid bruit and age are important risk factors for atherosclerotic and embolic stroke, respectively.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Brain_Ischemia_MeSH S_complications_MeSH Brain_Ischemia_complications_MeSH M_Cerebral_Hemorrhage_MeSH S_complications_MeSH Cerebral_Hemorrhage_complications_MeSH M_Cerebrovascular_Disorders_MeSH S_classification_MeSH Cerebrovascular_Disorders_classification_MeSH S_epidemiology_MeSH Cerebrovascular_Disorders_epidemiology_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Incidence_MeSH M_Male_MeSH M_Proportional_Hazards_Models_MeSH M_Reserpine_MeSH S_therapeutic_use_MeSH Reserpine_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Systole_MeSH 
****** 9660523
----K E
----T The role of combination therapy in the treatment of hypertension.
----A Antihypertensive therapy is indicated for reducing the risk of cardiovascular morbidity and mortality that accompanies arterial hypertension. Usually, pharmacological treatment is started as monotherapy, which, if unsuccessful, is followed by sequential monotherapy, or by combination therapy. Recent data indicate that combination therapy is required in more than 50% of the hypertensive population when the goal is to reduce blood pressure to below 140/90 mm Hg. The choice and doses of drugs used in combination therapy should be such that their synergistic effect on blood pressure is maximized, the tolerability of the drugs is maintained and side-effects are minimized. The combination of a dihydropyridine calcium antagonist with a beta-blocker or an angiotensin-converting enzyme (ACE) inhibitor is one of the most commonly used combination therapies. Two randomized, double-blind, parallel-group studies compared the antihypertensive effects of the dihydropyridine, barnidipine, with the beta-blocker, atenolol (n = 247), and the ACE inhibitor, enalapril (n = 155). The efficacy and tolerability of barnidipine in combination with either atenolol or enalapril was also investigated. Monotherapy with barnidipine was as effective in reducing blood pressure as monotherapy with either atenolol or enalapril. Combining barnidipine with either atenolol or enalapril reduced blood pressure further, and significantly increased the percentage of patients attaining the required reduction in blood pressure. When patients whose blood pressure was not adequately controlled by enalapril monotherapy were switched to barnidipine monotherapy, the majority then achieved the desired reduction in blood pressure. These results indicate that if barnidipine monotherapy fails to lower blood pressure to the desired values, its combination with either a beta-blocker or an ACE inhibitor is effective and well tolerated.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9658386
----K E
----T Prophylactic sodium valproate therapy in patients with drug-resistant migraine.
----A We assessed the efficacy of sodium valproate as a prophylactic agent in migraine headache. A prospective randomized study was conducted in adult patients who previously derived no significant benefit from most conventional prophylactic therapy for migraine. Twenty-seven patients with a diagnosis of migraine with aura or migraine without aura from a headache clinic received low dose sodium valproate for 3 months. Response to therapy was defined as 50% or greater reduction in the frequency of headache. Plasma drug level monitoring helped to identify four noncompliers who were excluded from the study. Seventeen (71%) patients observed improvement within 4-6 weeks of medication and remained well for 12 weeks. They were further followed up for 12-24 months. Two patients for side effects and 1 for nondrug-related problems were withdrawn from follow-up study. Twelve patients (60%) maintained their response for 12 months or longer. Clinical improvement (percentage reduction in the frequency of migraine attacks) correlated inversely with the plasma drug levels at 13-24 months and daily dose of valproate, among the responders, suggestive of a possible therapeutic window. In other words, patients who do not respond to low dose valproate are unlikely to benefit from further increase in dosage.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Premedication_MeSH M_Valproic_Acid_MeSH S_blood_MeSH Valproic_Acid_blood_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH 
****** 9649466
----K E
----T Propranolol plus prazosin compared with propranolol plus isosorbide-5-mononitrate in the treatment of portal hypertension.
----A BACKGROUND & AIMS: The association of prazosin to propranolol enhances the decrease in portal pressure but may cause hypotension and sodium retention. The aim of this study was to compare the portal pressure reduction and safety of the combination of propranolol plus prazosin with that of propranolol plus isosorbide-5-mononitrate (ISMN). METHODS: Fifty-six portal-hypertensive cirrhotics received randomly propranolol plus prazosin (n = 28) or propranolol plus ISMN (n = 28) orally for 3 months. Hemodynamics and liver and renal function were assessed at baseline and after 3 months. RESULTS: Propranolol plus prazosin caused a greater reduction in hepatic venous pressure gradient (HVPG) than propranolol plus ISMN (-24.2% +/- 11% vs. -16.1% +/- 11%; P < 0.01). A reduction in HVPG of > 20% was significantly more frequent in the propranolol plus prazosin group than in the propranolol plus ISMN group (85% vs. 53%; P < 0.05). Neither treatment modified hepatic blood flow, quantitative liver function test results, glomerular filtration rate, plasma renin activity, or plasma aldosterone level. Side effects occurred in 13 patients receiving propranolol plus prazosin compared with 7 receiving propranolol plus ISMN (P = 0.16). CONCLUSIONS: Propranolol plus prazosin has a greater portal pressure-lowering effect than propranolol plus ISMN. Both therapies were safe for liver and renal function. However, the combination of propranolol plus prazosin caused a greater decrease in arterial pressure and was less well tolerated than propranolol plus ISMN.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Hepatic_Veins_MeSH S_drug_effects_MeSH Hepatic_Veins_drug_effects_MeSH S_physiology_MeSH Hepatic_Veins_physiology_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prazosin_MeSH S_administration_&_dosage_MeSH Prazosin_administration_&_dosage_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH M_Venous_Pressure_MeSH S_drug_effects_MeSH Venous_Pressure_drug_effects_MeSH 
****** 9663729
----K E
----T Duplex-Doppler evaluation of the effects of propranolol and isosorbide-5-mononitrate on portal flow and splanchnic arterial circulation in cirrhosis.
----A BACKGROUND: A decrease in portal flow is an important pharmacological effect of drugs used for the prophylaxis of variceal bleeding. AIM: To assess the acute and chronic effects of propranolol, and the effect of the acute addition of isosorbide-5-mononitrate, on splanchnic circulation. METHODS: Measurements of portal blood flow volume (PBFV) and of Doppler ultrasound pulsatility index of the superior mesenteric, femoral and interlobar renal arteries were performed in 10 cirrhotic patients with varices at baseline, 90 min after propranolol or placebo, after 30 days of chronic propranolol treatment and 45 min after the addition of isosorbide-5-mononitrate. RESULTS: The mean PBFV was significantly lower at all times than at baseline, with the greatest mean percentage decrease achieved after the addition of isosorbide-5-mononitrate (> or = 20% in all patients). Acute changes, however, did not predict the chronic effects in many patients. Isosorbide-5-mononitrate significantly increased the mesenteric and femoral pulsatility indices, whereas no significant change was observed in the kidney. CONCLUSIONS: Propranolol significantly decreases PBFV, but chronic effects cannot be reliably predicted by the acute change. All patients achieved a decrease in PBFV of > or = 20% after the acute addition of isosorbide-5-mononitrate to chronic propranolol treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH S_ultrasonography_MeSH Esophageal_and_Gastric_Varices_ultrasonography_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_pharmacology_MeSH Isosorbide_Dinitrate_pharmacology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH S_ultrasonography_MeSH Liver_Cirrhosis_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_System_MeSH S_drug_effects_MeSH Portal_System_drug_effects_MeSH S_ultrasonography_MeSH Portal_System_ultrasonography_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultrasonography__Doppler__Duplex_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 9663914
----K E
----T Blood pressure screening, management and control in England: results from the health survey for England 1994.
----A OBJECTIVE: To assess the current levels of awareness, treatment and control of hypertension in England and to determine the number and type of drugs prescribed. DESIGN: A cross-sectional household-based survey of English adults. SUBJECTS: A random sample from the adult English population of 12,116 adults who participated in the 1994 Health Survey for England. MAIN OUTCOME MEASURES: Prevalences of treatment hypertension, awareness and control. RESULTS: Using a definition of hypertension as a systolic blood pressure > or = 160 mmHg or a diastolic blood pressure > or = 95 mmHg, or a patient's being administered antihypertensive treatment, the prevalence of awareness of hypertension was 63%. Among hypertensives, 50% were receiving treatment and 30% had their hypertension controlled (< 160 mmHg/95 mmHg). Awareness, treatment and control rates are considerably lower than the most recently reported rates from the USA. Diuretics and beta-blockers remain the most common antihypertensive agents used in England. CONCLUSION: There is considerable scope for improving the treatment and control of hypertension in the English adult population.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Blood_Pressure_MeSH P_Blood_Pressure_Determination_MeSH M_Comparative_Study_MeSH M_Cross-Sectional_Studies_MeSH M_England_MeSH S_epidemiology_MeSH England_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH P_Mass_Screening_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Random_Allocation_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9663926
----K E
----T Determinants of interindividual variation of renin and prorenin concentrations: evidence for a sexual dimorphism of (pro)renin levels in humans.
----A BACKGROUND: Plasma renin concentrations are an important factor in cardiovascular risk profiling. OBJECTIVE: To investigate the effects of sex, medication, and anthropometric factors that may contribute to the interindividual variation in the plasma concentrations of renin and its precursor prorenin. DESIGN AND METHODS: Prorenin and renin levels in 327 men and 383 women, aged 52-69 years, who participated in a 1994 reexamination of a previous population survey in Bavaria, were measured by immunoradiometric assay. RESULTS: Prorenin and renin levels in men were significantly higher than those in women, those in women without estrogen replacement therapy were significantly higher than those in women with estrogen replacement therapy, and those in diabetics were significantly higher than those in nondiabetics. Prorenin level was correlated negatively to blood pressure and positively to age and the use of diuretics; it was normal in subjects using angiotensin converting enzyme inhibitors and beta-adrenergic antagonists (beta-blockers). Renin level was correlated negatively to atrial natriuretic peptide level and the use of beta-blockers, and it was elevated above normal levels in subjects using angiotensin converting enzyme inhibitors and diuretics as well as in subjects who had previously suffered myocardial infarction. After exclusion of data for women being administered estrogen replacement therapy, multivariate analysis revealed that sex (P<0.001), age (P<0.02), blood pressure (P<0.002), diabetes (P<0.05), and the use of angiotensin converting enzyme inhibitors (P<0.002), beta-blockers (P<0.001), and diuretics (P<0.05) were independent determinants of plasma prorenin. Plasma renin was independently related to atrial natriuretic peptide level (P<0.01) and the use of angiotensin converting enzyme inhibitors (P<0.001), beta-blockers (P<0.001), and diuretics (P<0.05). CONCLUSIONS: These data demonstrate that there is a sexual dimorphism of prorenin levels in humans, suggesting that sex hormones affect the regulation of the renin gene. Data confirm previous reports of elevated prorenin levels in diabetics and older subjects, as well as of lower than normal prorenin levels in subjects with hypertension in smaller populations. Our findings may help to clarify the potential (patho)physiologic functions of prorenin and to identify the factors that influence the constitutive secretion and intracellular processing of this prohormone.
----P Journal_Article 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH S_drug_effects_MeSH Atrial_Natriuretic_Factor_drug_effects_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Cross-Sectional_Studies_MeSH M_Diabetes_Mellitus_MeSH S_blood_MeSH Diabetes_Mellitus_blood_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH M_Enzyme_Precursors_MeSH S_blood_MeSH Enzyme_Precursors_blood_MeSH S_drug_effects_MeSH Enzyme_Precursors_drug_effects_MeSH M_Estrogen_Replacement_Therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Germany_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Immunoradiometric_Assay_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_blood_MeSH Myocardial_Infarction_blood_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH M_Postmenopause_MeSH S_blood_MeSH Postmenopause_blood_MeSH S_drug_effects_MeSH Postmenopause_drug_effects_MeSH M_Prevalence_MeSH M_Random_Allocation_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH S_drug_effects_MeSH Renin_drug_effects_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Retrospective_Studies_MeSH P_Sex_Characteristics_MeSH 
****** 9665213
----K E
----T Beta-blocker therapy in young children with congestive heart failure under consideration for heart transplantation.
----A BACKGROUND: Although beta-blocker therapy for dilated or ischemic cardiomyopathy is now an accepted and effective treatment in adults, little is known about its efficacy in children. METHODS: We reviewed our experience with the use of metoprolol in four younger children with cardiomyopathy who were referred for consideration for heart transplantation because of severe congestive heart failure. RESULTS: Over a follow-up period of 12.6 +/- 6 months, left ventricular fractional shortening increased from 13.8% +/- 7% to 25.5% +/- 13%, and ejection fraction increased from 19.8% +/- 11% to 40.8% +/- 21% (p < 0.05). Two children became asymptomatic. CONCLUSION: Metoprolol may be effective in improving ejection fraction and symptoms in some young children with cardiomyopathy and congestive heart failure.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Comparative_Study_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_surgery_MeSH Heart_Failure__Congestive_surgery_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH P_Heart_Transplantation_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH 
****** 9669241
----K E
----T Results from late-breaking clinical trials sessions at ACC '98. American College of Cardiology.
----A 
----P Congresses 
----M P_Clinical_Trials_MeSH P_Heart_Diseases_MeSH M_Human_MeSH P_Randomized_Controlled_Trials_MeSH 
****** 9665894
----K E
----T Survival in treated hypertension: follow up study after two decades.
----A OBJECTIVE: To compare survival and cause specific mortality in hypertensive men with non-hypertensive men derived from the same random population, and to study mortality and morbidity from cardiovascular diseases in the hypertensive men in relation to effects on cardiovascular risk factors during 22-23 years of follow up. DESIGN: Prospective, population based observational study. SUBJECTS AND METHODS: 686 hypertensive men aged 47-55 at screening compared with 6810 non-hypertensive men. The hypertensive men were having stepped care treatment with either beta adrenergic blocking drugs, thiazide diuretics, or combination treatment. Mortality, morbidity, and adverse effects were registered at yearly examinations and from death certificates. MAIN OUTCOME MEASURES: All cause mortality and cause specific mortality. RESULTS: Treated hypertensive men had significantly impaired probability of total survival as well as survival from coronary heart disease and stroke. All cause mortality as well as coronary heart disease and stroke mortality were very similar in hypertensive men and normotensive men during the first decade, but increased steadily thereafter despite continuous good blood pressure control. Smoking, signs of target organ damage, and high serum cholesterol levels, but not blood pressure at screening, were significantly related to the incidence of coronary heart disease during follow up. In time dependent Cox's regression analysis, the incidence of coronary heart disease was significantly related only to serum cholesterol concentrations in the study. Cancer mortality was almost similar in treated hypertensive men (61/686, 8.9%) and non-hypertensive men (732/6810, 10.8%). CONCLUSION: Treated hypertensive men had impaired survival and increased mortality from cardiovascular disease compared with non-hypertensive men of similar age. These differences were observed during the second decade of follow up. During an observation period of 22-23 years-about 15 000 patient years-hypertensive men receiving diuretics and beta blockers had no increased risk of cancer or non-cardiovascular disease.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH M_Cause_of_Death_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Survival_Rate_MeSH 
****** 9672774
----K 1
----T Differential effects of selective beta-adrenergic blockade on insulin sensitivity and release in control subjects and in patients with angina and normal coronary arteries (syndrome X).
----A AIMS: Betablockers are very effective in patients with angina and angiographically smooth coronary arteries (syndrome X), but may exacerbate the state of insulin resistance that is known to be present in such patients. The aim of the study was to evaluate the effects of short-term treatment with atenolol on carbohydrate metabolism in syndrome X patients, as compared to normal subjects. METHODS AND RESULTS: Seventeen patients (15 females, 55 +/- 8 years, BMI 23.4 +/- 2.7 kg/m2) and 11 controls (5 females, 50 +/- 7 years, BMI 23.1 +/- 2.0 kg/m2) were studied twice by an intravenous glucose tolerance test (IVGTT, 0.5 g/kg) after ten days of both placebo and atenolol (100 mg o.d.), given in random order. Metabolic indices measuring glucose effectiveness and insulin sensitivity were derived from minimal model analysis of the glucose and insulin profiles measured during the IVGTT. Indices of first- and second-phase insulin release were also calculated from the IVGTT insulin response. Atenolol had different metabolic effects on normal subjects and syndrome X patients. Despite the fact that the drug was found to be effective in relieving symptoms of chest pain, it induced a significant (p < 0.05) worsening of insulin resistance in syndrome X patients. No such effect was observed in control subjects. On the other hand, atenolol produced a marked reduction (40%, p < 0.05) of first-phase insulin release in control subjects, but no significant change of the same index in syndrome X patients. CONCLUSION: These results show that betablockers are very effective for controlling symptoms and improving quality of life in syndrome X patients. However, they appear to further impair the ability to dispose glucose. Long-term studies on the net effects of beta-blockade administration for the treatment of such patients are warranted.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH S_statistics_&_numerical_data_MeSH Exercise_Test_statistics_&_numerical_data_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH S_statistics_&_numerical_data_MeSH Glucose_Tolerance_Test_statistics_&_numerical_data_MeSH M_Human_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH P_Insulin_Resistance_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Syndrome_X_MeSH S_blood_MeSH Syndrome_X_blood_MeSH S_drug_therapy_MeSH Syndrome_X_drug_therapy_MeSH M_Time_Factors_MeSH 
****** 9673599
----K E
----T Venous thromboembolism and cancer.
----A 
----P Journal_Article 
----M M_Aged_MeSH M_Cohort_Studies_MeSH M_Denmark_MeSH S_epidemiology_MeSH Denmark_epidemiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neoplasms_MeSH S_complications_MeSH Neoplasms_complications_MeSH S_diagnosis_MeSH Neoplasms_diagnosis_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH M_Pulmonary_Embolism_MeSH S_diagnosis_MeSH Pulmonary_Embolism_diagnosis_MeSH S_epidemiology_MeSH Pulmonary_Embolism_epidemiology_MeSH S_etiology_MeSH Pulmonary_Embolism_etiology_MeSH M_Risk_MeSH M_Thrombophlebitis_MeSH S_diagnosis_MeSH Thrombophlebitis_diagnosis_MeSH S_epidemiology_MeSH Thrombophlebitis_epidemiology_MeSH S_etiology_MeSH Thrombophlebitis_etiology_MeSH 
****** 9675624
----K E
----T Comparison of chlorthalidone, propranolol and bopindolol in six-month treatment of arterial hypertension.
----A The aim of this study was to test the hypothesis that prolonged treatment of mild to moderate hypertension with low-dose thiazide diuretics or beta blockers does not induce any of the major untoward biochemical changes, such as hypertriglyceridemia, hypercholesterolemia, hyperuricemia and electrolyte imbalances. The effect of these drugs was analyzed in 100 outpatients (52 males and 48 females) aged 52.0 +/- 7.9 years with mild to moderate hypertension, in a prospective 6-month study. After an appropriate workup, the patients were randomized to either 25 mg chlorthalidone (40 patients), 120 mg propranolol (30 patients), or 2 mg per day bopindolol (30 patients). A significant reduction of approximately 10% in systolic and diastolic blood pressure was recorded in all the groups. At the end of the 6th month, in the chlorthalidone group triglycerides increased to 3.0 +/- 2.1 mmol/l from 2.8 +/- 1.6 mmol/l, while cholesterol after an initial increase to 6.6 +/- 1.6 from 6.4 +/- 1.6 mmol/l returned to the baseline level. Uricemia and serum potassium concentration decreased by 4%. The body weight was reduced to 83.8 +/- 13.4 kg from 86.1 +/- 13.4 kg. There was no change in serum glucose level. In the propranolol group, as expected, heart rate decreased by 20%, but there were no significant changes in glucose and potassium plasma concentration. Triglycerides did not change significantly, while cholesterol, after a small increase, returned to the initial levels. Similar results were obtained in the bopindolol group, apart from the triglycerides, which increased significantly (to 2.5 +/- 1.1 from 2.2 +/- 0.4 mmol/l), probably because of the lower baseline concentration. We conclude that in prolonged treatment, chlorthalidone, propranolol and bopindolol do not induce significant untoward biochemical changes that alone might increase cardiovascular risk.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_administration_&_dosage_MeSH Chlorthalidone_administration_&_dosage_MeSH S_adverse_effects_MeSH Chlorthalidone_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_chemically_induced_MeSH Hyperlipidemia_chemically_induced_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Hypokalemia_MeSH S_chemically_induced_MeSH Hypokalemia_chemically_induced_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_administration_&_dosage_MeSH Pindolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Pindolol_analogs_&_derivatives_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Prospective_Studies_MeSH 
****** 9675959
----K 1
----T [Complex ventricular arrhythmias and carvedilol: efficacy in hemodialyzed uremic patients]
----A Carvedilol has been shown to be effective in systemic hypertension and coronary artery disease in patients with end-stage renal disease, on maintenance hemodialysis. The aim of our study was to assess the effects of carvedilol on ventricular arrhythmias in these patients. Ninety-eight uremic patients maintained on hemodialysis, with complex ventricular arrhythmias (class III, IV and V of Lown's classification), not only during dialysis, were included in the study. They were divided into two groups, with mild-to-moderate hypertension or coronary artery disease. The efficacy and safety of carvedilol (50 mg/day) was compared to placebo in a 6-week randomized, double-blind study. Carvedilol significantly reduced, in both hypertensive and ischemic patients, total ventricular premature contractions (82.7 +/- 11.3 vs 358.1 +/- 73.9, p < 0.001; 88.3 +/- 24.4 vs 369.9 +/- 77.8, p < 0.001), repetitive ventricular premature contractions (1.3 +/- 1.3 vs 6.3 +/- 3.5, p < 0.001; 1.2 +/- 0.7 vs 6.9 +/- 2.6, p < 0.001) and episodes of ventricular tachycardia (1.1 +/- 1.2 vs 11.8 +/- 7.5, p < 0.001; 1.4 +/- 1.2 vs 14.0 +/- 8.3, p < 0.001). In placebo-treated patients, instead, these parameters were not significantly changed (329.1 +/- 76.5 vs 361.7 +/- 71.7, NS, and 324.6 +/- 79.7 vs 359.3 +/- 58.1, NS; 6.2 +/- 3.7 vs 7.3 +/- 3.7, NS, and 4.9 +/- 2.2 vs 6.1 +/- 3.2, NS; 9.8 +/- 6.3 vs 13.3 +/- 8.0, NS, and 9.0 +/- 6.2 vs 12.4 +/- 7.8, NS). Carvedilol confirmed a significant effect on myocardial ischemia and systemic hypertension. No significant side effects were reported. Ventricular arrhythmias are frequent in patients with end-stage renal disease maintained on hemodialysis. They are often due to an underlying cardiac disease, namely systemic hypertension with left ventricular hypertrophy and coronary artery disease. The results of our study show that the antiarrhythmic effect of carvedilol is linked, at least partly, to an improvement of the underlying cardiac disease. Uremic patients have a chronic increase in adrenergic tone, with a direct correlation between norepinephrine plasmatic concentration and frequence of premature ventricular contractions. Beta-blockers are very important in these patients because of their modulation on the adrenergic system. They also reduce potassium flow, from extracellular to intracellular fluid. Therefore carvedilol can affect the sudden hypokalemia occurring in the first phase of hemodialysis treatment, that may be an important cause of intradialytic arrhythmias.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial Review Review_Literature 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Kidney_Failure__Chronic_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH S_therapy_MeSH Kidney_Failure__Chronic_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH P_Renal_Dialysis_MeSH M_Tachycardia__Ventricular_MeSH S_complications_MeSH Tachycardia__Ventricular_complications_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH M_Uremia_MeSH S_etiology_MeSH Uremia_etiology_MeSH S_therapy_MeSH Uremia_therapy_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9679720
----K E
----T Effect of single-drug therapy on reduction of left atrial size in mild to moderate hypertension: comparison of six antihypertensive agents.
----A BACKGROUND: Cardiac effects of hypertension include increased left ventricular (LV) mass and LV hypertrophy, as well as increased left atrial size, a predictor of stroke and atrial fibrillation. Although literature on reduction of LV mass with antihypertensive therapy is extensive, little information is available on effects of treatment on left atrial size. METHODS AND RESULTS: Patients with mild to moderate hypertension (diastolic blood pressure 95 to 109 mm Hg) were randomly allocated to treatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-masked trial. Two-dimensional targeted M-mode echocardiography was used to assess left atrial size and LV mass at baseline, 8 weeks, and 1 and 2 years. Longitudinal analysis examined changes in left atrial size from the baseline study, statistically adjusting for age, race, pretreatment left atrial size and LV mass, and serial measurements of systolic blood pressure, body weight, urinary sodium excretion, and physical activity score. Without adjustment for covariates, only hydrochlorothiazide was associated with decreases in left atrial size from baseline at 8 weeks (-1.0 +/- 5.2 mm; P=0.052), 1 year (-2.0 +/- 5.1 mm; P=0.02), and 2 years (4.6+/-7.2 mm; P=0.002). After adjustment for effects of covariates, patients with normal left atrial size had greater reduction (-3.3 mm) in left atrial size at 2 years with hydrochlorothiazide than with any other drug. For patients with left atrial enlargement, left atrial size decreased significantly with hydrochlorothiazide, atenolol, clonidine, and diltiazem at 1 year and with all treatments at 2 years. However, reduction at 2 years was greater with hydrochlorothiazide than with captopril or prazosin. CONCLUSIONS: Antihypertensive drugs differ in their effects on left atrial size. Hydrochlorothiazide was associated with greater overall reduction of left atrial size than other drugs effective for the treatment of hypertension. Reduction of left atrial size with therapy is in part independent of factors known to influence left atrial size, including LV mass and reduction of LV mass with treatment. The clinical benefit of reducing left atrial size with antihypertensive treatment remains to be determined.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH P_Echocardiography_MeSH M_Heart_Atria_MeSH S_drug_effects_MeSH Heart_Atria_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 9683206
----K E
----T Do inhibitors of angiotensin-I-converting enzyme protect against risk of cancer?
----A BACKGROUND: Previous studies have reported an increased risk of cancer with calcium-channel blockers in man. Other work in animals suggests that inhibitors of angiotensin-I-converting enzyme (ACE) protect against cancer. We aimed to assess the risk of cancer in hypertensive patients receiving ACE inhibitors or other antihypertensive drugs. METHODS: Our retrospective cohort study was based on the records of 5207 patients who attended the Glasgow Blood Pressure Clinic between Jan 1, 1980, and Dec 31, 1995. The patients' records are linked with the Registrar General Scotland and the West of Scotland Cancer Registry. FINDINGS: Compared with the West of Scotland controls, the relative risks of incident and fatal cancer among the 1559 patients receiving ACE inhibitors were 0.72 (95% CI 0.55-0.92) and 0.65 (0.44-0.93). Among the 3648 patients receiving antihypertensive drugs other than ACE inhibitors (calcium-channel blockers 1416, diuretics 2099, beta-blockers 2681), the corresponding relative risks were 110 (0.97-1.22) and 1.03 (0.87-1.20). The relative risk of cancer was lowest in women on ACE inhibitors: 0.63 (0.41-0.93) for incident cancer; 0.48 (0.23-0.88) for fatal cancer; and 0.37 (0.12-0.87) for female-specific cancers. The reduced relative risk of cancer in patients on ACE inhibitors was greatest with follow-up of longer than 3 years. Calcium-channel blockers, diuretics, and beta-blockers had no apparent effect on risk of cancer. INTERPRETATION: Long-term use of ACE inhibitors may protect against cancer. The status of this finding is more that of hypothesis generation than of hypothesis testing; randomised controlled trials are needed.
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neoplasms_MeSH S_epidemiology_MeSH Neoplasms_epidemiology_MeSH S_prevention_&_control_MeSH Neoplasms_prevention_&_control_MeSH M_Registries_MeSH S_statistics_&_numerical_data_MeSH Registries_statistics_&_numerical_data_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Scotland_MeSH S_epidemiology_MeSH Scotland_epidemiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9683312
----K E
----T Rationale and design for the Controlled ONset Verapamil INvestigation of Cardiovascular Endpoints (CONVINCE) Trial.
----A The Controlled ONset Verapamil INvestigation of Cardiovascular Endpoints (CONVINCE) Trial is a randomized, prospective, double-blind, parallel-group, two-arm, actively controlled, multicenter, international 5-year clinical trial involving 15,000 patients. CONVINCE will compare the incidence of fatal or nonfatal myocardial infarction (MI), fatal or nonfatal stroke, or cardiovascular-disease-related death in two antihypertensive treatment regimens. One treatment arm begins with controlled onset-extended release (COER)-verapamil, which has its major antihypertensive effect 6-12 hours after administration. The other arm (standard of care (SOC)) begins with either hydrochlorothiazide (HCTZ) or atenolol, one of which is preselected by the investigator for an individual patient prior to randomization. Secondary objectives include comparisons of the regimens for each of the components of the primary endpoint (separately), death or hospitalization related to cardiovascular disease, efficacy in lowering blood pressure to goal, primary events occurring between 6 am and noon, all-cause mortality, withdrawals from blinded therapy, cancer, and hospitalizations due to bleeding. Patients may be enrolled if they are hypertensive and at least 55 years of age and have an established second risk factor for cardiovascular disease. Initial medications include COER-verapamil (180 mg/d), HCTZ (12.5 mg/d), or atenolol (50 mg/d). Initial doses are doubled if blood pressure (BP) does not reach goal (systolic BP < 140 mm and diastolic BP < 90 mm Hg). If BP is not controlled by the higher dose of the initial medication, HCTZ is added to COER-verapamil, or the SOC choice not initially selected is added in the SOC arm. An ACE-inhibitor is recommended (although nearly any open-label medication is allowed) as the third step for patients whose BP is not adequately controlled or who have a contraindication to one of the two SOC medications. Patients take two sets of tablets daily, one in the morning and one in the evening. Although most patients switch from an established antihypertensive medication to randomized treatment, untreated patients with stages I-III hypertension (SBP between 140 and 190 or DBP between 90 and 110 mm Hg) are eligible. Outcomes are monitored by an independent Data and Safety Monitoring Board. Enrollment began during the third quarter of 1996, and follow-up is to be completed in the third quarter of 2002.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9700441
----K I
----T An evidence-based approach to the treatment of esophageal variceal bleeding.
----A Esophageal varices are a life threatening cause of gastrointestinal bleeding. Management includes both primary prevention of variceal bleeding and treatment of actively bleeding varices. Evidence from randomized controlled trials indicates that beta blockers and nitrates may prevent the initial episode of bleeding varices. Ample data from randomized controlled trials indicate that band ligation is more effective than scleropathy for the treatment of bleeding esophageal varices. Somatostatin may decrease rebleeding rates with or without endoscopic therapy. No effective treatment has been developed for the treatment of patients who fail endoscopic therapy.
----P Journal_Article Meta-Analysis 
----M M_Adult_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH P_Evidence-Based_Medicine_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_MEDLINE_MeSH M_Meta-Analysis_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9700713
----K E
----T Cerebral hemodynamics in young hypertensive subjects and effects of atenolol treatment.
----A The aim of this study was to evaluate changes in cerebral hemodynamics in young patients with uncomplicated hypertension before and after effective antihypertensive treatment with a beta-blocker drug. Changes in mean flow velocity in the middle cerebral artery from normal condition to hypercapnia were evaluated by means of a transcranial Doppler in 42 hypertensive patients and 21 healthy subjects comparable for age and sex distribution. We obtained hypercapnia with breath-holding and evaluated cerebrovascular reactivity with the breath-holding index (BHI). After a baseline evaluation (time 0), patients were randomly assigned to a placebo (group 1) or atenolol (group 2) therapy. The evaluation was repeated after 30 (time 1) and 60 (time 2) days of treatment. Before treatment, hypertensive patients had significantly lower BHI values (0.96 +/- 0.1 group 1 and 0.85 +/- 0.3 group 2) than controls (1.69 +/- 0.4) (P < 0.0001). During treatment, mean blood pressure significantly decreased in group 2 patients. In the same group, BHI values significantly increased with respect to the pre-treatment evaluation: 1.39 +/- 0.2 at time 1 and 1.44 +/- 0.2 at time 2 (P < 0.0001). On the contrary, mean blood pressure and BHI values remained unchanged in the placebo group. Furthermore, BHI values were significantly higher in group 2 than in group 1 patients at times 1 (P < 0.001) and 2 (P < 0.0001). These findings suggest that hypertension causes reduced capability of cerebral vessels to adapt to functional changes. This condition, which is reversible after treatment, could be implicated in the increased susceptibility to ischemic stroke in hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Flow_Velocity_MeSH M_Carbon_Dioxide_MeSH S_blood_MeSH Carbon_Dioxide_blood_MeSH M_Cerebral_Arteries_MeSH S_physiology_MeSH Cerebral_Arteries_physiology_MeSH S_physiopathology_MeSH Cerebral_Arteries_physiopathology_MeSH S_ultrasonography_MeSH Cerebral_Arteries_ultrasonography_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Reference_Values_MeSH M_Ultrasonography__Doppler__Transcranial_MeSH 
****** 9702935
----K E
----T Comparison of irbesartan vs felodipine in the regression after 1 year of left ventricular hypertrophy in hypertensive patients (the SILVER trial). Study of Irbesartan in Left VEntricular hypertrophy Regression.
----A The SILVER (Study of Irbesartan in Left VEntricular hypertrophy Regression) trial is designed to test the hypothesis that the newly developed angiontensin-II receptor antagonist, irbesartan, will produce a greater reduction in left ventricular (LV) mass than felodipine ER, in a population of hypertensive patients defined by seated diastolic blood pressure (SeDBP) in the range 95-115 mmHg or seated systolic blood pressure (SeSBP) in the range 160-200 mm Hg. A population of 360 men and women of non-childbearing potential, >18 years of age, with hypertension, newly diagnosed or after a 3-week washout from previous anti-hypertensive or vasodilator therapies, will be randomised at approximately 80-90 European sites. Add-on therapy with hydrochlorothiazide and atenolol will be allowed for blood pressure control. Patients will be studied by two-dimensional and M-mode echocardiography at baseline (central validation of LV hypertrophy), on randomisation day, and after 6 and 12 months randomised therapy. Blinded analysis of echocardiograms will be performed at a central laboratory, which will provide measurements of the LV mass index (LVMI), determined by M-mode readings according to Devereux formula and using the Penn convention. The primary end-point of the study will be the change in LVMI from baseline to 12 months. The study power is 90% to detect differences between groups from baseline of approximately 8 g/m2.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9702620
----K E
----T Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy.
----A STUDY OBJECTIVE: To examine the acute hemodynamic effects of intravenous (i.v.) nicardipine and its ability to attenuate the hyperdynamic response to electroconvulsive therapy (ECT), when used alone or in combination with labetalol. DESIGN: Prospective, randomized, double-blind, positive-control, clinical investigation. SETTING: University hospital. PATIENTS: 36 patients undergoing ECT. INTERVENTIONS: In a series of three studies, the hemodynamic effects of nicardipine were assessed prior to, during, and after ECT. After administration of glycopyrrolate 0.1 mg i.v., placebo (saline) or nicardipine was administered by rapid infusion (1, 2.5, 5, 10, and 15 mg) or bolus injection (1.25, 2.5, and 5 mg), either alone or in combination with labetalol 10 mg i.v. Unconsciousness was induced with methohexital 1 mg/kg i.v.; succinylcholine 1.2 to 1.5 mg/kg i.v. was administered for muscle relaxation. A bilateral electrical stimulus was delivered and the durations of motor and electroencephalographic (EEG) seizures were noted. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure (MAP) and heart rate (HR) values were recorded at 1- to 5-minute intervals throughout the study period. When administered as a rapid infusion, nicardipine 5 mg i.v. produced a significant decrease in MAP; however, nicardipine dosages of 10 to 15 mg i.v. did not produce a significantly greater decrease in MAP than 5 mg. Bolus administration of nicardipine 1.25 to 5 mg produced a rapid onset of its hemodynamic effects without exacerbating the cardiovascular depressant effects of methohexital. However, the decrease in MAP was accompanied by an increase in HR after administration of the 5 mg i.v. bolus dose. The acute hyperdynamic response to ECT was most effectively controlled by nicardipine 2.5 to 5 mg i.v. bolus, in combination with labetalol 10 mg i.v. Seizure duration was not significantly altered by the use of nicardipine as part of the anesthetic regimen for ECT. CONCLUSION: Nicardipine 2.5 mg i.v. bolus in combination with labetalol 10 mg i.v. was the most effective pretreatment regimen for preventing the acute hyperdynamic response to ECT. However, this combination produced a 20% decrease in MAP immediately prior to ECT and a lower MAP at the time of discharge.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anesthetics__Intravenous_MeSH S_administration_&_dosage_MeSH Anesthetics__Intravenous_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH P_Electroconvulsive_Therapy_MeSH M_Electroencephalography_MeSH M_Glycopyrrolate_MeSH S_administration_&_dosage_MeSH Glycopyrrolate_administration_&_dosage_MeSH S_therapeutic_use_MeSH Glycopyrrolate_therapeutic_use_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Injections__Intravenous_MeSH M_Labetalol_MeSH S_administration_&_dosage_MeSH Labetalol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Labetalol_therapeutic_use_MeSH M_Methohexital_MeSH S_administration_&_dosage_MeSH Methohexital_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Muscarinic_Antagonists_MeSH S_administration_&_dosage_MeSH Muscarinic_Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Muscarinic_Antagonists_therapeutic_use_MeSH M_Neuromuscular_Depolarizing_Agents_MeSH S_administration_&_dosage_MeSH Neuromuscular_Depolarizing_Agents_administration_&_dosage_MeSH M_Nicardipine_MeSH S_administration_&_dosage_MeSH Nicardipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Placebos_MeSH M_Prospective_Studies_MeSH M_Seizures_MeSH S_physiopathology_MeSH Seizures_physiopathology_MeSH S_prevention_&_control_MeSH Seizures_prevention_&_control_MeSH M_Succinylcholine_MeSH S_administration_&_dosage_MeSH Succinylcholine_administration_&_dosage_MeSH 
****** 9707705
----K E
----T How safe is carvedilol in NIDDM patients with hypertension?
----A 
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9710178
----K E
----T Secondary prevention of coronary heart disease.
----A Despite the significant reduction in cardiovascular mortality during the past three decades, atherosclerotic coronary heart disease (CHD) remains the leading cause of death and disability in the United States. Randomized clinical trials in patients with CHD have provided convincing evidence that risk factor modification is beneficial in decreasing all-cause mortality and cardiovascular morbidity and mortality. Multifactorial coronary risk reduction provides the most substantial benefit. Coronary risk reduction is associated with a decrease in cardiovascular-related hospital admissions, a reduced need for myocardial revascularization procedures, and an improved quality of life for the patients so treated. Control of coronary risk factors is an integral component of the optimal care of the patient with CHD.
----P Journal_Article Review Review__Tutorial 
----M M_Algorithms_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_rehabilitation_MeSH Coronary_Disease_rehabilitation_MeSH M_Decision_Trees_MeSH M_Exercise_MeSH P_Health_Behavior_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH P_Life_Style_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH M_Risk_Factors_MeSH 
****** 9715821
----K I
----T Over 20 years' experience of beta-blockade in heart failure.
----A The use of beta-blocker therapy in heart failure was contraindicated for many years because it was considered to block necessary sympathetic compensatory responses to reduced cardiac function. However, early studies provided promising results in terms of improved symptoms and work capacity and reduced heart size. Small-scale studies have been completed over the past 20 years but until large-scale, long-term, randomized trials were conducted, the potential of beta-blockers in heart failure was not confirmed. The results of randomized trials published to date have included over 3,000 patients and the results show improvements in left ventricular function and heart rate. Significant improvements in New York Heart Association classification were also shown. Although no conclusive effect on mortality was shown, the first Cardiac Insufficiency Bisoprolol Study (CIBIS) indicated a trend toward improved survival during long-term treatment with bisoprolol. Ongoing studies have been specifically designed to investigate the effects of beta-blockers on survival. One of these trials, CIBIS II, which was terminated early in 1998 because of a positive effect on survival, is expected to report in late summer 1998. Such trials will also examine the different mechanisms of action of beta-blockers in heart failure and the influence of causes on the effects of beta-blockade.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9715823
----K E
----T Use of carvedilol in chronic heart failure: challenges in therapeutic management.
----A In controlled trials, long-term treatment of patients with chronic heart failure with beta-blockers improves symptoms, slows progression of disease, and reduces morbidity and mortality rates. However, in some patients the introduction of therapy can be associated with a period of clinical instability, including risks of fluid retention, hypotension, and bradycardia. Appropriate patient selection and optimization of background therapy can minimize the risk during the introduction of therapy. With vigilance for early signs of clinical deterioration and appropriate adjustment of background medications, the care of most patients exhibiting clinical instability can be successfully managed so the patient is able to continue with the long-term therapy, a prerequisite to realizing beneficial effects. With the initiation of carvedilol, any evidence of fluid retention warrants a prompt increase in the diuretic dosage, and in more pronounced cases the carvedilol dose may need to be reduced or interrupted. In contrast, symptoms of hypotension (most commonly dizziness) generally resolve without intervention, although persistent problems may necessitate adjusting the timing of dose administration or perhaps temporarily reducing the dose of vasodilators or diuretics (the latter with care to avoid fluid retention). Bradycardia should be managed as standard practice would indicate. During long-term treatment, adjustments in beta-blocker dosage may be required in the event of an exacerbation of heart failure. Dosages should be adjusted as would be the case with other heart-failure medications, based on the severity of the clinical decompensation, but with care to minimize abrupt changes unless mandated by the patient's condition and to avoid precipitating ischemia or further deterioration. The occurrence of effects such as these does not necessarily indicate that a patient cannot respond favorably to long-term beta-blockade, but all require understanding, vigilance, and the availability of medical personnel, especially during the introduction of this therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Controlled_Clinical_Trials_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9717036
----K E
----T Does sublingual 17 beta-oestradiol have any effects on exercise capacity and myocardial ischaemia in post-menopausal women with stable coronary artery disease?
----A BACKGROUND: A variety of vascular effects have been ascribed to 17 beta-oestradiol. These effects may partially explain the reduced incidence of cardiovascular disease found in post-menopausal women on oestrogen replacement therapy. OBJECTIVES: To evaluate the effects of 2 mg sublingual 17 beta-oestradiol on exercise capacity, exercise-induced myocardial ischaemia and circulating levels of endothelin-1 in post-menopausal women with stable coronary artery disease. METHODS: Twelve post-menopausal women, mean age 61 (range 52-72) years, with angiographically verified significant coronary artery disease, were randomly assigned to 2 mg of sublingual 17 beta-oestradiol, 2.5 mg of buccal nitroglycerine and to placebo in a double-blind cross-over study design with at least 2 days between each of the study arms. Antianginal medications, with the exception of beta-blockers, were discontinued before investigation. All study patients underwent a maximal bicycle exercise test 30 min after drug intake. Blood was withdrawn immediately before and up to 8 h after medication for analyses of circulating levels of oestradiol and endothelin-1. RESULTS: The mean serum levels of oestradiol increased from a control level of 72 +/- 28 pmol.l-1 to 3557 +/- 1731 pmol.l-1 after 30 min and to 5028 +/- 3971 pmol.l-1 after 60 min with a gradual decline thereafter. Sublingual 17 beta-oestradiol did not induce any improvement in exercise duration when compared with nitroglycerin and placebo (500 +/- 112 s, 505 +/- 107 s, 498 +/- 157 s), and did not influence time to onset of ST-segment depression (358 +/- 89 s, 436 +/- 93 s, 384 +/- 116 s). The plasma levels of endothelin-1 did not change after administration of 17 beta-oestradiol, nitroglycerin or placebo. CONCLUSIONS: No effects of exercise capacity, exercise-induced acute ischaemia, or plasma levels of endothelin-1 were found after a single dose of 2 mg 17 beta-oestradiol in post-menopausal women with documented coronary artery disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Sublingual_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH M_Estradiol_MeSH S_administration_&_dosage_MeSH Estradiol_administration_&_dosage_MeSH P_Estrogen_Replacement_Therapy_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Nitroglycerin_MeSH S_administration_&_dosage_MeSH Nitroglycerin_administration_&_dosage_MeSH M_Postmenopause_MeSH S_drug_effects_MeSH Postmenopause_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9720548
----K E
----T Tamsulosin treatment of 19,365 patients with lower urinary tract symptoms: does co-morbidity alter tolerability?
----A PURPOSE: We compare the tolerability and blood pressure effects of 0.4 mg. tamsulosin once daily in patients with lower urinary symptoms suggestive of benign prostatic obstruction with or without concomitant disease and/or antihypertensive medication. MATERIALS AND METHODS: Data from 2 open label, observational studies (study 1, 9,507 patients treated for 4 weeks and study 2, 9,858 patients treated for 12 weeks) were analyzed for global tolerability and effects on blood pressure stratifying for co-morbidity (none, diabetes, hypertension, other cardiovascular disease) and co-medication (diuretics, beta-blockers, calcium channel blockers, angiotensin converting enzyme inhibitors). RESULTS: Overall 90 and 95% of patients in studies 1 and 2, respectively, reported good or very good tolerability. While global tolerability was slightly reduced in patients with concomitant disease or some forms of medication (p < 0.05), it was rated as good or very good by more than 90 and 95% of patients even in those groups. In control patients, that is those with neither co-morbidity nor co-medication, the tamsulosin induced blood pressure reductions were similar to those previously reported for placebo treatment but were statistically significant (p < 0.05). Mean additional blood pressure reductions in patients with concomitant disease or medication were not more than 2 mm. Hg. CONCLUSIONS: Tamsulosin is well tolerated and has marginal effects on blood pressure in the majority of patients. It largely maintains its good global tolerability and minimal blood pressure effects in patients with cardiovascular co-morbidity or diabetes, or those on co-medication with antihypertensive agents.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Drug_Tolerance_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prostatic_Hyperplasia_MeSH S_complications_MeSH Prostatic_Hyperplasia_complications_MeSH S_drug_therapy_MeSH Prostatic_Hyperplasia_drug_therapy_MeSH M_Sulfonamides_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH 
****** 9731558
----K E
----T Effects of propranolol on the hepatic hemodynamic response to physical exercise in patients with cirrhosis.
----A Physical exercise increases portal pressure (hepatic venous pressure gradient [HVPG]) in patients with cirrhosis. It is unknown if this deleterious effect is associated with changes in gastroesophageal collateral blood flow and if these can be prevented by propranolol administration. The aim of this study was to characterize the effects of propranolol on the splanchnic hemodynamic response to exercise in patients with cirrhosis. Twenty-three patients with cirrhosis and portal hypertension had hemodynamic measurements in baseline conditions, and during moderate cycling exercise (40 W) under double-blind propranolol or placebo administration. In patients receiving placebo, HVPG significantly increased during exercise (from 16.7 +/- 0.9 to 19.0 +/- 1.0 mm Hg; P < .01), hepatic blood flow (HBF) decreased (-18% +/- 4%; P < .01), while azygos blood flow (AzBF) was unchanged (4% +/- 12%; ns). In patients receiving propranolol, portal pressure did not increase during exercise, but decreased from 16.3 +/- 1.0 to 12.9 +/- 1.1 mm Hg (P < .01). The lack of increase in HVPG in response to exercise in patients receiving propranolol may be related to a more pronounced decrease in HBF, as compared with patients receiving placebo, and to a blunted increase in cardiac output (CO). Moderate physical exercise adversely influences the hepatic hemodynamics in patients with cirrhosis, causing a significant increase in portal pressure. This is effectively prevented by propranolol pretreatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH P_Exercise_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Liver_MeSH S_drug_effects_MeSH Liver_drug_effects_MeSH S_physiology_MeSH Liver_physiology_MeSH M_Liver_Cirrhosis_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9732337
----K E
----T Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group.
----A OBJECTIVE: To determine whether tight control of blood pressure prevents macrovascular and microvascular complications in patients with type 2 diabetes. DESIGN: Randomised controlled trial comparing tight control of blood pressure aiming at a blood pressure of <150/85 mm Hg (with the use of an angiotensin converting enzyme inhibitor captopril or a beta blocker atenolol as main treatment) with less tight control aiming at a blood pressure of <180/105 mm Hg. SETTING: 20 hospital based clinics in England, Scotland, and Northern Ireland. SUBJECTS: 1148 hypertensive patients with type 2 diabetes (mean age 56, mean blood pressure at entry 160/94 mm Hg); 758 patients were allocated to tight control of blood pressure and 390 patients to less tight control with a median follow up of 8.4 years. MAIN OUTCOME MEASURES: Predefined clinical end points, fatal and non-fatal, related to diabetes, deaths related to diabetes, and all cause mortality. Surrogate measures of microvascular disease included urinary albumin excretion and retinal photography. RESULTS: Mean blood pressure during follow up was significantly reduced in the group assigned tight blood pressure control (144/82 mm Hg) compared with the group assigned to less tight control (154/87 mm Hg) (P<0.0001). Reductions in risk in the group assigned to tight control compared with that assigned to less tight control were 24% in diabetes related end points (95% confidence interval 8% to 38%) (P=0.0046), 32% in deaths related to diabetes (6% to 51%) (P=0.019), 44% in strokes (11% to 65%) (P=0.013), and 37% in microvascular end points (11% to 56%) (P=0.0092), predominantly owing to a reduced risk of retinal photocoagulation. There was a non-significant reduction in all cause mortality. After nine years of follow up the group assigned to tight blood pressure control also had a 34% reduction in risk in the proportion of patients with deterioration of retinopathy by two steps (99% confidence interval 11% to 50%) (P=0.0004) and a 47% reduced risk (7% to 70%) (P=0.004) of deterioration in visual acuity by three lines of the early treatment of diabetic retinopathy study (ETDRS) chart. After nine years of follow up 29% of patients in the group assigned to tight control required three or more treatments to lower blood pressure to achieve target blood pressures. CONCLUSION: Tight blood pressure control in patients with hypertension and type 2 diabetes achieves a clinically important reduction in the risk of deaths related to diabetes, complications related to diabetes, progression of diabetic retinopathy, and deterioration in visual acuity.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Albuminuria_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Diabetic_Retinopathy_MeSH S_prevention_&_control_MeSH Diabetic_Retinopathy_prevention_&_control_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypoglycemia_MeSH S_etiology_MeSH Hypoglycemia_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Patient_Compliance_MeSH M_Peripheral_Vascular_Diseases_MeSH S_prevention_&_control_MeSH Peripheral_Vascular_Diseases_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Visual_Acuity_MeSH M_Weight_Gain_MeSH S_drug_effects_MeSH Weight_Gain_drug_effects_MeSH 
****** 9732338
----K E
----T Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. UK Prospective Diabetes Study Group.
----A OBJECTIVE: To determine whether tight control of blood pressure with either a beta blocker or an angiotensin converting enzyme inhibitor has a specific advantage or disadvantage in preventing the macrovascular and microvascular complications of type 2 diabetes. DESIGN: Randomised controlled trial comparing an angiotensin converting enzyme inhibitor (captopril) with a beta blocker (atenolol) in patients with type 2 diabetes aiming at a blood pressure of <150/<85 mm Hg. SETTING: 20 hospital based clinics in England, Scotland, and Northern Ireland. SUBJECTS: 1148 hypertensive patients with type 2 diabetes (mean age 56 years, mean blood pressure 160/94 mm Hg). Of the 758 patients allocated to tight control of blood pressure, 400 were allocated to captopril and 358 to atenolol. 390 patients were allocated to less tight control of blood pressure. MAIN OUTCOME MEASURES: Predefined clinical end points, fatal and non-fatal, related to diabetes, death related to diabetes, and all cause mortality. Surrogate measures of microvascular and macrovascular disease included urinary albumin excretion and retinopathy assessed by retinal photography. RESULTS: Captopril and atenolol were equally effective in reducing blood pressure to a mean of 144/83 mm Hg and 143/81 mm Hg respectively, with a similar proportion of patients (27% and 31%) requiring three or more antihypertensive treatments. More patients in the captopril group than the atenolol group took the allocated treatment: at their last clinic visit, 78% of those allocated captopril and 65% of those allocated atenolol were taking the drug (P<0.0001). Captopril and atenolol were equally effective in reducing the risk of macrovascular end points. Similar proportions of patients in the two groups showed deterioration in retinopathy by two grades after nine years (31% in the captopril group and 37% in the atenolol group) and developed clinical grade albuminuria >=300 mg/l (5% and 9%). The proportion of patients with hypoglycaemic attacks was not different between groups, but mean weight gain in the atenolol group was greater (3.4 kg v 1.6 kg). CONCLUSION: Blood pressure lowering with captopril or atenolol was similarly effective in reducing the incidence of diabetic complications. This study provided no evidence that either drug has any specific beneficial or deleterious effect, suggesting that blood pressure reduction in itself may be more important than the treatment used.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Diabetic_Retinopathy_MeSH S_prevention_&_control_MeSH Diabetic_Retinopathy_prevention_&_control_MeSH M_Follow-Up_Studies_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_metabolism_MeSH Hemoglobin_A__Glycosylated_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypoglycemia_MeSH S_chemically_induced_MeSH Hypoglycemia_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Patient_Compliance_MeSH M_Peripheral_Vascular_Diseases_MeSH S_prevention_&_control_MeSH Peripheral_Vascular_Diseases_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Visual_Acuity_MeSH M_Weight_Gain_MeSH S_drug_effects_MeSH Weight_Gain_drug_effects_MeSH 
****** 9732339
----K E
----T Cost effectiveness analysis of improved blood pressure control in hypertensive patients with type 2 diabetes: UKPDS 40. UK Prospective Diabetes Study Group.
----A OBJECTIVES: To estimate the economic efficiency of tight blood pressure control, with angiotensin converting enzyme inhibitors or beta blockers, compared with less tight control in hypertensive patients with type 2 diabetes. DESIGN: Cost effectiveness analysis incorporating within trial analysis and estimation of impact on life expectancy through use of the within trial hazards of reaching a defined clinical end point. Use of resources driven by trial protocol and use of resources in standard clinical practice were both considered. SETTING: 20 hospital based clinics in England, Scotland, and Northern Ireland. SUBJECTS: 1148 hypertensive patients with type 2 diabetes from UK prospective diabetes study randomised to tight control of blood pressure (n=758) or less tight control (n=390). MAIN OUTCOME MEASURE: Cost effectiveness ratios based on (a) use of healthcare resources associated with tight control and less tight control and treatment of complications and (b) within trial time free from diabetes related end points, and life years gained. RESULTS: Based on use of resources driven by trial protocol, the incremental cost effectiveness of tight control compared with less tight control was cost saving. Based on use of resources in standard clinical practice, incremental cost per extra year free from end points amounted to pound1049 (costs and effects discounted at 6% per year) and pound434 (costs discounted at 6% per year and effects not discounted). The incremental cost per life year gained was pound720 (costs and effects discounted at 6% per year) and pound291 (costs discounted at 6% per year and effects not discounted). CONCLUSIONS: Tight control of blood pressure in hypertensive patients with type 2 diabetes substantially reduced the cost of complications, increased the interval without complications and survival, and had a cost effectiveness ratio that compares favourably with many accepted healthcare programmes.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_economics_MeSH Atenolol_economics_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Captopril_MeSH S_economics_MeSH Captopril_economics_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cost_of_Illness_MeSH M_Cost-Benefit_Analysis_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_economics_MeSH Diabetes_Mellitus__Type_II_economics_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Health_Services_MeSH S_economics_MeSH Health_Services_economics_MeSH S_utilization_MeSH Health_Services_utilization_MeSH M_Hospitalization_MeSH S_economics_MeSH Hospitalization_economics_MeSH M_Human_MeSH M_Hypertension_MeSH S_economics_MeSH Hypertension_economics_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Life_Expectancy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Quality-Adjusted_Life_Years_MeSH M_Sensitivity_and_Specificity_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 9734114
----K 1
----T [Risk factors of adverse effects of angiotensin-converting enzyme inhibitors. Apropos of 30,072 patients treated by trandolapril]
----A SUMMARY: The aim of the present study was to investigate the incidence of adverse effects and the prognostic value of various risk factors in a large population of unselected hypertensive patients treated with the ACE inhibitor trandolapril. Among the 30 072 patients investigated in this post marketing retrospective study, 1813 patients (6.0 per cent) reported an adverse effect. The five most frequent side effects were coughing (3.1 per cent), dizziness (0.7 per cent), headache (0.6 per cent) asthenia (0.5 per cent) and nausea (0.3 per cent). Intolerance risk factors for trandolapril were researched using both univariate and multivariate analysis. In the univariate analysis, a prior intolerance of an ACE inhibitor and female gender were strongly correlated with either overall intolerance or coughing. The most relevant variables for the occurrence of adverse effects, listed according to their entry order in the multivariate analysis, were: prior intolerance of ACE inhibitors (OR: 4.19, 95 per cent CI: 3.66-4.78), female gender (OR: 1.46, 95 per cent CI: 1.31-1.63), prior intolerance of other antihpertensive agents (OR: 1.27, 95 per cent CI: 1.14-1.41), smoking (OR: 0.76, 95 per cent CI: 0.66-0.87) and combination with a beta blocker (OR: 1.31, 95 per cent CI: 1.08-1.58). A prior intolerance of an ACE inhibitor appears to be a very strong predictor of coughing (OR: 6.14, 95 per cent CI: 5.24-7.19). The following variables, namely female gender (OR: 1.61, 95 per cent CI: 1.40-1.85), age 60-80 (OR: 1.25, 95 per cent CI: 1.09-1.44) and prior intolerance of other antihypertensive agents (OR: 1.20, 95 per cent CI: 1.03-2.39) appear less significant.
----P Case_Reports Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Data_Interpretation__Statistical_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_adverse_effects_MeSH Indoles_adverse_effects_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Product_Surveillance__Postmarketing_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 9737492
----K E
----T Who reviews the reviewers? Feasibility of using a fictitious manuscript to evaluate peer reviewer performance.
----A STUDY OBJECTIVE: To determine whether a fictitious manuscript into which purposeful errors were placed could be used as an instrument to evaluate peer reviewer performance. METHODS: An instrument for reviewer evaluation was created in the form of a fictitious manuscript into which deliberate errors were placed in order to develop an approach for the analysis of peer reviewer performance. The manuscript described a double-blind, placebo control study purportedly demonstrating that intravenous propranolol reduced the pain of acute migraine headache. There were 10 major and 13 minor errors placed in the manuscript. The work was distributed to all reviewers of Annals of Emergency Medicine for review. RESULTS: The manuscript was sent to 262 reviewers; 203 (78%) reviews were returned. One-hundred ninety-nine reviewers recommended a disposition for the manuscript: 15 recommended acceptance, 117 rejection, and 67 revision. The 15 who recommended acceptance identified 17.3% (95% confidence interval [CI] 11.3% to 23.4%) of the major and 11.8% (CI 7.3% to 16.3%) of the minor errors. The 117 who recommended rejection identified 39.1 % (CI 36.3% to 41.9%) of the major and 25.2% (CI 23.0% to 27.4%) of the minor errors. The 67 who recommended revision identified 29.6% (CI 26.1% to 33.1%) of the major and 22.0% (CI 19.3% to 24.8%) of the minor errors. The number of errors identified differed significantly across recommended disposition. Sixty-eight percent of the reviewers did not realize that the conclusions of the work were not supported by the results. CONCLUSION: These data suggest that the use of a preconceived manuscript into which purposeful errors are placed may be a viable approach to evaluate reviewer performance. Peer reviewers in this study failed to identify two thirds of the major errors in such a manuscript.
----P Journal_Article 
----M M_Confidence_Intervals_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Data_Interpretation__Statistical_MeSH M_Double-Blind_Method_MeSH M_Evaluation_Studies_MeSH M_Feasibility_Studies_MeSH M_Human_MeSH M_Manuscripts__Medical_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Pain_Measurement_MeSH M_Patient_Selection_MeSH M_Peer_Review__Research_MeSH S_standards_MeSH Peer_Review__Research_standards_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Publishing_MeSH S_standards_MeSH Publishing_standards_MeSH M_Randomized_Controlled_Trials_MeSH S_standards_MeSH Randomized_Controlled_Trials_standards_MeSH M_Research_Design_MeSH S_standards_MeSH Research_Design_standards_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9738164
----K I
----T Beta-blocker therapy for congestive heart failure: a systemic overview and critical appraisal of the published trials.
----A OBJECTIVE: To evaluate the effect of beta-blockers on mortality and morbidity, and to provide an appraisal of the reliability of the available data. DATA SOURCES: MEDLINE search for trials of beta-blockers for congestive heart failure (CHF). STUDY SELECTION: All randomized trials of beta-blockers versus placebo, or greater than one month's duration, in patients with CHF. Eighteen published trials involving 2986 patients were selected. DATA EXTRACTION: Independently by two authors. DATA SYNTHESIS: The Yusuf-Peto method for combining data was used. Data were available on mortality in 2841 patients (95%), on hospitalization for heart failure in 1514 (51%) and on heart transplantation in 2330 (79%). There was a lower rate of death in the active treatment group (131 of 1606) [8.2] versus 155 of 1235 [12.6%]; OR = 72; 99% CI 0.51 to 1.00), a lower rate of hospitalization for heart failure (137 of 756 [18.1%] versus 218 of 758 [28.7%]; OR = 0.54; 99% CI 0.39 to 0.74) and a trend towards a lower proportion of patients receiving heart transplantation (15 of 1354 [l.1%] versus 26 of 976 [2.7%]; OR = 0.45; 99% CI 0.20 to 1.03). Ventricular function improved; however, there was no effect on exercise duration. Although the effects on mortality were nominally statistically significant, the use of formal methods of interim monitoring adapted for meta-analyses suggests that substantially more patients still need to be studied in large scales trials to provide reliable and conclusive evidence. CONCLUSIONS: While the available data on the use of beta-blockers in CHF appear to be promising, they are neither complete nor robust. The routine use of beta-blockers in patients with heart failure should wait the results of ongoing studies.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Drug_Evaluation_MeSH M_Evaluation_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Reproducibility_of_Results_MeSH 
****** 9741499
----K E
----T A prospective randomized trial of triage angiography in acute coronary syndromes ineligible for thrombolytic therapy. Results of the medicine versus angiography in thrombolytic exclusion (MATE) trial.
----A OBJECTIVES: The purpose of this study was to determine if early triage angiography with revascularization, if indicated, favorably affects clinical outcomes in patients with suspected acute myocardial infarction who are ineligible for thrombolysis. BACKGROUND: The majority of patients with acute myocardial infarction and other acute coronary syndromes are considered ineligible for thrombolysis and therefore are not afforded the opportunity for early reperfusion. METHODS: This multicenter, prospective, randomized trial evaluated in a controlled fashion the outcomes following triage angiography in acute coronary syndromes ineligible for thrombolytic therapy. Eligible patients (n=201) with <24 h of symptoms were randomized to early triage angiography and subsequent therapies based on the angiogram versus conventional medical therapy consisting of aspirin, intravenous heparin, nitroglycerin, beta-blockers, and analgesics. RESULTS: In the triage angiography group, 109 patients underwent early angiography and 64 (58%) received revascularization, whereas in the conservative group, 54 (60%) subsequently underwent nonprotocol angiography in response to recurrent ischemia and 33 (37%) received revascularization (p=0.004). The mean time to revascularization was 27+/-32 versus 88+/-98 h (p=0.0001) and the primary endpoint of recurrent ischemic events or death occurred in 14 (13%) versus 31 (34%) of the triage angiography and conservative groups, respectively (45% risk reduction, 95% CI 27-59%, p=0.0002). There were no differences between the groups with respect to initial hospital costs or length of stay. Long-term follow-up at a median of 21 months revealed no significant differences in the endpoints of late revascularization, recurrent myocardial infarction, or all-cause mortality. CONCLUSIONS: Early triage angiography in patients with acute coronary syndromes who are not eligible for thrombolytics reduced the composite of recurrent ischemic events or death and shortened the time to definitive revascularization during the index hospitalization. Despite more frequent early revascularization after triage angiography, we found no long-term benefit in cardiac outcomes compared with conservative medical therapy with revascularization prompted by recurrent ischemia.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH P_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Hospital_Mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_radiography_MeSH Myocardial_Infarction_radiography_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Myocardial_Revascularization_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH P_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH P_Triage_MeSH 
****** 9741504
----K E
----T Atenolol use and clinical outcomes after thrombolysis for acute myocardial infarction: the GUSTO-I experience. Global Utilization of Streptokinase and TPA (alteplase) for Occluded Coronary Arteries.
----A OBJECTIVES: We assessed the use and effects of acute intravenous and later oral atenolol treatment in a prospectively planned post hoc analysis of the GUSTO-I dataset. BACKGROUND: Early intravenous beta blockade is generally recommended after myocardial infarction, especially for patients with tachycardia and/or hypertension and those without heart failure. METHODS: Besides one of four thrombolytic strategies, patients without hypotension, bradycardia or signs of heart failure were to receive atenolol 5 mg intravenously as soon as possible, another 5 mg intravenously 10 min later and 50 to 100 mg orally daily during hospitalization. We compared the 30-day mortality of patients given no atenolol (n=10,073), any atenolol (n=30,771), any intravenous atenolol (n=18,200), only oral atenolol (n=12,545) and both intravenous and oral drug (n=16,406), after controlling for baseline differences and for early deaths (before oral atenolol could be given). RESULTS: Patients given any atenolol had a lower baseline risk than those not given atenolol. Adjusted 30-day mortality was significantly lower in atenolol-treated patients, but patients treated with intravenous and oral atenolol treatment vs. oral treatment alone were more likely to die (odds ratio, 1.3; 95% confidence interval, 1.0 to 1.5; p=0.02). Subgroups had similar rates of stroke, intracranial hemorrhage and reinfarction, but intravenous atenolol use was associated with more heart failure, shock, recurrent ischemia and pacemaker use than oral atenolol use. CONCLUSIONS: Although atenolol appears to improve outcomes after thrombolysis for myocardial infarction, early intravenous atenolol seems of limited value. The best approach for most patients may be to begin oral atenolol once stable.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Risk_MeSH M_Streptokinase_MeSH S_administration_&_dosage_MeSH Streptokinase_administration_&_dosage_MeSH S_adverse_effects_MeSH Streptokinase_adverse_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH P_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH 
****** 9743424
----K I
----T Effects of atenolol on postoperative myocardial ischemia.
----A 
----P Comment Letter 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH 
****** 9743509
----K I
----T Clinical effects of beta-adrenergic blockade in chronic heart failure: a meta-analysis of double-blind, placebo-controlled, randomized trials.
----A BACKGROUND: beta-Blockers have improved symptoms and reduced the risk of cardiovascular events in studies of patients with heart failure, but it is unclear which end points are most sensitive to the therapeutic effects of these drugs. METHODS AND RESULTS: We combined the results of all 18 published double-blind, placebo-controlled, parallel-group trials of beta-blockers in heart failure. From this combined database of 3023 patients, we evaluated the strength of evidence supporting an effect of treatment on left ventricular ejection fraction, NYHA functional class, hospitalizations for heart failure, and death. beta-Blockers exerted their most persuasive effects on ejection fraction and on the combined risk of death and hospitalization for heart failure. beta-Blockade increased the ejection fraction by 29% (P<10(-9)) and reduced the combined risk of death or hospitalization for heart failure by 37% (P<0.001). Both effects remained significant even if >90% of the trials were eliminated from the analysis or if a large number of trials with a neutral result were added to the analysis. In contrast, the effect of beta-blockade on NYHA functional class was of borderline significance (P=0.04) and disappeared with the addition or removal of only 1 moderate-size study. Although beta -blockade reduced all-cause mortality by 32% (P=0.003), this effect was only moderately robust and varied according to the type of ss-blocker tested, ie, the reduction of mortality risk was greater for nonselective beta-blockers than for beta1-selective agents (49% versus 18%, P=0.049). However, selective and nonselective beta-blockers did not differ in their effects on other measures of clinical efficacy. CONCLUSIONS: These analyses indicate that there is persuasive evidence supporting a favorable effect of beta-blockade on ejection fraction and the combined risk of death and hospitalization for heart failure. In contrast, the effect of these drugs on other end points requires additional study.
----P Clinical_Trial Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 9750252
----K E
----T Construction of a continuous stopping boundary from an alpha spending function.
----A Lan and DeMets (1983, Biometrika 70, 659-663) proposed a flexible method for monitoring accumulating data that does not require the number and times of analyses to be specified in advance yet maintains an overall Type I error, alpha. Their method amounts to discretizing a preselected continuous boundary by clumping the density of the boundary crossing time at discrete analysis times and calculating the resultant discrete-time boundary values. In this framework, the cumulative distribution function of the continuous-time stopping rule is used as an alpha spending function. A key assumption that underlies this method is that future analysis times are not chosen on the basis of the current value of the statistic. However, clinical trials may be monitored more frequently when they are close to crossing the boundary. In this situation, the corresponding continuous-time boundary should be used. Here we demonstrate how to construct a continuous stopping boundary from an alpha spending function. This capability is useful in the design of clinical trials. We use the Beta-Blocker Heart Attack Trial (BHAT) and AIDS Clinical Trials Group protocol 021 for illustration.
----P Journal_Article 
----M M_AIDS-Related_Opportunistic_Infections_MeSH S_prevention_&_control_MeSH AIDS-Related_Opportunistic_Infections_prevention_&_control_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Biometry_MeSH S_methods_MeSH Biometry_methods_MeSH M_Clinical_Trials_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Pneumonia__Pneumocystis_MeSH S_prevention_&_control_MeSH Pneumonia__Pneumocystis_prevention_&_control_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9755356
----K E
----T Serotonergic synergism: the risks and benefits of combining the selective serotonin reuptake inhibitors with other serotonergic drugs.
----A It has become common clinical practice to combine the selective serotonin reuptake inhibitors with other serotonergic agents for augmentation or adjunctive purposes. The empirical basis for using these combinations remains limited, but is growing. Also growing is a literature that suggests that even the most apparently benign combinations of serotonergic drugs carry at least some risk of serious pharmacokinetic or pharmacodynamic drug interactions, such as a serotonin syndrome.
----P Journal_Article 
----M M_Antidepressive_Agents_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Depressive_Disorder_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH M_Drug_Synergism_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Monoamine_Oxidase_Inhibitors_MeSH S_administration_&_dosage_MeSH Monoamine_Oxidase_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Monoamine_Oxidase_Inhibitors_therapeutic_use_MeSH M_Serotonin_Agonists_MeSH S_administration_&_dosage_MeSH Serotonin_Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Serotonin_Antagonists_MeSH S_administration_&_dosage_MeSH Serotonin_Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Serotonin_Antagonists_therapeutic_use_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_administration_&_dosage_MeSH Serotonin_Uptake_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9759992
----K E
----T Valsartan and atenolol in patients with severe essential hypertension.
----A The aim of this study was to evaluate the efficacy and tolerability of valsartan, a new angiotensin II receptor antagonist, versus atenolol in the treatment of severe primary hypertension. A total of 103 adult out-patients were randomised to receive either valsartan 160 mg or atenolol 100 mg once daily for 6 weeks. If necessary, additional blood pressure (BP) control could be provided as add-on therapy. Both valsartan and atenolol decreased mean sitting diastolic BP (DBP) and mean sitting systolic BP (SBP): least squares mean change from baseline in DBP; valsartan, -20.0 mm Hg; atenolol, -20.4 mm Hg: in SBP; valsartan, -30.0 mm Hg; atenolol, -25.5 mm Hg. There was no statistically significant difference between the treatment groups. Add-on hydrochlorothiazide (HCTZ) 25 mg was required by 97.2% of patients receiving atenolol and 83.6% of patients receiving valsartan; additional verapamil SR 240 mg was also required by 58.3% of patients receiving atenolol and 64.2% receiving valsartan. Valsartan was well tolerated, with a comparable incidence of treatment-related adverse experiences in both groups. In conclusion valsartan 160 mg is as well tolerated and effective as atenolol 100 mg in lowering BP in severely hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH M_Valine_MeSH S_administration_&_dosage_MeSH Valine_administration_&_dosage_MeSH S_adverse_effects_MeSH Valine_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH 
****** 9761084
----K I
----T Comparison of metoprolol and sotalol in preventing ventricular tachyarrhythmias after the implantation of a cardioverter/defibrillator.
----A The purpose of this prospective study was to evaluate, on an intention-to-treat basis, the efficacy of d,l-sotalol and metoprolol with regards to the recurrence of arrhythmic events after implantable cardioverter defibrillator (ICD) implantation. After ICD implantation, 70 patients were randomly assigned to treatment with either metoprolol (mean dosage 104+/-37 mg/day in 35 patients) or d,l-sotalol (mean dosage 242+/-109 mg/day in 35 patients). During follow up ventricular tachycardia (VT), fast VT, and ventricular fibrillation (VF) episodes were calculated. Metoprolol treatment led to a marked reduction in the recurrence of arrhythmic events. Actuarial rates for absence of VT recurrence at 1 and 2 years were significantly higher in the metoprolol group compared with the d,l-sotalol group (83% and 80% vs 57% and 51%, respectively, p=0.016). The actuarial rates for absence of fast VT or VF were 80% in the metoprolol group compared with 46% in the d,l-sotalol group (p=0.002). During a follow up of 26+/-16 months, there were 3 deaths in the metoprolol group compared with 6 deaths in the d,l-sotalol group. Actuarial rates of overall survival were not significantly different in the 2 groups (91% vs 83%, p=0.287). In this prospective, randomized, controlled study the recurrence rate of ventricular tachyarrhythmias in patients treated with metoprolol was lower than in patients treated by d,l-sotolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH P_Defibrillators__Implantable_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Survival_Rate_MeSH M_Tachycardia__Ventricular_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Treatment_Outcome_MeSH 
****** 9762290
----K E
----T Predictive factors of variceal bleeding control by emergency sclerotherapy. Multicenter Group.
----A OBJECTIVES: Acute bleeding from esophageal varices is a major complication of cirrhosis. Despite the large number of published studies no predictive factors of control of bleeding have been identified. We assessed the clinical and biological factors predictive of bleeding control within the first 2 weeks after a bleeding episode in a homogeneous group of patients enrolled in a large multicenter trial, who underwent a standardized emergency sclerotherapy session. METHODS: 101 patients with cirrhosis were enrolled. All had endoscopy-proven variceal bleeding, and the interval between hematemesis or melena and emergency sclerotherapy was always less than 24 hours. A second sclerotherapy session and other methods for the prevention of rebleeding were allowed after 5 days. RESULTS: Treatment failed in 16 patients after 24 hours and in a total of 33 patients after 15 days. Three of the 17 variables included in multivariate logistic analysis were associated with failure at 24 hours: encephalopathy (P = 0.006, OR = 4.0), blood transfusion prior to sclerotherapy (P = 0.012, OR = 6.2) and previous propranolol therapy (P = 0.022, OR = 4.6). Two variables were associated with failure between 24 hours and day 15 in patients successfully controlled after 24 hours: an interval between the onset of bleeding and sclerotherapy of less than 12 hours (P = 0.010) and blood transfusion (P = 0.018). After 15 days, three variables were associated with failure in a multivariate Cox model: encephalopathy (P = 0.0025, OR = 2.3), time to sclerotherapy (P = 0.022, OR 2.3) and blood transfusion before sclerotherapy (P = 0.0005, OR = 4.0). CONCLUSION: Encephalopathy, the severity of bleeding, assessed in terms of transfusion requirements, and the time between clinically overt bleeding and sclerotherapy are the main predictive factors of failure of the control of bleeding after emergency sclerotherapy for acute bleeding from esophageal varices.
----P Clinical_Trial Journal_Article Multicenter_Study 
----M M_Emergencies_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH P_Sclerotherapy_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 9764058
----K E
----T Beta adrenergic blockers lower renin in patients treated with ACE inhibitors and diuretics.
----A OBJECTIVE: To examine the effect of concomitant intake of beta blockers with angiotensin converting enzyme (ACE) inhibitors, diuretics, or both on plasma renin concentrations in a population based sample (MONICA survey, Augsburg, Germany). SUBJECT AND METHODS: 728 individuals were studied, of whom 171 were treated using monotherapy (ACE inhibitor (n = 21), diuretic (n = 10), or beta blocker (n = 72)), or combination treatment (ACE inhibitor + diuretic (n = 32), ACE inhibitor + beta blocker (n = 7), diuretic + beta blocker (n = 22), ACE inhibitor + diuretic + beta blocker (n = 7)). The remaining 557 individuals were untreated. Indications for treatment were hypertension (75%), coronary artery disease with (12%) or without (3%) hypertension, or unknown (10%). RESULTS: Mean (SEM) renin concentrations in individuals treated with an ACE inhibitor (41 (8) mU/l), a diuretic (41 (10) mU/l), or the combination of an ACE inhibitor and a diuretic (54 (10) mU/l) were raised compared with untreated individuals (17 (1) mU/l; p < 0.05 each). Monotherapy with a beta blocker, however, decreased mean renin concentrations (12 (1) mU/l; p < 0.01 v untreated). Renin concentrations in individuals taking a beta blocker with either an ACE inhibitor (21 (8) mU/l), or a diuretic (22 (4) mU/l), or with both an ACE inhibitor and a diuretic (21 (7) mU/L), were significantly lower compared with renin concentrations in groups not receiving beta blocker treatment (p < 0.05 each). CONCLUSION: These data suggest that the upregulation of renin by treatment with ACE inhibitors, diuretics, or both can be largely prevented by concomitant beta blocker treatment.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9777817
----K E
----T Age-race subgroup compared with renin profile as predictors of blood pressure response to antihypertensive therapy. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A CONTEXT: Renin profiling and age-race subgroup may help select single-drug therapy for stage 1 and stage 2 hypertension. OBJECTIVE: To compare the plasma renin profiling and age-race subgroup methods as predictors of response to single-drug therapy in men with stage 1 and 2 hypertension as defined by the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. DESIGN: The Veterans Affairs Cooperative Study on Single-Drug Therapy of Hypertension, a randomized controlled trial. SETTING: Fifteen Veterans Affairs hypertension centers. PATIENTS: A total of 1105 ambulatory men with entry diastolic blood pressure (DBP) of 95 to 109 mm Hg, of whom 1031 had valid plasma and urine samples for renin profiling. INTERVENTIONS: Randomization to 1 of 6 antihypertensive drugs: hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem (sustained release), or prazosin. MAIN OUTCOME MEASURE: Treatment response as assessed by percentage achieving goal DBP (<90 mm Hg) in response to a single drug that corresponded to patients' renin profile vs a single drug that corresponded to patients' age-race subgroup. RESULTS: Clonidine and diltiazem had consistent response rates regardless of renin profile (76%, 67%, and 80% for low, medium, and high renin, respectively, for clonidine and 83%, 82%, and 83%, respectively, for diltiazem for patients with baseline DBP of 95-99 mm Hg). Hydrochlorothiazide and prazosin were best in low- and medium-renin profiles; captopril was best in medium- and high-renin profiles (low-, medium-, and high-renin response rates were 82%, 78%, and 14%, respectively, for hydrochlorothiazide; 88%, 67%, and 40%, respectively, for prazosin; and 51%, 83%, and 100%, respectively, for captopril for patients with baseline DBP of 95-99 mm Hg). Response rates for patients with baseline DBP of 95 to 99 mm Hg by age-race subgroup ranged from 70% for clonidine to 90% for prazosin for younger black men, from 50% for captopril to 97% for diltiazem for older black men, from 70% for hydrochlorothiazide to 92% for atenolol for younger white men, and from 84% for hydrochlorothiazide to 95% for diltiazem for older white men. Patients with a correct treatment for their renin profile but incorrect for age-race subgroup had a response rate of 58.7%; patients with an incorrect treatment for their renin profile but correct for age-race subgroup had a response rate of 63.1% (P = .30). After controlling for DBP and interactions with treatment group, age-race subgroup (P<.001) significantly predicted response to single-drug therapy, whereas renin profile was of borderline significance (P= .05). CONCLUSIONS: In these men with stage 1 and stage 2 hypertension, therapeutic responses were consistent with baseline renin profile, but age-race subgroup was a better predictor of response.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_European_Continental_Ancestry_Group_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Matched-Pair_Analysis_MeSH M_Middle_Aged_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9783498
----K E
----T Bisoprolol in the treatment of hypertension in the elderly.
----A The aim of the study was to examine the hypotensive efficacy and tolerance of bisoprolol in elderly patients. Sixty patients (40 <65 years and 20 >65 years) with mild-to-moderate essential hypertension (diastolic blood pressure (DBP) between 95 and 109 mm Hg) were included in the study. After a 2-week run-in period on placebo, patients began bisoprolol therapy (5 mg/d) for 12 weeks. After 4 weeks the dose was increased to 10 mg/d in those with a DBP > or =95 mm Hg. Additionally, in 10 patients over 65 years old, 24-h ambulatory BP monitoring (ABPM) was performed, after placebo and after bisoprolol (5 mg) administration. The hypotensive efficacy of bisoprolol in the elderly and younger patients was similar. Before and after treatment the mean difference of systolic BP (SBP) was 19.6 +/- 12.5 mm Hg and DBP 9.6 +/- 6.2 mm Hg in the younger patients and 16.1 +/- 13.6 mmHg and 9.5 +/- 6.0 mmHg in the elderly patients. Bisoprolol produced a similar reduction in heart rate (23.1% vs 17.1%) in the estimated groups. The tolerance of bisoprolol was good in both groups. There were no significant differences in adverse drug reactions between the groups.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_Determination_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Treatment_Outcome_MeSH 
****** 9791144
----K E
----T Effect of bradykinin-receptor blockade on the response to angiotensin-converting-enzyme inhibitor in normotensive and hypertensive subjects.
----A BACKGROUND: Angiotensin-converting-enzyme (ACE) inhibitors not only decrease the production of angiotensin II but also decrease the degradation of bradykinin. In this study, a specific bradykinin-receptor antagonist, icatibant acetate (HOE 140), was used to determine the contribution of bradykinin to the short-term effects of ACE inhibition on blood pressure and plasma renin activity in both normotensive and hypertensive subjects. METHODS: We compared the hemodynamic, renal, and endocrine effects of captopril alone (25 mg), captopril plus icatibant (100 microg per kilogram of body weight), the angiotensin II subtype 1-receptor antagonist losartan (75 mg), and placebo in 20 subjects with normal blood pressure and 7 subjects with hypertension. The subjects were studied while they were salt depleted (i.e., in balance on a diet in which they were allowed 10 mmol of sodium per day). The drugs were administered on four separate study days in a single-blind, randomized fashion. RESULTS: The coadministration of icatibant significantly attenuated the hypotensive effect of captopril (maximal decrease in mean arterial pressure for all subjects combined, 10.5+/-1.0 mm Hg, as compared with 14.0+/-1.0 mm Hg for captopril alone; P=0.001), in such a way that the decrease in blood pressure after the administration of captopril plus icatibant was similar to that after the administration of losartan (maximal decrease in mean arterial pressure, 11.0+/-1.7 mm Hg). Icatibant did not alter the renal hemodynamic response to captopril, but it significantly altered the change in plasma renin activity in response to ACE inhibition (-0.4+/-0.4 ng of angiotensin I per milliliter per hour, as compared with 2.0+/-0.7 ng per milliliter per hour for captopril alone; P=0.007). The magnitude of these effects was similar in both the normotensive and the hypertensive subjects, as well as in both the black subjects and the white subjects. CONCLUSIONS: These data confirm that bradykinin contributes to the short-term effects of ACE inhibition on blood pressure in normotensive and hypertensive persons and suggest that bradykinin also contributes to the short-term effects of ACE inhibition on the renin-angiotensin system.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Bradykinin_MeSH S_analogs_&_derivatives_MeSH Bradykinin_analogs_&_derivatives_MeSH S_pharmacology_MeSH Bradykinin_pharmacology_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Diet__Sodium-Restricted_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH M_Male_MeSH M_Receptors__Bradykinin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Bradykinin_antagonists_&_inhibitors_MeSH M_Reference_Values_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 9789703
----K E
----T Doxorubicin-induced cardiomyopathy treated with carvedilol.
----A Even today, heart failure due to doxorubicin-induced dilated cardiomyopathy seems to have a poor prognosis, as it is often irreversible and relatively unresponsive to standard medical treatment. This paper describes the first case of a patient complaining of severe symptoms of congestive heart failure due to doxorubicin-induced dilated cardiomyopathy unresponsive to standard medical treatment (digoxin, diuretics, and angiotensin-converting enzyme inhibitor), who showed complete clinical recovery and significant improvement of left ventricular dysfunction after carvedilol treatment. It also illustrates the possibility that carvedilol may be a first-choice drug for the treatment of this disease.
----P Case_Reports Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antineoplastic_Agents_MeSH S_adverse_effects_MeSH Antineoplastic_Agents_adverse_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_chemically_induced_MeSH Cardiomyopathy__Congestive_chemically_induced_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_radiography_MeSH Cardiomyopathy__Congestive_radiography_MeSH M_Doxorubicin_MeSH S_adverse_effects_MeSH Doxorubicin_adverse_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_radiography_MeSH Heart_Failure__Congestive_radiography_MeSH M_Human_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Radiography__Thoracic_MeSH M_Time_Factors_MeSH 
****** 9794346
----K E
----T Effectiveness of three different doses of carvedilol for exertional angina. Carvedilol-Angina Study Group.
----A Carvedilol is a nonselective beta-receptor antagonist with vasodilating properties primarily due to selective alpha-1 antagonism. This 4-treatment, 5-period, double-blind, crossover study evaluated the efficacy and safety of 3 doses of carvedilol (12.5, 25, and 50 mg given twice daily) versus placebo in 122 patients with chronic stable angina. Carvedilol in doses of 25 mg twice daily and 50 mg twice daily was statistically superior to placebo with respect to time to angina (placebo: 316 seconds; 25 mg carvedilol: 337 seconds, p = 0.0039; 50 mg: 345 seconds, p <0.0001) and time to 1-mm ST-segment depression (placebo: 301 seconds; 25 mg: 313 seconds; 50 mg: 323 seconds; p <0.0001). The percentage of patients reporting any adverse experience was slightly less in those receiving placebo (placebo: 28.4%; 12.5 mg: 33.1%; 25 mg: 34.5%; 50 mg: 31.9%). Carvedilol is effective and safe in treating patients with chronic stable angina.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 9794735
----K E
----T Risk factors associated with alterations in carotid intima-media thickness in hypertension: baseline data from the European Lacidipine Study on Atherosclerosis.
----A BACKGROUND: The possibility that calcium antagonists exert an anti-atherosclerotic action at least partly independently of the blood-pressure-lowering effect is supported by results of a large number of experimental studies and can now be investigated by quantitative B-mode ultrasound imagining of the carotid artery walls. DESIGN: The European Lacidipine Study on Atherosclerosis (ELSA) is a prospective, randomized, double-blind, multinational trial comparing effects of 4-year treatment based on the long-acting, highly lipophilic calcium antagonist lacidipine with those of treatment based on the beta-blocker atenolol on the development of carotid artery wall alterations in patients (aged 45-75 years) with mild-to-moderate hypertension (systolic blood pressure 150-210 mmHg and diastolic blood pressure 95-115 mmHg). While the intervention study is progressing, this article summarizes baseline data obtained from the whole cohort of 2259 patients randomly allocated to treatment. METHODS: Baseline ultrasound data were obtained from two replicate examinations performed shortly before random allocation to treatment by certified sonographers at 23 referral centres and read at the ultrasound coordinating centre at the Wake Forest University School of Medicine. Intima-media thickness was measured at up to 12 different sites in the carotid artery tree and expressed as the mean of the maxima at these sites (Mmax), the mean of the maxima at four sites in the distal common carotid artery and bifurcation (CBMmax) and the maximum intima-media thickness (Tmax). Baseline demographic and clinical measurements were performed by investigators in 410 peripheral clinical units and 24 h ambulatory blood pressure monitorings read and validated by members of a centralized unit at the University of Milan. The statistical analysis centre at the Technische Universitat Munchen received and analysed all baseline data, by calculating means +/- SD, medians and ranges and performing correlation (Spearman correlation coefficients) and multiple regression analyses. RESULTS: Prevalence of carotid artery wall alterations among the hypertensive patients randomly allocated to treatment in the ELSA was very high: 82% had Tmax > or = 1.3 mm ('plaques' according to protocol) and 17% had Tmax > or = 1.0 and < 1.3 mm ('thickening'), with a median of two plaques per patient. We found significant correlations between ultrasound measurements and the following demographic and clinical variables: age, sex, systolic blood pressure and pulse pressure (both clinic and ambulatory), concentrations of total, high-density lipoprotein and low-density lipoprotein cholesterol and triglycerides, smoking habit and duration of hypertension. We found no significant correlation to diastolic blood pressure and glucose concentration. A multiple regression analysis indicated significant variables in the following rank order: age, 24 h ambulatory pulse pressure, sex, low-density lipoprotein cholesterol concentration, triglyceride concentration, smoking and clinic systolic blood pressure. CONCLUSIONS: Analysis of baseline data from the ELSA has shown that there is an extremely marked prevalence of carotid artery wall alterations among mild-to-moderate, middle-aged hypertensive patients. In addition to age, systolic blood pressure and pulse pressure, particularly if they are accurately measured by ambulatory monitoring, play a major role, somewhat greater than those of sex, low-density lipoprotein cholesterol concentration and smoking, in influencing intima-media thickness.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH M_Aged_MeSH M_Arteriosclerosis_MeSH S_etiology_MeSH Arteriosclerosis_etiology_MeSH S_prevention_&_control_MeSH Arteriosclerosis_prevention_&_control_MeSH S_ultrasonography_MeSH Arteriosclerosis_ultrasonography_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH M_Carotid_Arteries_MeSH S_ultrasonography_MeSH Carotid_Arteries_ultrasonography_MeSH M_Dihydropyridines_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 9799042
----K I
----T Sexual function in hypertensive males treated with lisinopril or atenolol: a cross-over study.
----A To evaluate the effect of antihypertensive treatment on sexual activity, 90 hypertensive men, aged 40 to 49 years, all married and without history of sexual dysfunction were treated with 100 mg of atenolol or 20 mg of lisinopril for 16 weeks, according to a double-blind, randomized, cross-over design. During the first month of therapy, sexual activity, assessed as number of sexual intercourse episodes per month, significantly declined with both atenolol (from 7.8 +/- 4.3 to 4.5 +/- 2.8, P < .01 v placebo) and lisinopril (from 7.1 +/- 4.0 to 5.0 +/- 2.5, P < .05 v placebo). Ongoing with the treatment, sexual activity tended toward recovery in the lisinopril (7.7 +/- 4.0 sexual intercourse episodes per month, P = NS v placebo), but not in the atenolol group (4.2 +/- 2.8, P < .01 v placebo), with a statistically significant difference between the two drugs (P < .01). The percentage of patients who complained of sexual dysfunction symptoms was significantly higher in the atenolol- than in the lisinopril-treated group (17% v 3%, P < .05). These findings suggest that atenolol induces a chronic worsening of sexual activity, whereas lisinopril causes only a temporary decline.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Libido_MeSH S_drug_effects_MeSH Libido_drug_effects_MeSH M_Lisinopril_MeSH S_adverse_effects_MeSH Lisinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Sex_Characteristics_MeSH M_Sexual_Behavior_MeSH S_drug_effects_MeSH Sexual_Behavior_drug_effects_MeSH 
****** 9803188
----K E
----T Current hypertension control is just not good enough.
----A 
----P Comment Editorial 
----M M_Age_Distribution_MeSH M_Cerebrovascular_Disorders_MeSH S_epidemiology_MeSH Cerebrovascular_Disorders_epidemiology_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Incidence_MeSH M_Kidney_Failure__Chronic_MeSH S_epidemiology_MeSH Kidney_Failure__Chronic_epidemiology_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH P_Patient_Education_MeSH M_Practice_Guidelines_MeSH M_Prevalence_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 9803197
----K E
----T Treatment of hypertension: insights from the JNC-VI report.
----A The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI) provides updated guidelines for the treatment of hypertension. Antihypertensive drug therapy may be initiated either after a trial of lifestyle modifications or immediately after the diagnosis is made, depending on the patient's other cardiovascular risk factors and the presence of clinical cardiovascular disease. In general, therapy may begin with diuretics or beta-adrenergic blockers in patients under age 65, unless a concomitant condition warrants another, more tailored choice. Low dosages should be used initially, but if the blood pressure is not successfully reduced to 140/90 mm Hg or below, another drug should be added or should replace the initial choice. General principles of therapy include the use of once-a-day formulations and combination drugs as well as cost considerations.
----P Journal_Article Review Review__Tutorial 
----M M_Algorithms_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Life_Style_MeSH M_United_States_MeSH 
****** 9809921
----K I
----T Etiology and response to drug treatment in heart failure.
----A Clinical trials in heart failure (HF) tend to randomize patients according to demographic characteristics and severity of left ventricular dysfunction, without taking account of the precise diagnosis. This article reviews results from recent trials suggesting that the etiology of HF, and particularly whether it is ischemic or nonischemic, may influence the long-term prognosis and the response to treatment. Some studies, but not all, suggest that nonischemic HF has a better prognosis than ischemic HF. The data on the benefits of angiotensin-converting enzyme inhibitors in ischemic versus nonischemic HF are conflicting. Carvedilol, and recently, bisoprolol have been shown to reduce mortality in ischemic and nonischemic HF, whereas metoprolol has, to date, improved prognosis only in dilated cardiomyopathy. Better responses to digoxin, amlodipine and amiodarone have been reported in non-ischemic HF. There is at present no clear explanation for the apparent therapeutic differences between ischemic and nonischemic HF. Absence of a rigorous definition of "nonischemic HF" in many studies makes interpretation of the results difficult. Further studies to clarify the effects of etiology of HF on the response to treatment could be particularly important for preventing progression to more advanced stages, in which any type of drug therapy may have limited value in prolonging survival. An individualized therapeutic approach, based on etiology of HF and possibly other factors such as plasma drug levels or the levels of neurohormones, could result in major progress in treating HF patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiac_Glycosides_MeSH S_therapeutic_use_MeSH Cardiac_Glycosides_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_diagnosis_MeSH Cardiomyopathy__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Diagnosis__Differential_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH S_diagnosis_MeSH Myocardial_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9809925
----K I
----T Randomized, double-blind, placebo-controlled study of carvedilol on the prevention of nitrate tolerance in patients with chronic heart failure.
----A OBJECTIVES: This study was designed to evaluate the effect of carvedilol on nitrate tolerance in patients with chronic heart failure. BACKGROUND: The attenuation of cyclic guanosine 5'-monophosphate (cGMP) production due to inactivation of guanylate cyclase by increased superoxide has been reported as a mechanism of nitrate tolerance. Carvedilol has been known to combine alpha/beta-blockade with antioxidant properties. METHODS: To evaluate the effect of carvedilol on nitrate tolerance, 40 patients with chronic heart failure were randomized to four groups that received either carvedilol (2.5 mg once a day [carvedilol group, n=10]), metoprolol (30 mg once a day [metoprolol group, n=10]), doxazosin (0.5 mg once a day [doxazosin group, n=10]) or placebo (placebo group, n=10). Vasodilatory response to nitroglycerin (NTG) was assessed with forearm plethysmography by measuring the change in forearm blood flow (FBF) before and 5 min after sublingual administration of 0.3 mg NTG, and at the same time blood samples were taken from veins on the opposite side to measure platelet cGMP. Plethysmography and blood sampling were obtained serially at baseline (day 0); 3 days after carvedilol, metoprolol, doxazosin or placebo administration (day 3); and 3 days after application of a 10-mg/24-h NTG tape concomitantly with carvedilol, metoprolol, doxazosin or placebo (day 6). RESULTS: There was no significant difference in the response of FBF (%FBF) and cGMP (%cGMP) to sublingual NTG on day 0 and day 3 among the four groups. On day 6, %FBF and %cGMP were significantly lower in the metoprolol, doxazosin and placebo groups than on day 0 and day 3, but these parameters in the carvedilol group were maintained. CONCLUSIONS: These results indicated that carvedilol may prevent nitrate tolerance in patients with chronic heart failure during continuous therapy with NTG.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Blood_Platelets_MeSH S_metabolism_MeSH Blood_Platelets_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Cyclic_GMP_MeSH S_biosynthesis_MeSH Cyclic_GMP_biosynthesis_MeSH S_blood_MeSH Cyclic_GMP_blood_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Drug_Hypersensitivity_MeSH S_blood_MeSH Drug_Hypersensitivity_blood_MeSH S_etiology_MeSH Drug_Hypersensitivity_etiology_MeSH S_prevention_&_control_MeSH Drug_Hypersensitivity_prevention_&_control_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_adverse_effects_MeSH Nitroglycerin_adverse_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 9809926
----K I
----T Preventive effects of carvedilol on nitrate tolerance--a randomized, double-blind, placebo-controlled comparative study between carvedilol and arotinolol.
----A OBJECTIVES: This study was designed to compare the preventive efect of nitrate tolerance between carvedilol with antioxidant properties and arotinolol without antioxidant properties. BACKGROUND: The attenuation of cyclic guanosine monophosphate (cGMP) production due to inactivation of guanylate cyclase by increased superoxide has been reported as a mechanism of nitrate tolerance. Carvedilol has been known to combine alpha- and beta-blockade with antioxidant properties. METHODS: To evaluate the preventive effect of nitrate tolerance, 24 patients with untreated hypertension were randomized to receive either carvedilol (10 mg twice a day [carvedilol group, n=8]), arotinolol (10 mg twice a day [arotinolol group, n=8]), or placebo (placebo group, n=8). Vasodilatory response to nitroglycerin (NTG) was assessed with forearm plethysmography by measuring the change in forearm blood flow (FBF) before and 5 min after sublingual administration of 0.3 mg NTG, and at the same time blood samples were taken from veins on the opposite side to measure platelet cGMP. Plethysmography and blood sampling were obtained serially at baseline (day 0), 3 days after carvedilol, arotinolol or placebo administration (day 3) and 3 days after application of a 20 mg/24 h NTG tape concomitantly with carvedilol, arotinolol or placebo (day 6). RESULTS: There was no significant difference in the response of FBF (%FBF) and cGMP (%cGMP) to sublingual administration of NTG on days 0 and 3 among the three groups. On day 6, %FBF and %cGMP were significantly lower in the arotinolol group and the placebo group than days 0 and 3, but these parameters in the carvedilol group were maintained. CONCLUSIONS: The results indicated that carvedilol with antioxidant properties may prevent the development of nitrate tolerance during continuous therapy with NTG compared with arotinolol without antioxidant properties.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Blood_Platelets_MeSH S_metabolism_MeSH Blood_Platelets_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cyclic_GMP_MeSH S_biosynthesis_MeSH Cyclic_GMP_biosynthesis_MeSH S_blood_MeSH Cyclic_GMP_blood_MeSH M_Double-Blind_Method_MeSH M_Drug_Hypersensitivity_MeSH S_blood_MeSH Drug_Hypersensitivity_blood_MeSH S_etiology_MeSH Drug_Hypersensitivity_etiology_MeSH S_prevention_&_control_MeSH Drug_Hypersensitivity_prevention_&_control_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_adverse_effects_MeSH Nitroglycerin_adverse_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH 
****** 9809930
----K E
----T Rationale and design of the International Verapamil SR/Trandolapril Study (INVEST): an Internet-based randomized trial in coronary artery disease patients with hypertension.
----A OBJECTIVES: The primary objective of the International Verapamil SR/Trandolapril Study (INVEST) is to compare the risk for adverse outcomes (all-cause mortality, nonfatal myocardial infarction [MI] or nonfatal stroke) in hypertensive patients with coronary artery disease (CAD) treated with either a calcium antagonist-based or a noncalcium antagonist-based strategy. BACKGROUND: Treatment recommendations for hypertension include initial therapy with a diuretic or beta-adrenergic blocking agent, for which reductions in morbidity and mortality are documented from randomized trials but are less than expected from epidemiologic data. For this reason, recent attention has focused on calcium antagonists or angiotensin-converting enzyme inhibitors. While these agents reduce blood pressure, outcome data from large randomized trials are lacking, but some case-control data, dominated by short-acting dihydropyridines, suggest an increased risk of cardiovascular events. These studies had methodologic limitations and did not differentiate among calcium antagonist types and formulations. Several studies differentiating among calcium antagonist types and an overview of published randomized trials show no increased risk with verapamil and suggestion for benefit in CAD patients. METHODS: A total of 27,000 CAD patients with hypertension will be randomized at 1,500 primary care sites to receive either a calcium antagonist-based (verapamil) or beta-blocker/diuretic-based (atenolol/hydrochlorothiazide) antihypertensive care strategy. The study uses a novel, electronic "paper-less" system for direct on-screen data entry, randomization and drug distribution from a mail pharmacy linked to the coordination center via the Internet. RESULTS: Contract negotiations with the United States and international sites are ongoing. Patients being enrolled are predominantly elderly (72% aged 60 years or older) men (54%), with either an abnormal coronary angiogram or prior MI (71%). In addition to hypertension, CAD and elderly age, most patients (89%) have one or more associated conditions (diabetes, dyslipidemia, smoking, cerebral or peripheral vascular disease, etc.) contributing to increased risk for adverse outcome. While 26% have diabetes, most of these are noninsulin dependent. Using the protocol strategies, target blood pressures (according to JNC VI) have been reached in 58% at the fourth visit, and as expected most (89%) are requiring multiple antihypertensive drugs. CONCLUSION: The design and baseline characteristics of the initial patients recruited for a prospective, randomized, international, multicenter study comparing two therapeutic strategies to control hypertension in CAD patients are described.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Research_Design_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 9808602
----K E
----T Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension.
----A BACKGROUND: Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined. METHODS AND RESULTS: In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. CONCLUSIONS: Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 9814627
----K E
----T Combination of enalapril and low-dose thiazide reduces normoalbuminuria in essential hypertension.
----A OBJECTIVE: To examine the effect of the combination of enalapril with a very low dose of hydrochlorothiazide versus atenolol on urinary albumin excretion in normoalbuminuric patients with mild to moderate essential hypertension. A secondary objective was to compare the effects of the two regimens in patients with different levels of albuminuria. DESIGN: A 12 weeks, randomized, double-blind, double-dummy, multicenter, comparative study with two parallel groups. SETTING: General practices in Denmark and Finland. PATIENTS: The subjects comprised 174 patients with mild to moderate essential hypertension, normal serum creatinine and no proteinuria. INTERVENTIONS: Enalapril/hydrochlorothiazide (20/6 mg) daily or atenolol (50 mg) daily. MAIN OUTCOME MEASURES: Urinary albumin: creatinine ratio and blood pressure. RESULTS: At baseline, normoalbuminuria was found in 74 and 85 patients in the enalapril/hydrochlorothiazide and atenolol groups, respectively. Blood pressure was reduced similarly by both treatments. The ratio of urinary albumin to creatinine in normoalbuminuric patients was significantly reduced during treatment with enalapril/hydrochlorothiazide at 20/6 mg (from geometic mean x/divided by antilog SD of 0.53 x/divided by 1.77 to 0.47 x/divided by 1.58 mg/mmol, P=0.02) but was unchanged during atenolol treatment (0.55 x/divided by 1.74 and 0.58 x/divided by 1.87 mg/mmol). The difference between the two treatments was statistically significant (P=0.03) and was predominantly achieved through a reduction of albuminuria in the upper-normal range during enalapril/hydrochlorothiazide treatment. CONCLUSIONS: Therapy with enalapril/hydrochlorothiazide at 20/6 mg and atenolol at 50 mg once daily reduced blood pressure similarly in patients with essential hypertension. Suppression of urinary albumin excretion within the normoalbuminuric range was observed during treatment with enalapril/hydrochlorothiazide at 20/6 mg.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Albuminuria_MeSH S_drug_therapy_MeSH Albuminuria_drug_therapy_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH S_urine_MeSH Albuminuria_urine_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_urine_MeSH Creatinine_urine_MeSH M_Diuretics__Thiazide_MeSH S_administration_&_dosage_MeSH Diuretics__Thiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9814628
----K E
----T Sex differences in antihypertensive drug use: determinants of the choice of medication for hypertension.
----A OBJECTIVE: To describe and explain sex differences in antihypertensive drug use. DESIGN AND METHODS: From 1987 to 1995, two cross-sectional population-based surveys of cardiovascular disease risk factors in The Netherlands were carried out among 56026 men and women aged 20-59 years. Polytomous logistic regression modelling was used to adjust for potential confounders of the association between sex and use of different antihypertensive drugs. RESULTS: The response rate was 40% for men and 46% for women. Of these respondents, 40% (1041) of the hypertensive men and 59% (1403) of the hypertensive women were being treated pharmacologically; 57% (595) of the treated men and 54% (760) of the treated women were on monotherapy for hypertension with a diuretic (men 14.8%, women 37.2%), a beta-blocker (men 59.0%, women 45.3%), a calcium antagonist (men 8.6%, women 5.0%) or an angiotensin converting enzyme inhibitor (men 17.7%, women 12.5%). Among those on monotherapy for hypertension, women were less likely than men to be using a beta-blocker [prevalence odds ratio (POR), female/male=0.34; 95% confidence interval (CI) 0.24-0.47], a calcium antagonist (POR=0.27, 95% CI 0.15-0.48) or an angiotensin converting enzyme inhibitor (POR=0.34, 95% CI 0.22-0.52) than a diuretic. These sex differences persisted after adjustment for all factors that could have influenced the choice of these antihypertensive drugs (indications and contra-indications for the four antihypertensive drug classes). The sex differences in antihypertensive drug use were smaller among hypertensives with a history of cardiovascular disease (adjusted PORs, female/male, for beta-blockers, calcium antagonists and ACE inhibitors, respectively, compared to diuretics were 0.80 with 95% CI 0.20-3.24, 0.40 with 95% CI 0.10-0.48 and 0.64 with 95% CI 0.12-3.39) than among those without such a history. CONCLUSIONS: The different patterns of antihypertensive drug use among hypertensive men and women seem irrational, and cannot be explained by factors known to influence antihypertensive drug choice. Among hypertensives with a history of cardiovascular disease, the sex differences were smaller than among those without such a history. Further research is required to explain the sex differences in the choice of antihypertensive drug by prescribers, and to investigate the consequences of these differences for long-term patient outcomes.
----P Journal_Article 
----M M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Sectional_Studies_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Drug_Utilization_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Netherlands_MeSH M_Questionnaires_MeSH M_Retrospective_Studies_MeSH P_Sex_Characteristics_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9818888
----K E
----T Long-term outcome of migraine therapy: predictive value of the frontotemporal nitroglycerin test.
----A We evaluated whether type of response to the migraine-induction test with a nitroglycerin ointment applied to the frontotemporal head region could predict the efficacy of antimigraine therapy. Forty-two patients with migraine without aura underwent the test before and 2 months after antimigraine therapy. Two and 4 months after treatment withdrawal, most subjects with a negative response to the post-treatment test maintained treatment benefit, whereas benefit was lost in patients with an early onset migraine response.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Female_MeSH M_Flunarizine_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_chemically_induced_MeSH Migraine_chemically_induced_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH M_Nitroglycerin_MeSH S_diagnostic_use_MeSH Nitroglycerin_diagnostic_use_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9819786
----K E
----T Comparison between moexipril and atenolol in obese postmenopausal women with hypertension.
----A The present study investigated the effect of the new ACE-inhibitor moexipril versus the beta 1-adrenergic blocker atenolol on metabolic parameters, adverse events (AEs) and sitting systolic (SSBP) and sitting diastolic blood pressure (SDBP) in obese postmenopausal women with hypertension (stage I and II). After a 4-week placebo run-in phase, 116 obese, postmenopausal women with primary hypertension were randomised into two treatment groups receiving once daily dosages of either moexipril 7.5 mg or atenolol 25 mg initially (mean age: 57 +/- 7 years in both groups; mean weight: 94 kg in the moexipril group and 89 kg in the atenolol group, corresponding to a body mass index (BMI) of 35.2 kg/m2 and 34.1 kg/m2 in both groups, respectively). After 4 and 8 weeks, the dosages were uptitrated to moexipril 15 mg, or if necessary to moexipril 15 mg/hydrochlorothiazide (HCTZ) 25 mg, or to atenolol 50 mg and atenolol 50 mg/HCTZ 25 mg, in patients whose blood pressure was not sufficiently controlled. At endpoint, metabolic parameters (total cholesterol, triglycerides, LDL, HDL, glucose, insulin) were not significantly altered in either treatment group. Most frequent adverse events under monotherapy (moexipril/atenolol) were asthenia (5.3/13.0%), headache (13.2/21.7%), cough (7.9/6.5%), pharyngitis (21.1/8.7%) and peripheral oedema (5.3/13.0%). Overall at least one AE was reported in 66% of the patients treated with moexipril and in 78% of those treated with atenolol. Reduction of SSBP/SDBP at endpoint was 14.7 +/- 1.9/10.0 +/- 1.1 and 8.7 +/- 1.9/8.4 +/- 1.1 mmHg after treatment with moexipril and atenolol, respectively. The results showed that moexipril and atenolol are equally effective in reducing blood pressure without adversely affecting blood lipids and carbohydrate metabolism.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isoquinolines_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_blood_MeSH Obesity_blood_MeSH S_complications_MeSH Obesity_complications_MeSH P_Postmenopause_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 9820105
----K 1
----T [Changes in pharmacotherapy of hypertension 1989-1996 in patients with diabetes mellitus]
----A The authors investigated in a retrospective study in a group of diabetics changes in the pharmacotherapy of hypertension. In 1989-1996 2308 diabetics had spa treatment in the Military Balneological Institute in Karlovy Vary and 1058 of these patients had hypertension (45.8%). The patients were from all parts of the Czech Republic and before 1993 from the whole Czechoslovak Federal Republic. The authors investigated the pharmacotherapy of hypertension and focused attention on four basic groups of antihypertensive drugs (beta-blockers, diuretics, Ca channel blockers and ACE inhibitors). They recorded a marked drop of the number of patients taking diuretics (from 62% to 24%), and a slight decline in the group taking beta-blockers). They recorded an increase in Ca channel blockers (from 7% to 54%) and in recent years of ACE inhibitors (from practically zero to 24%). They draw attention to the dominant ratio of some drugs in selected groups of antihypertensives and discuss whether they are suitable for the treatment of hypertension in patients with diabetes mellitus. The number of patients without pharmacotherapy of hypertension declined but was not statistically significant.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Drug_Utilization_MeSH S_trends_MeSH Drug_Utilization_trends_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH 
****** 9823789
----K E
----T Advances in the medical management of acute coronary syndromes.
----A Many advances in the treatment of acute coronary syndromes have been realized over recent years. In ST elevation myocardial infarction, new aggressive thrombolytic regimens improve early reperfusion and improve survival. The current focus is on bolus thrombolysis, glycoprotein IIb/IIIa inhibition, and low-molecular-weight heparin as adjuncts. In unstable angina and non-ST elevation myocardial infarction, two major advances are IIb/IIIa inhibition and low-molecular-weight heparin, each of which significantly improves the outcome of patients and which have just been approved for use by the Food and Drug Administration. Following acute coronary syndromes, cholesterol lowering with statin drugs has a major effect, even in the large group of patients with average cholesterol levels. Use of clopidogrel, a more potent antiplatelet agent than aspirin, appears to decrease recurrent ischemic events, which has highlighted the potential benefits of oral IIb/IIIa inhibitors, which are much more potent antiplatelet agents. An additional focus has been on ensuring that patients actually receive the currently available medications. With a great number of new medical treatments, the outcome of patients with acute coronary syndromes has improved and will continue to improve as we enter the next millennium.
----P Journal_Article Review Review__Academic 
----M M_Acute_Disease_MeSH M_Animals_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Enzyme_Inhibitors_therapeutic_use_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH P_Myocardial_Revascularization_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Platelet_Glycoprotein_GPIIb-IIIa_Complex_MeSH S_antagonists_&_inhibitors_MeSH Platelet_Glycoprotein_GPIIb-IIIa_Complex_antagonists_&_inhibitors_MeSH M_Syndrome_MeSH P_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH 
****** 9824025
----K E
----T Predicting severe angiographic coronary artery disease using computerization of clinical and exercise test data.
----A Currently the standard exercise test is shifting from being a tool for the cardiologist to utilization by the nonspecialist. This change could be facilitated by computerization similar to the interpretation programs available for the resting ECG. Therefore, we sought to determine if computerization of both exercise ECG measurements and prediction equations can substitute for visual analysis performed by cardiologists to predict which patients have severe angiographic coronary artery disease. We performed a retrospective analysis of consecutive patients referred for evaluation of possible or known coronary artery disease who underwent both exercise testing with digital recording of their exercise ECGs and coronary angiography at two university-affiliated Veteran's Affairs medical centers and a Hungarian hospital. There were 2,385 consecutive male patients with complete data who had exercise tests between 1987 and 1997. Measurements included clinical and exercise test data, and visual interpretation of the ECG paper tracings and > 100 computed measurements from the digitized ECG recordings and compilation of angiographic data from clinical reports. The computer measurements had similar diagnostic power compared with visual interpretation. Computerized ECG measurements from maximal exercise or recovery were equivalent or superior to all other measurements. Prediction equations applied by computer were only able to correctly classify two or three more patients out of 100 tested than ECG measurements alone. beta-Blockers had no effect on test characteristics while ST depression on the resting ECG decreased specificity. By setting probability limits using the scores from the equations, the population was divided into high-, intermediate-, and low-probability groups. A strategy using further testing in the intermediate group resulted in 86% sensitivity and 85% specificity for identifying patients with severe coronary disease. We conclude that computerized exercise ST measurements are comparable to visual ST measurements by a cardiologist and computerized scores only minimally improved the discriminatory power of the test. However, using these scores in a stratification algorithm allows the nonspecialist physician to improve the discriminatory characteristics of the standard exercise test even when resting ST depression is present. Computerization permitted accurate identification of patients with severe coronary disease who require referral.
----P Journal_Article 
----M M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_radiography_MeSH Coronary_Disease_radiography_MeSH P_Electrocardiography_MeSH P_Exercise_Test_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_ROC_Curve_MeSH M_Retrospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH P_Signal_Processing__Computer-Assisted_MeSH 
****** 9830766
----K 1
----T [Influence of risk factors and pharmacological treatment on mortality in patients with essential hypertension]
----A BACKGROUND: The V JNC consensus stated that although new antihypertensive agents, such as angiotensin converting enzyme inhibitors and calcium channel blockers, are considered safer drugs, there is no firm evidence from large controlled trials that these drugs are associated with a lower cardiovascular mortality. AIM: To study the association between cardiovascular risk factors, blood pressure levels, pharmacological treatment and mortality in a group of hypertensive patients followed at an hypertension outpatient clinic. PATIENTS AND METHODS: Patients with essential hypertension were treated with different antihypertensive medications, according to physicians criteria, and controlled until death or loss from follow up. Causes of death were obtained from hospital records and death certificates. Survival was analyzed using life tables, comparisons between groups of patients were done using chi square or a Cox's proportional hazards model. RESULTS: Three hundred thirty-nine hypertensive patients aged 33 to 80 years old were followed for a mean period of 9.8 +/- 4.9 years. Eighty-six were treated with beta blockers, 64 with diuretics, 133 with calcium antagonists and 56 with ACE inhibitors. Blood pressure dropped similarly with all medications. During follow up, 79 patients died. Life table analysis showed that patients with a history of angina, diabetes or myocardial infarction had higher mortality rates. Similarly, patients treated with beta blockers and diuretics had higher mortality than patients treated with calcium antagonists or angiotensin converting enzyme inhibitors. The proportional hazards model showed that the effect of treatment modality persisted after correction for the other risk factors for mortality. CONCLUSIONS: In this series of hypertensive patients, those treated with beta blockers or diuretics had higher mortality rates than those receiving calcium channel antagonists or angiotensin converting enzyme inhibitors.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 9833172
----K E
----T Nephroprotection by antihypertensive therapy.
----A Morbidity and mortality due to end-stage renal failure has become a major health concern in recent years and there is clear evidence that arterial hypertension constitutes a powerful risk factor for the progression of renal disease. Several studies have documented the benefit of blood pressure control on renal function, and it is increasingly recognized that antihypertensive therapy aimed at reducing blood pressure well below the target value of 140/90 mmHg further improves the overall renal survival rate. Different classes of antihypertensive agents show disparate specific nephroprotective properties that are unrelated to their blood pressure lowering properties. ACE inhibitors and calcium channel blockers have been reported to ameliorate renal function by favorably modifying renal and intraglomerular hemodynamics. In addition, both drugs exert beneficial effects on non-hemodynamic parameters of renal function. In contrast, beta-blockers and diuretics, although still being solely recommended as first line drugs in the management of arterial hypertension, can have adverse effects on renal function. Recently, long-term randomized controlled trials have consistently demonstrated the superior nephroprotective value of ACE inhibitors on renal function outcome. Whether AT1 receptor antagonists have similar effects on long-term renal survival is still under investigation. The outcome of forthcoming clinical trials is likely to influence clinical guidelines and optimize the medical regimen of human essential hypertension in patients with chronic renal insufficiency.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH 
****** 9836247
----K E
----T Differential chronergy of propranolol effects on heart rate in healthy and hypertensive subjects.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 9853182
----K E
----T The impact of beta-receptor blocker addition to high-dose angiotensin-converting enzyme inhibitor-nitrate therapy in heart failure.
----A BACKGROUND: The natural history of heart failure is one of continued worsening of cardiac function. Beta-receptor blocker therapy has been effective in improving clinical status and left ventricular function in patients with heart failure. Similarly, high doses of angiotensin-converting enzyme (ACE) inhibitors with nitrates partially reverse the ventricular remodeling of heart failure. HYPOTHESIS: We tested the hypothesis that beta-blocker therapy added to high-dose ACE inhibitor-nitrates would potentiate the reversal of heart failure. METHODS: Thirteen patients, aged 52 +/- 8 years, with moderate to severe heart failure, 12 of whom were referred for transplant consideration, with heart failure duration of 4.8 +/- 2.2 years, were prospectively followed for 12 months. Baseline echocardiographic ejection fraction was 19 +/- 8%, and presenting New York Heart Association class was 2.9 +/- 0.7. Angiotensin-converting enzyme inhibitors and nitrates were uptitrated over 6 months to a final dose of lisinopril 53 +/- 31 mg/day, and isosorbide dinitrate 217 +/- 213 mg/day. At 6 months, beta-blocker therapy with atenolol was initiated and titrated to a final dose of 46 +/- 23 mg/day. Two-dimensional Doppler echocardiography and metabolic stress testing were performed at baseline, at 6 months on lisinopril-nitrates only, and at 12 months on combined ACE inhibitor-nitrate and beta-blocker therapy. RESULTS: New York Heart Association classification improved from 2.9 +/- 0.7 to 1.8 +/- 0.8 on lisinopril-nitrates (p < 0.05), and to 1.5 +/- 0.5 with the addition of beta blockade (p = NS). On follow-up, peak oxygen consumption rose from 17 +/- 7 ml O2/kg/min at baseline to 21 +/- 5 ml O2/kg/min at 6 months on lisinopril-nitrates (p = 0.06) without further change on beta blockade. Ejection fraction rose from 19 +/- 8 to 33 +/- 14% on lisinopril-nitrates at 6 months (p = 0.005) and to 36 +/- 18% on beta blockade at 12 months (p = NS). CONCLUSION: High-dose ACE inhibitor-nitrate therapy significantly improved patient clinical status and left ventricular systolic function in heart failure. The addition of beta-receptor blockade over and above high-dose ACE inhibitor-nitrates was well tolerated but had no further impact on symptomatic status, exercise tolerance, or left ventricular systolic function. The potential for pharmacologic reversal of heart failure remodeling may be finite despite the use of complementary therapies. Larger placebo-controlled and randomized trials of beta-receptor blockade added to high-dose ACE inhibitor-nitrate therapy are needed to confirm these observations.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9854453
----K E
----T Effects of beta-blockers on the concentration and oxidizability of plasma lipids.
----A 1. beta-blockers improve morbidity and mortality after myocardial infarction, probably by several mechanisms. We investigated potentially relevant effects of beta-blockers in vivo and in vitro on plasma lipid oxidizability. Forty-two healthy men were randomized to receive placebo (13), metoprolol (14) or propranolol (15). 2. At 4 weeks, the effects on heart rate, blood pressure and lipids appeared similar and subjects taking a beta-blocker were combined. Compared with placebo, those on a beta-blocker gained 0.5 kg in weight (P = 0.04), heart rate fell from 63 to 52 beats/min (P < 0.0001) and blood pressure fell from 116/74 to 113/69 mmHg (P < 0.005); high-density lipoprotein (HDL)-cholesterol fell from 1.26 to 1.11 mmol/l (P = 0.005), there being no change in the ratio of free to esterified cholesterol in HDL, and there was an apparent rise in serum triacylglycerols from 1.18 to 1.43 mmol/l (P = 0.15 when adjusted for weight gain). Low-density lipoprotein (LDL)-cholesterol and lipoprotein (a) did not change. In this study, the oxidizability of LDL was unaffected by beta-blocker therapy. beta-blockade was not associated with any change in LDL fatty acid profile, or beta-carotene or alpha-tocopherol content which might account for the reduced LDL oxidizability previously reported in patients treated with beta-blockers. Furthermore, neither atenolol nor propranolol, at concentrations up to 100 mumol/l, had any effect on in vitro oxidizability of LDL obtained from healthy volunteers. 3. In contrast to the favourable haemodynamic effects conferred by beta-blockers, the effects on weight and serum triacylglycerols and HDL-cholesterol appear to be adverse and we did not demonstrate any changes in lipid oxidizability which might be relevant to the protective effects of beta-blockers in patients with coronary disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Comparative_Study_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Lipid_Peroxidation_MeSH S_drug_effects_MeSH Lipid_Peroxidation_drug_effects_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH S_metabolism_MeSH Lipids_metabolism_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH S_chemistry_MeSH Lipoproteins__LDL_Cholesterol_chemistry_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 9857888
----K E
----T Potential impact of evidence-based medicine in acute coronary syndromes: insights from GUSTO-IIb. Global Use of Strategies to Open Occluded Arteries in Acute Coronary Syndromes trial.
----A OBJECTIVES: The purpose of this study to determine whether use of cardiac medications reflects evidence-based recommendations for patients with non-ST elevation acute coronary syndromes. BACKGROUND: Agency for Health Care Policy and Research practice guidelines for unstable angina recommend the use of cardiac medications based on evidence from randomized trials. It is unknown whether practitioners in the U.S., Canada and Europe follow these recommendations in patients with non-ST elevation acute coronary syndromes. METHODS: We studied 7,743 patients with non-ST elevation acute coronary syndromes enrolled in the international Global Use of Strategies to Open Occluded Arteries in Acute Coronary Syndromes trial. The use of aspirin, beta-adrenergic blocking agents, angiotensin-converting enzyme inhibitors and calcium channel blocking agents was determined at discharge for all patients and "ideal" patients (those with indications and no contraindications). Using published estimates of relative mortality reductions with these drugs, we calculated the lives that could have been saved at 1 year if discharge medication use had better matched guideline recommendations. RESULTS: Overall, guideline adherence at discharge in "ideal" patients was 85.6% for aspirin, 59.1% for beta-blockers and 51.7% for angiotensin-converting enzyme inhibitors. Calcium channel blockers were given to 26.7% of patients with a contraindication to these drugs. These rates were similar across locations of enrollment. Women and older patients less often received aspirin when "ideal," and younger patients more often received calcium channel blockers when they were contraindicated. If medication use had been more evidence-based, 1-year mortality might have been reduced by a relative 22%. CONCLUSIONS: There is significant room for improvement in the use of recommended drugs in patients with non-ST elevation acute coronary syndromes. Medication use that more closely follows recommendations could reduce mortality in this population.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH P_Evidence-Based_Medicine_MeSH M_Female_MeSH P_Guideline_Adherence_MeSH M_Human_MeSH M_Male_MeSH M_Patient_Selection_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9856962
----K E
----T Characteristics of 9194 patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint Reduction in Hypertension.
----A -Losartan was the first available orally administered selective antagonist of the angiotensin II type 1 receptor developed for the treatment of hypertension. The Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of the beta-blocker atenolol on the reduction of cardiovascular morbidity and mortality. Patients with essential hypertension, aged between 55 and 80 years, and ECG-documented left ventricular hypertrophy (LVH) were included. Altogether, 9223 patients in Scandinavia, the United Kingdom, and the United States were randomized from June 1995 through April 1997, and 9194 remain after exclusion of a study center at which irregularities were discovered. This population of hypertensives (mean systolic/diastolic blood pressure, 174.4/97.8 mm Hg) with LVH comprises women (54.1%) and men, mostly retired from active work (mean age, 66.9 years), with a high prevalence of overweight (mean body mass index, 28.0 kg/m2), diabetes mellitus (12.3%), lipid disorders (18.0%), and symptoms or signs of coronary heart disease (15.1%). There were fewer current smokers (<17%) than in the general population, and approximately 7% were nonwhite. Almost 30% of participants had been untreated for at least 6 months when screened for the study. Only 1557 persons who entered the placebo run-in period of 14 days were excluded, predominantly because of sitting blood pressures above or below the predetermined range of 160-200/95-115 mm Hg and ECG-LVH criteria not met. By application of simple 12-lead ECG criteria for LVH (Cornell voltage QRS duration product formula plus Sokolow-Lyon voltage read by a core laboratory), hypertensive patients with LVH with an average 5-year coronary heart disease risk of 22.3% according to the Framingham score were identified. This population is now being treated (goal, <140/90 mm Hg) in adherence with the protocol for at least 4 years after final enrollment (ie, through April 2001) and until at least 1040 patients suffer myocardial infarction, stroke, or cardiovascular death.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Body_Mass_Index_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_blood_MeSH Hypertrophy__Left_Ventricular_blood_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_diagnosis_MeSH Hypertrophy__Left_Ventricular_diagnosis_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9866432
----K E
----T Controversies in perioperative medicine.
----A Coexisting medical problems are common in surgical patients. Due to the lack of convincing studies, however, the optimal strategies for perioperative management of many medical problems remain unclear. Thus, practices are often based on inconclusive clinical studies or extrapolated from current understanding of pathophysiology. This article reviews guidelines and practices for endocarditis prophylaxis, perioperative anticoagulation in patients with mechanical heart valves, glucose control in diabetic patients undergoing surgery, and the use of beta-blockers to prevent postoperative cardiac complications. In addition, the strength of the evidence supporting these practices is evaluated.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_analysis_MeSH Blood_Glucose_analysis_MeSH M_Diabetes_Mellitus_MeSH S_blood_MeSH Diabetes_Mellitus_blood_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus_prevention_&_control_MeSH M_Disease_MeSH M_Endocarditis__Bacterial_MeSH S_prevention_&_control_MeSH Endocarditis__Bacterial_prevention_&_control_MeSH M_Guidelines_MeSH M_Heart_Diseases_MeSH S_prevention_&_control_MeSH Heart_Diseases_prevention_&_control_MeSH M_Heart_Valve_Prosthesis_MeSH M_Human_MeSH P_Perioperative_Care_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Surgical_Procedures__Operative_MeSH 
****** 9870118
----K E
----T Do intensive blood pressure lowering and low-dose ASA help our hypertensive patients?
----A 
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Hemorrhage_MeSH S_chemically_induced_MeSH Hemorrhage_chemically_induced_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_administration_&_dosage_MeSH Platelet_Aggregation_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Platelet_Aggregation_Inhibitors_adverse_effects_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH 
****** 9870122
----K E
----T Community management of heart failure.
----A OBJECTIVE: To review therapies for treating patients with heart failure (HF). QUALITY OF EVIDENCE: Recommendations in this paper are mainly based on the results of randomized controlled trials. To a lesser extent, data from smaller, more physiologic studies are included. Where appropriate, recommendations are based on the results of a consensus conference. MAIN MESSAGE: Although pharmacologic therapy is the main strategy for treating HF patients, general measures, such as counseling and advice about regular physical activity, are an important component of management. Use of angiotensin-converting enzyme inhibitors (ACE-I) is central to treating HF patients, because these agents decrease mortality and morbidity significantly. Digoxin does not reduce mortality but does reduce morbidity. Angiotensin II antagonists, although found to provide clinical benefit equal to ACE-I, have not been found as yet to have similar effects on mortality and morbidity. Diuretics and nitrates are useful for treating these patients' symptoms. Calcium channel blockers should generally be avoided. CONCLUSIONS: Angiotensin-converting enzyme inhibitors are the therapy of choice for HF patients and should be used in all cases unless there are contraindications or clear evidence of intolerance. All other therapies are used mainly for symptom relief.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Controlled_Clinical_Trials_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Exercise_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Outpatients_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9874045
----K E
----T Two- to three-year follow-up of patients with single-vessel coronary artery disease randomized to PTCA or medical therapy (results of a VA cooperative study). Veterans Affairs Cooperative Studies Program ACME Investigators. Angioplasty Compared to Medicine.
----A Despite increasing use of percutaneous transluminal coronary angioplasty (PTCA) to treat stenotic coronary artery disease, there are relatively few prospective studies evaluating its long-term effectiveness. We prospectively randomized 212 stable patients with provocable myocardial ischemia and single-vessel subocclusive coronary disease to receive primary therapy with either PTCA or medical therapy. This report presents the clinical follow-up of these patients at a mean, after randomization, of 2.4 years for interview and 3.0 years for exercise testing. Of the 212 patients originally randomized, 175 received an extended follow-up interview, and 132 underwent exercise testing; 62% of patients in the PTCA group were angina free compared with 47% of patients in the medical group (p <0.05). Furthermore, exercise duration as measured by treadmill testing was prolonged by 1.33 minutes over baseline in the PTCA group, whereas it decreased by 0.28 minutes in the medical group (p <0.04). Although the angina-free time on the treadmill was not different (p=0.50), fewer patients in the medical group developed angina on the treadmill at 3 years than those in the PTCA group (p=0.04). By 36 months, excluding the initial randomized PTCA, use of PTCA and use of coronary artery bypass surgery were not different in the 2 treatment groups. These data indicate that some of the early benefits derived from PTCA in patients with single-vessel coronary artery disease are sustained, making it an attractive therapeutic option for these patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_prevention_&_control_MeSH Angina_Pectoris_prevention_&_control_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_methods_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_methods_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Disease-Free_Survival_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH M_United_States_Department_of_Veterans_Affairs_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9878936
----K E
----T Epidemiology of myocardial infarction in France: therapeutic and prognostic implications of heart failure during the acute phase.
----A BACKGROUND: The aim of this study was to assess the 1-year outcome of acute myocardial infarction, in current practice, according to the presence or absence of heart failure. This was an epidemiologic, prospective survey involving 2152 patients recruited in November 1995 from 312 French coronary care units. METHODS AND RESULTS: All consecutive patients admitted within 48 hours for confirmed acute myocardial infarction to the participating centers in November 1995 were included. For each patient, baseline parameters, as well as clinical course and therapeutic treatment during the first 5 days, were collected. For the purpose of this study, the diagnosis of heart failure required a left ventricular ejection fraction </=35% and/or a Killip class >1. During the 1-year follow-up, date and cause of death were recorded. Kaplan-Meier survival curves were analyzed with the log rank test. Cox multivariate analyses were used to assess the independent prognostic factors among 5-day survivors. Eight hundred twenty-one (38%) patients exhibited heart failure during the first 5 days after myocardial infarction. Patients with heart failure were 10 years older and were more likely to be hypertensive or diabetic; use of primary revascularization (33% vs 47%, P <.001) and beta-blockers (40% vs 79%, P <.001) was less frequent, whereas prescription of angiotensin-converting enzyme (ACE) inhibitors was enhanced (56% vs 41%, P <.001). Mortality rate was strongly related to both left ventricular ejection fraction (P <. 001) and Killip class (P <.001). One-year mortality rate was 39.7% in patients with heart failure compared with 7.1% in patients without heart failure (P <.001). A significant reduction in mortality rates was observed with beta-blockers (risk ratio 0.63 [0. 45 to 0.89], P =.01) and ACE inhibitors (risk ratio 0.73 [0.54 to 0. 99], P =.04). It was more pronounced in patients with heart failure. CONCLUSIONS: Results of this French observational survey are in line with previous epidemiologic studies and with major therapeutic trials. Patients with heart failure after acute myocardial infarction constitute a high-risk group. They appear to derive a greater benefit from treatment with both beta-blockers and ACE inhibitors than from each class on its own.
----P Journal_Article Multicenter_Study 
----M M_Acute_Disease_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Disease-Free_Survival_MeSH M_Female_MeSH M_France_MeSH S_epidemiology_MeSH France_epidemiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_epidemiology_MeSH Myocardial_Infarction_epidemiology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 9886905
----K E
----T Study population and treatment titration in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT).
----A OBJECTIVES: To ascertain the baseline characteristics of the high-risk hypertensive patients entering the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT). To determine the success of single and combination therapy in achieving target blood pressures in such a population. DESIGN: INSIGHT is a double-blind, prospective outcome trial comparing the efficacy of the calcium channel blocker, nifedipine GITS, and the thiazide, co-amilozide, in preventing myocardial infarction and stroke. We recruited 2996 men and 3454 women, aged 55-80 years, with blood pressure during placebo run-in >150/95 mmHg or isolated systolic blood pressure >160 mmHg from nine countries. Treatment allocation to nifedipine GITS 30 mg daily or co-amilozide (hydrochlorothiazide 25 mg/amiloride 5 mg) once daily was performed by minimization rather than randomization to balance additional risk factors. This was followed by four optional increases in treatment: dose-doubling of the primary drug, addition of atenolol 25/50 mg or enalapril 5/10 mg, and then any other hypotensive drug excluding calcium blockers or diuretics. Target blood pressure was 140/90 mmHg or a fall > or = 20/10 mmHg. RESULTS: Blood pressure at randomization was 172+/-15 / 99+/-9 mmHg. Thirteen per cent of the patients were previously untreated. The proportions of each additional risk factors were: smoking > 10/day, 29%; cholesterol > 6.43 mmol/l, 52%; family history of premature myocardial infarction or stroke, 21%; diabetes mellitus 20%; left ventricular hypertrophy, 10%; previous myocardial infarction, other presentations of coronary heart disease, and peripheral vascular disease, each 6%; proteinuria, 3%. Fifty-five per cent of patients had one additional risk factor, whereas 33%, 9% and 3% had two, three or more additional risk factors, respectively. The blood pressure (and falls in blood pressure) at the end of titration and at 1 year after minimization was 139+/-12 / 82+/-7 mmHg (33+/-15 / 17+/-9) in the 5226 patients still on randomized treatment The numbers requiring the four treatment increments were, respectively, 1591, 780, 597 and 294, meaning that almost 70% of patients on randomized treatment in INSIGHT are receiving only the primary drug. At one year, 69% of patients had a blood pressure < or = 140/90 mmHg. CONCLUSION: INSIGHT is one of the first double-blind comparisons of active antihypertensive treatments, requiring high-risk patients to achieve sufficient power. Despite this requirement, it is possible to achieve good blood pressure control in most patients without the addition of multiple additional treatments that may dilute any differences between the primary agents.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 9890389
----K I
----T Effect of cocaine on cardiac biochemical functions.
----A The role of cocaine in cardiac ischemia and subsequent reversible and irreversible pathologic changes is well established. Nevertheless, the mechanisms leading to cardiac injury and irreversible cellular changes remain elusive. Reactive oxygen species (ROSs) are the critical mediators of cellular damage during ischemia-reperfusion. To explore the response of cardiac oxidative stress parameters to intravenous (i.v.) And intraperitoneal (i.p.) cocaine exposure, cardiac total glutathione (GSH, GSSG), malonaldialdehyde (MDA), Mn-superoxide dismutase (Mn-SOD), catalase (CAT), GSH-peroxidase (GSH-px), and GSH s-transferase (GST) were measured, along with biochemical and histologic markers indicative of cardiac injury. Repeated i.p. cocaine exposure produced significant impairment in cardiac integrity, demonstrated by increased circulating lactate (2.4-fold; p < 0.0001), creatine kinase (2.2-fold; p < 0.0001), and creatinine levels (1.7-fold; p < 0.0001). Infiltration of neutrophils into myocardial cavities also was evident. These changes paralleled increases in cardiac MDA (25%; p < 0.04), GSSG (55%; p < 0.001), protein carbonyls (23%; p < 0.05), and Mn-SOD (23%; p < 0.05) levels, indicative of oxidative stress, decreases in GSH (35%; p < 0.01), adenosine triphosphate (ATP; 26%; p < 0.04), GSH-px (28%; p < 0.03), CAT (32%; p < 0.01), and GST (50%; p < 0.001) levels. Intravenous cocaine administration also had similar effects on cardiac oxidative stress measures. In conclusion, our data indicate that cocaine administration compromised the heart's antioxidant defense system.
----P Journal_Article 
----M M_Animals_MeSH M_Antioxidants_MeSH S_metabolism_MeSH Antioxidants_metabolism_MeSH M_Apoptosis_MeSH S_drug_effects_MeSH Apoptosis_drug_effects_MeSH M_Catalase_MeSH S_metabolism_MeSH Catalase_metabolism_MeSH M_Cocaine_MeSH S_administration_&_dosage_MeSH Cocaine_administration_&_dosage_MeSH S_pharmacology_MeSH Cocaine_pharmacology_MeSH M_Glutathione_MeSH S_metabolism_MeSH Glutathione_metabolism_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiology_MeSH Heart_physiology_MeSH M_Injections__Intraperitoneal_MeSH M_Injections__Intravenous_MeSH M_Lipid_Peroxides_MeSH S_metabolism_MeSH Lipid_Peroxides_metabolism_MeSH M_Male_MeSH M_Myocardium_MeSH S_enzymology_MeSH Myocardium_enzymology_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Oxidative_Stress_MeSH S_drug_effects_MeSH Oxidative_Stress_drug_effects_MeSH M_Rats_MeSH M_Rats__Sprague-Dawley_MeSH M_Superoxide_Dismutase_MeSH S_metabolism_MeSH Superoxide_Dismutase_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9890408
----K E
----T Analysis of arrhythmias in the Circadian Antiischemia Program in Europe (CAPE) study.
----A The aim of this study was to analyze whether, in patients with long-standing (>4 years) coronary artery disease (CAD), the addition of the long-acting calcium channel blocker (CCB) amlodipine to conventional treatment [beta-blockers (BBLs) and nitrates] during anginal attacks would have a proarrhythmic effect. This was tested by analyzing data from patients who had taken part in the Circadian Anti-ischemia Program in Europe (CAPE) trial. After a 2-week, single-blind, run-in period (Phase 1), patients were randomized to amlodipine, 5 mg/day (first 4 weeks) and 10 mg/day (second 4 weeks), or placebo for 8 weeks (Phase 2). The 48-h Holter data were analyzed for 167 amlodipine-treated patients and 83 placebo patients based on a 2:1 randomization scheme. Sixty-three per cent of amlodipine patients and 67% of placebo patients were receiving concomitant BBLs, and >90% had taken sublingual nitrates during anginal attacks, as basic antiischemic therapy. After 7 weeks of therapy, when 48-h Holter monitoring was repeated, there were no significant changes in the frequency of ventricular arrhythmias in the placebo or amlodipine groups for all patients or subgroups of patients with or without BBLs. Also, between-group comparisons showed no significant differences in arrhythmias between amlodipine and placebo patients. In summary, amlodipine (5-10 mg/day) given to patients with severe, chronic CAD receiving conventional antiischemic therapy, did not produce any proarrhythmic effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Arrhythmia_MeSH S_chemically_induced_MeSH Arrhythmia_chemically_induced_MeSH S_complications_MeSH Arrhythmia_complications_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Europe_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Program_Evaluation_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 9894381
----K E
----T Antiarrhythmic therapy in the post-infarction setting: update from major amiodarone studies.
----A Many deaths among hospital survivors of acute myocardial infarction are due to sustained ventricular tachycardia and ventricular fibrillation. This has prompted the evaluation of prophylactic antiarrhythmic drugs and devices. Although it is widely agreed that antiarrhythmic treatment is useful, it is not certain which therapy provides optimal results. Increasing recognition of the efficacy of amiodarone has prompted the design of several trials of the drug. This paper focuses on primary prophylactic antiarrythmic therapy in the post-infarction setting and particularly on recent amiodarone trials.
----P Journal_Article Review Review__Tutorial 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Pilot_Projects_MeSH 
****** 9918893
----K E
----T Effect of beta-blockade on baroreceptor and autonomic function in heart failure.
----A Although beta-adrenoreceptor antagonists appear to be beneficial in chronic heart failure there is little information on their effects on autonomic and baroreceptor function which may have important prognostic implications. We sought to determine first whether beta-adrenoreceptor blockade will improve baroreceptor function and vagal tone in chronic heart failure, and second whether there were any differences between standard therapy with metoprolol and the second-generation vasodilating beta-blocker celiprolol. In this double-blind randomized placebo-controlled study 50 patients with stable chronic heart failure received either celiprolol 200 mg daily, metoprolol 50 mg twice daily or placebo for 12 weeks after a 4-week dose titration period. Thirty-five healthy normal subjects were also studied. Baroreceptor gain was assessed non-invasively by cross-spectral analysis of R-R and systolic blood pressure low- and high-frequency components (the alpha angle) during controlled respiration. High-frequency power was used as a measure of vagal modulation. Satisfactory recordings for analysis were obtained in 31 patients with heart failure. The results showed that at baseline baroreceptor gain (alphaHF) was significantly depressed in patients with heart failure compared with the normal control group (4.95+/-0. 55 versus 11.73+/-1.32 ms/mmHg, P<0.0001). After 12 weeks of treatment with metoprolol baroreceptor gain improved significantly whether measured while supine (P=0.03) or standing (P=0.009), and this was associated with a significant increase in R-R HF power (P=0. 008). There were no significant changes after treatment with celiprolol or placebo. We conclude that metoprolol but not celiprolol therapy restores baroreceptor gain towards normal and increases vagal tone in chronic heart failure. The ancillary properties of celiprolol do not appear to provide any advantages over metoprolol for the restoration of autonomic and baroreceptor function in heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Blood_Pressure_MeSH M_Case-Control_Studies_MeSH M_Celiprolol_MeSH S_therapeutic_use_MeSH Celiprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Pressoreceptors_MeSH S_drug_effects_MeSH Pressoreceptors_drug_effects_MeSH M_Signal_Processing__Computer-Assisted_MeSH M_Statistics__Nonparametric_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9924849
----K E
----T Efficacy and safety of carvedilol in patients with chronic heart failure receiving concomitant amiodarone therapy. Australia/New Zealand Heart Failure Research Collaborative Group.
----A BACKGROUND: The beta-blocker/vasodilator carvedilol is found to have beneficial effects in patients with chronic heart failure. However, the safety and efficacy of this agent in the presence of concomitant amiodarone therapy has not been previously determined. METHODS AND RESULTS: We retrospectively analyzed the Australia/New Zealand Carvedilol Heart Failure Research Collaborative Group study of 415 patients with mild to moderate ischemic heart failure where amiodarone was administered as part of the treatment therapy (in 52 patients). After the open-label carvedilol run-in, patients received carvedilol (target dose 25 mg twice daily) or placebo for an average of 19 months. The main adverse events during this double-blind period were worsened heart failure, hypotension/dizziness, bradycardia/atrioventricular block, and aggravation of angina. By Chi square analysis, carvedilol and amiodarone together were not associated with a greater overall incidence of adverse effects than either drug alone. The beneficial effects of carvedilol on left ventricular ejection that were observed in the main trial were preserved in the presence of amiodarone. CONCLUSIONS: Carvedilol is a useful additional therapy for patients with chronic heart failure already receiving amiodarone. Carvedilol can be added to amiodarone in these patients without expectation of increased adverse effects or loss of clinical efficacy.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 9926443
----K E
----T Clinical implications for the Acute Infarction Ramipril Efficacy extension (AIREX) Study.
----A It is now clear that angiotensin-converting enzyme (ACE) inhibitor treatment after myocardial infarction (MI) reduces mortality and morbidity. However, the benefits of ACE inhibition are not homogeneous and are largely confined to high-risk patients who have subjective or objective evidence of left ventricular (LV) dysfunction. How long treatment should continue is a vexed question, which also arises with other agents, for example beta-blocker use after MI. The AIREX study assessed the long-term magnitude and duration of the survival benefits observed with ramipril in patients after MI who have clinically defined heart failure. The mortality status of all 603 patients recruited from the UK centres involved in the AIRE study was verified at an extended 5-year follow-up (3 years after the AIRE study closed). Ramipril assignation was associated with a 36% relative and a 11% absolute mortality risk reduction. These findings strongly support the view to select patients on the basis of impaired LV function and reinforce the previously reported conclusions of the "selective" ACE inhibition post-MI trials. Using this approach, the survival benefit is not only of large magnitude but also sustained over many years. These results also argue for life-long treatment with an ACE inhibitor, once a decision to treat an individual patient after MI has been made.
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Follow-Up_Studies_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Morbidity_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Survival_Analysis_MeSH 
****** 9928753
----K E
----T Improved efficacy with maintained tolerability in the treatment of primary hypertension. Comparison between the felodipine-metoprolol combination tablet and monotherapy with enalapril. Swedish Multicentre Group.
----A In this multicentre, double-blind, parallel-group study, 120 out-patients with mild to moderate primary hypertension were randomised, after a 4-week single-blind placebo run-in period, to a combination tablet of felodipine-metoprolol 5/50 mg (Logimax, Mobloc, Astra) once daily or enalapril 10 mg once daily. If blood pressure (BP) remained suboptimally controlled after 4 weeks (supine diastolic BP >90 mm Hg 24-h post dose), the dose was doubled for a further 4 weeks. After 8 weeks felodipine-metoprolol reduced supine BP significantly more than enalapril (19.7/12.0 mmHg and 11.1/7.2 mm Hg, respectively). The mean differences in change in BP between treatments were 8.6/4.8 mm Hg in favour of felodipine-metoprolol (P = 0.001/P <0.001). A statistically significant difference to the advantage of felodipine-metoprolol was also seen in standing BP. Even though the dose was increased in a larger proportion of patients in the enalapril group (61%) than in the felodipine-metoprolol group (40%), fewer enalapril-treated patients achieved adequate BP control (41% vs 63% on felodipine-metoprolol, P <0.05). Both treatments were well tolerated. Three patients treated with felodipine-metoprolol and four with enalapril discontinued treatment due to adverse events. A similar number of patients reported adverse events in each treatment group. In conclusion, a combination tablet of felodipine-metoprolol 5/50-10/100 mg once daily reduced BP more effectively than enalapril 10-20 mg once daily 24 h post dose. The result was expected, but a more important observation was that both treatments were tolerated to a similar degree. Obviously, a considerable BP reduction may be well tolerated, as was the main purpose to demonstrate in this study.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tablets_MeSH S_adverse_effects_MeSH Tablets_adverse_effects_MeSH M_Treatment_Outcome_MeSH 
****** 9932994
----K 5
----T Brimonidine tartrate 0.2% twice daily vs timolol 0.5% twice daily: 1-year results in glaucoma patients. Brimonidine Study Group.
----A PURPOSE: To compare the long-term efficacy and safety of brimonidine 0.2% twice daily with timolol 0.5% twice daily in patients with glaucoma or ocular hypertension. METHODS: Of the 926 patients enrolled in the study, 837 met the protocol entry criteria and received either brimonidine 0.2% twice daily (n = 466) or timolol 0.5% (n = 371) twice daily in each eye for 1 year. RESULTS: Brimonidine and timolol significantly reduced mean intraocular pressure (P < .001) from baseline levels at every scheduled follow-up visit, both at hour 2 (peak) and hour 12 (trough). At weeks 1 and 2 and months 3 and 12, significantly greater mean decreases in intraocular pressure (P < .040) at peak were observed in patients treated with brimonidine than those treated with timolol. The mean intraocular pressure decrease at trough was significantly greater for timolol than for brimonidine at each follow-up visit (P < .001). With the exception of ocular allergy (in 11.5% of patients using brimonidine and less than 1% using timolol), fewer than 3% of patients in either treatment group withdrew from the study prematurely as a result of a specific adverse event. Patients receiving timolol experienced significant decreases in heart rate (P < .001) from baseline at all follow-up visits. No significant changes in heart rate were seen in patients treated with brimonidine. Neither medication produced clinically significant changes in blood pressure. CONCLUSION: Brimonidine is safe and effective in the long-term lowering of intraocular pressure in patients with glaucoma or ocular hypertension, with efficacy comparable to that of timolol but without a notable negative chronotropic effect on the heart.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Agonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH S_administration_&_dosage_MeSH Ophthalmic_Solutions_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 9931077
----K E
----T Safety of nifedipine in angina pectoris: a meta-analysis.
----A -Our objective was to compare cardiovascular event rates in patients with stable angina receiving nifedipine as monotherapy or combination therapy and in active drug controls. A MEDLARS search of published articles from 1966 to 1995 in English, French, German, Italian, or Spanish, supplemented by a manual search of bibliographies, identified 60 randomized controlled trials that met protocol criteria. Blinded articles were extracted by 2 physicians. The pooled risks of death, withdrawal, and cardiovascular event were computed and expressed as odds ratios (ORs) for all nifedipine formulations and relative to same study control drug regimens. Thirty cardiovascular events were reported in 2635 nifedipine exposures (1.14%) and 19 events in 2655 other active drug exposures (0.72%). Unadjusted ORs for nifedipine versus controls were 1.40 (95% CI, 0.56 to 3.49) for major events (death, nonfatal myocardial infarction, stroke, revascularization procedure), 1.75 (95% CI, 0.83 to 3.67) for increased angina, and 1.61 (95% CI, 0.91 to 2.87) for all events (major events plus increased angina). Episodes of increased angina were more frequent on immediate-release nifedipine (OR, 4.19 [95% CI, 1.41 to 12.49]) and on nifedipine monotherapy (OR, 2.61 [95% CI, 1.30 to 5.26]). The OR for immediate-release nifedipine was significantly higher than that for sustained-release/extended-release nifedipine (P=0.001), and the OR for nifedipine monotherapy was higher than that for nifedipine combination therapy (P=0.03). Increased risks of cardiovascular events in patients with stable angina on nifedipine were due primarily to more episodes of increased angina, confined to the immediate-release formulation and to nifedipine monotherapy.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_mortality_MeSH Angina_Pectoris_mortality_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Dosage_Forms_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Nifedipine_adverse_effects_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Nitrates_MeSH S_administration_&_dosage_MeSH Nitrates_administration_&_dosage_MeSH M_Odds_Ratio_MeSH M_Placebos_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 9934342
----K E
----T Effect of initial drug choice on persistence with antihypertensive therapy: the importance of actual practice data.
----A BACKGROUND: Rational medical decisions should be based on the best possible evidence. Clinical trial results, however, may not reflect conditions in actual practice. In hypertension, for example, trials indicate equivalent antihypertensive efficacy and safety for many medications, yet blood pressure frequently remains uncontrolled, perhaps owing to poor compliance. This paper examines the effect of initial choice of treatment on persistence with therapy in actual practice. METHODS: The authors examined all outpatient prescriptions for antihypertensive medications filled in Saskatchewan between 1989 and 1994 by over 22,000 patients with newly diagnosed hypertension whose initial treatment was with a diuretic, beta-blocker, calcium-channel blocker or angiotensin-converting-enzyme (ACE) inhibitor. Rates of persistence over the first year of treatment were compared. RESULTS: After 6 months, persistence with therapy was poor and differed according to the class of initial therapeutic agent: 80% for diuretics, 85% for beta-blockers, 86% for calcium-channel blockers and 89% for ACE inhibitors (p < 0.001). These differences remained significant when age, sex and health status in the previous year were controlled for. Changes in the therapeutic regimen were also associated with lack of persistence. INTERPRETATION: A relation not seen in clinical trials--between persistence with treatment and initial antihypertensive medication prescribed--was found in actual practice. This relation also indicates the importance of real-world studies for evidence-based medicine.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Decision_Making_MeSH P_Evidence-Based_Medicine_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH S_statistics_&_numerical_data_MeSH Patient_Compliance_statistics_&_numerical_data_MeSH M_Primary_Health_Care_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10339027
----K E
----T Cholesterol and coronary heart disease: screening and treatment.
----A 
----P Journal_Article 
----M M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Cost-Benefit_Analysis_MeSH M_Diet_MeSH P_Disease_Management_MeSH M_Exercise_MeSH M_Great_Britain_MeSH S_epidemiology_MeSH Great_Britain_epidemiology_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_diagnosis_MeSH Hypercholesterolemia_diagnosis_MeSH S_therapy_MeSH Hypercholesterolemia_therapy_MeSH P_Mass_Screening_MeSH M_Population_Surveillance_MeSH M_Smoking_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9952147
----K E
----T Dexmedetomidine failed to block the acute hyperdynamic response to electroconvulsive therapy.
----A BACKGROUND: Orally administered clonidine (0.2-0.3 mg) has been reported to decrease the acute hypertensive response to electroconvulsive therapy (ECT) without prolonging early recovery. This preliminary study was designed to evaluate the acute hemodynamic effects of the investigational alpha2-adrenergic agonist, dexmedetomidine, in patients undergoing a series of ECT treatments. METHODS: Six patients undergoing a series of three to six consecutive ECT treatments were studied according to a randomized, double-blind, placebo-controlled protocol All patients received either saline or dexmedetomidine, 0.5 or 1.0 microg/kg intravenously, 10-30 min before induction of anesthesia for ECT using a standardized anesthesia protocol. In addition to assessing the cardiovascular variables, the duration of seizure activity, degree of sedation, and time to discharge from the Phase I recovery unit were assessed. RESULTS: Although dexmedetomidine produced dose-related increases in the level of sedation before the ECT procedure, it failed to decrease the peak blood pressure and heart rate responses after the ECT treatment. The 0.5 and 1.0 microg/kg doses of dexmedetomidine prolonged the times to orientation and to discharge from the Phase I unit. CONCLUSIONS: The results of this pilot study suggest that dexmedetomidine (0.5-1.0 microg/kg given intravenously) is not beneficial in controlling the acute hyperdynamic response after ECT.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Analgesics__Non-Narcotic_MeSH S_administration_&_dosage_MeSH Analgesics__Non-Narcotic_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Depressive_Disorder_MeSH S_therapy_MeSH Depressive_Disorder_therapy_MeSH M_Double-Blind_Method_MeSH M_Electroconvulsive_Therapy_MeSH S_adverse_effects_MeSH Electroconvulsive_Therapy_adverse_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Hypnotics_and_Sedatives_MeSH S_administration_&_dosage_MeSH Hypnotics_and_Sedatives_administration_&_dosage_MeSH M_Imidazoles_MeSH S_administration_&_dosage_MeSH Imidazoles_administration_&_dosage_MeSH M_Medetomidine_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9973007
----K E
----T Ventricular rate control in chronic atrial fibrillation during daily activity and programmed exercise: a crossover open-label study of five drug regimens.
----A OBJECTIVES: We compared the effects of five pharmacologic regimens on the circadian rhythm and exercise-induced changes of ventricular rate (VR) in patients with chronic atrial fibrillation (CAF). BACKGROUND: Systematic comparison of standardized drug regimens on 24 h VR control in CAF have not been reported. METHODS: In 12 patients (11 male, 69+/-6 yr) with CAF, the effects on VR by 5 standardized daily regimens: 1) 0.25 mg digoxin, 2) 240 mg diltiazem-CD, 3) 50 mg atenolol, 4) 0.25 mg digoxin + 240 mg diltiazem-CD, and 5) 0.25 mg digoxin + 50 mg atenolol; were studied after 2 week treatment assigned in random order. The VR data were analyzed by ANOVA with repeated measures. The circadian phase differences were evaluated by cosinor analysis. RESULTS: The 24-h mean (+/-SD) values of VR (bpm) were - digoxin: 78.9 +/- 16.3, diltiazem: 80.0+/-15.5, atenolol: 75.9+/-11.7, digoxin + diltiazem: 67.3+/-14.1 and digoxin + atenolol: 65.0+/-9.4. Circadian patterns were significant in each treatment group (p < 0.001). The VR on digoxin + atenolol was significantly lower than that on digoxin (p < 0.0001), diltiazem (p < 0.0002) and atenolol (p < 0.001). The time of peak VR on Holter was significantly delayed with regimens 3 and 5 which included atenolol (p < 0.03). During exercise, digoxin and digoxin + atenolol treatments resulted in the highest and lowest mean VR respectively. The exercise Time-VR plots of all groups were nearly parallel (p = ns). The exercise duration was similar in all treatment groups (p = ns). CONCLUSIONS: This study indicates that digoxin and diltiazem, as single agents at the doses tested, are least effective for controlling ventricular rate in atrial fibrillation during daily activity. Digoxin + atenolol produced the most effective rate control reflecting a synergistic effect on the AV node. The data provides a basis for testing the effects of chronic suppression of diurnal fluctuations of VR on left atrial and ventricular function in CAF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH P_Heart_Rate_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 9989534
----K I
----T Sympathetic activation in heart failure and its treatment with beta-blockade.
----A Multiple models explaining the pathogenesis of heart failure have been put forth during the past 5 decades. These models were modified as clinical evidence supported or refuted their assumptions. During the past 2 decades, heart failure models emphasized the importance of neurohormonal systems in heart failure progression. The positive impact that angiotensin-converting enzyme inhibitors have had on mortality from heart failure has bolstered the neurohormonal theory. Attention recently has turned to the sympathetic nervous system and its potential deleterious effects on the cardiovascular system in heart failure. The sympathetic nervous system can negatively impact the cardiovascular system in heart failure in several ways, including down-regulating beta1-receptors, exerting direct toxic effects on the myocardium, and contributing to myocardial remodeling and life-threatening arrhythmias. Beta-adrenergic blockers have shown promise for reducing morbidity and mortality in heart failure, but definitive reductions in mortality remain to be shown by future investigations.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Conduction_System_MeSH S_drug_effects_MeSH Heart_Conduction_System_drug_effects_MeSH S_physiopathology_MeSH Heart_Conduction_System_physiopathology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH M_Hormones_MeSH S_metabolism_MeSH Hormones_metabolism_MeSH M_Human_MeSH M_Multicenter_Studies_MeSH M_Neuropeptides_MeSH S_metabolism_MeSH Neuropeptides_metabolism_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH 
****** 9988956
----K E
----T Aggressive blood pressure lowering is safe, but benefit is still hard to prove.
----A In the Hypertension Optimal Treatment (HOT) study, hypertensive patients who were randomly assigned to undergo antihypertensive treatment to achieve a goal diastolic blood pressure of 80 mm Hg or lower did not experience fewer cardiovascular events than did patients who received treatment with goal pressures of 85 or 90 mm Hg. Such aggressive antihypertensive treatment was safe and well tolerated, and did result in fewer cardiovascular events in the subset of patients with diabetes. All patients were randomly assigned to take aspirin 75 mg/day or placebo, and patients in the aspirin group had a 15% lower rate of major cardiovascular events and myocardial infarctions than did patients who received placebo. This finding establishes the efficacy of aspirin in preventing strokes and myocardial infarctions in hypertensive patients.
----P Clinical_Trial Journal_Article Meta-Analysis Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_pharmacology_MeSH Aspirin_pharmacology_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Disorders_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_pharmacology_MeSH Fibrinolytic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_pharmacology_MeSH Platelet_Aggregation_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Quality_of_Life_MeSH M_Risk_Factors_MeSH 
****** 9989964
----K E
----T Neurohumoral prediction of benefit from carvedilol in ischemic left ventricular dysfunction. Australia-New Zealand Heart Failure Group.
----A BACKGROUND--Plasma neurohormones were analyzed for prediction of adverse outcomes and response to treatment in 415 patients with ischemic left ventricular dysfunction randomly assigned to receive carvedilol or placebo. METHODS AND RESULTS--Atrial natriuretic peptide, brain natriuretic peptide (BNP), or norepinephrine (NE) levels above the group median were associated with increased mortality rates and heart failure. On multivariate analysis, both BNP and NE interacted with treatment to predict death or heart failure independent of age, New York Heart Association class, and left ventricular ejection fraction. For placebo, supramedian levels of BNP were associated with 3-fold the mortality rate of inframedian levels (20/104; 19% vs 6/99; 6%; P<0.01). For carvedilol, mortality rate was comparable in these 2 subgroups (12/109; 11% vs 8/94; 9%; NS). Corresponding rates for heart failure were 29/104 (28%) versus 3/99 (3%; P<0.001) for placebo and 16/109 (15%) versus 7/94 (7%; NS) for carvedilol. High NE levels did not predict additional benefit from carvedilol, which significantly reduced heart failure admissions only in those with NE levels below the median (13.1% to 4. 0%; P<0.01). In the 23% of the study population with supramedian BNP but inframedian levels of NE, carvedilol reduced hospital admission with heart failure by >90% (P<0.001). CONCLUSIONS--Carvedilol reduced mortality rates and heart failure in those with higher pretreatment BNP levels but lesser activation of plasma NE. Neurohumoral profiling may guide introduction of beta-blockade in heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Argipressin_MeSH S_blood_MeSH Argipressin_blood_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Ischemia_MeSH S_blood_MeSH Myocardial_Ischemia_blood_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Neuropeptides_MeSH S_blood_MeSH Neuropeptides_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 10023937
----K I
----T Beta-blockers for mild to moderate heart failure.
----A 
----P Comment Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Animals_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Severity_of_Illness_Index_MeSH 
****** 10023943
----K I
----T The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial.
----A BACKGROUND: In patients with heart failure, beta-blockade has improved morbidity and left-ventricular function, but the impact on survival is uncertain. We investigated the efficacy of bisoprolol, a beta1 selective adrenoceptor blocker in decreasing all-cause mortality in chronic heart failure. METHODS: In a multicentre double-blind randomised placebo-controlled trial in Europe, we enrolled 2647 symptomatic patients in New York Heart Association class III or IV, with left-ventricular ejection fraction of 35% or less receiving standard therapy with diuretics and inhibitors of angiotensin-converting enzyme. We randomly assigned patients bisoprolol 1.25 mg (n=1327) or placebo (n=1320) daily, the drug being progressively increased to a maximum of 10 mg per day. Patients were followed up for a mean of 1.3 years. Analysis was by intention to treat. FINDINGS: CIBIS-II was stopped early, after the second interim analysis, because bisoprolol showed a significant mortality benefit. All-cause mortality was significantly lower with bisoprolol than on placebo (156 [11.8%] vs 228 [17.3%] deaths with a hazard ratio of 0.66 (95% CI 0.54-0.81, p<0.0001). There were significantly fewer sudden deaths among patients on bisoprolol than in those on placebo (48 [3.6%] vs 83 [6.3%] deaths), with a hazard ratio of 0.56 (0.39-0.80, p=0.0011). Treatment effects were independent of the severity or cause of heart failure. INTERPRETATION: Beta-blocker therapy had benefits for survival in stable heart-failure patients. Results should not, however, be extrapolated to patients with severe class IV symptoms and recent instability because safety and efficacy has not been established in these patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH 
****** 10024334
----K E
----T Irbesartan reduces QT dispersion in hypertensive individuals.
----A Angiotensin type 1 receptor antagonists have direct effects on the autonomic nervous system and myocardium. Because of this, we hypothesized that irbesartan would reduce QT dispersion to a greater degree than amlodipine, a highly selective vasodilator. To test this, we gathered electrocardiographic (ECG) data from a multinational, multicenter, randomized, double-blind parallel group study that compared the antihypertensive efficacy of irbesartan and amlodipine in elderly subjects with mild to moderate hypertension. Subjects were treated for 6 months with either drug. Hydrochlorothiazide and atenolol were added after 12 weeks if blood pressure (BP) remained uncontrolled. ECGs were obtained before randomization and at 6 months. A total of 188 subjects (118 with baseline ECGs) were randomized. We analyzed 104 subjects who had complete ECGs at baseline and after 6 months of treatment. Baseline characteristics between treatments were similar, apart from a slight imbalance in diastolic BP (irbesartan [n=53] versus amlodipine [n=51], 99.2 [SD 3. 6] versus 100.8 [3.8] mm Hg; P=0.03). There were no significant differences in BP normalization (diastolic BP <90 mm Hg) between treatments at 6 months (irbesartan versus amlodipine, 80% versus 88%; P=0.378). We found a significant reduction in QT indexes in the irbesartan group (QTc dispersion mean, -11.4 [34.5] milliseconds, P=0.02; QTc max, -12.8 [35.5] milliseconds, P=0.01), and QTc dispersion did not correlate with the change in BP. The reduction in QT indexes with amlodipine (QTc dispersion, -9.7 [35.4] milliseconds, P=0.06; QTc max, -8.6 [33.2] milliseconds, P=0.07) did not quite reach statistical significance, but there was a correlation between the change in QT indexes and changes in systolic BP. In conclusion, irbesartan improved QT dispersion, and this effect may be important in preventing sudden cardiac death in at-risk hypertensive subjects.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_pharmacology_MeSH Amlodipine_pharmacology_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_pharmacology_MeSH Biphenyl_Compounds_pharmacology_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH S_physiopathology_MeSH Heart_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_physiology_MeSH Receptors__Angiotensin_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_pharmacology_MeSH Tetrazoles_pharmacology_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 10025200
----K E
----T [Current use of beta-blockers in coronary artery disease]
----A This article presents the results of a retrospective analysis of the use of beta-blockers and current dosing of these agents in patients with coronary artery disease. While 70 to 78% of patients admitted to Norwegian university hospitals during 1990-1997 for angiographic evaluation of chest pain used beta-blockers, only 43-60% of patients with stable coronary artery disease enrolled in the 4S study in Norway received such treatment. High risk groups such as diabetics and patients with peripheral artery disease were less likely to receive beta-blockers during the early period, but were not treated differentially compared to low risk patients during recent years. Only 15% of patients with congestive heart failure received oral beta-blockers, and only 10.5% intravenous beta-blockade during acute myocardial infarction. The dosing of the most common beta-blockers were low, approximately 50% of doses shown to improve survival after acute myocardial infarction.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Diabetes_Mellitus_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus_prevention_&_control_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 10027497
----K E
----T Carvedilol and the Food and Drug Administration approval process: an introduction.
----A We discuss briefly the new drug carvedilol (Coreg), a beta-blocker, alpha-blocker, and antioxidant. This drug was developed for congestive heart failure in a series of trials, four in the United States and one in Australia and New Zealand, briefly summarized in this document. We also summarize the classical paradigm of the U.S. Food and Drug Administration (FDA) for drug approval and the FDA's use of advisory committees. This document serves as background to the discussion of carvedilol's approval.
----P Comment Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Approval_MeSH S_methods_MeSH Drug_Approval_methods_MeSH S_statistics_&_numerical_data_MeSH Drug_Approval_statistics_&_numerical_data_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Public_Policy_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH M_United_States_MeSH M_United_States_Food_and_Drug_Administration_MeSH S_standards_MeSH United_States_Food_and_Drug_Administration_standards_MeSH 
****** 10027498
----K E
----T Carvedilol and the Food and Drug Administration (FDA) approval process: the FDA paradigm and reflections on hypothesis testing.
----A Carvedilol (Coreg), a beta- and alpha-blocker and an antioxidant drug, was evaluated for moderate to severe heart failure patients in a program containing four United States and one Australia/New Zealand study. The data were evaluated twice by the Cardiovascular and Renal Drugs Advisory Committee of the U.S. Food and Drug Administration (FDA). These meetings resulted in opposite decisions by the advisory committee. The crux of the argumentation was the two-positive-trial FDA paradigm. Carvedilol did not meet the usual paradigm because an exercise end point was not statistically different from placebo in three U.S. trials. Most other end points were highly significant, and death, which was monitored across the U.S. program, was different with p < 0.0001. Here we argue that the usual paradigm is very useful but not an absolute principle, that the usual paradigm can sometimes miss the strength of evidence even in the primary end points, and that rational decision making requires on occasion that other evidence must lead to approval. Control of the type I error rate should be taken very seriously, should rarely be violated, and serves the biomedical community well. It is not an absolute principle, however, but rather must be considered in context.
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Approval_MeSH S_methods_MeSH Drug_Approval_methods_MeSH S_statistics_&_numerical_data_MeSH Drug_Approval_statistics_&_numerical_data_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Public_Policy_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_United_States_MeSH M_United_States_Food_and_Drug_Administration_MeSH S_standards_MeSH United_States_Food_and_Drug_Administration_standards_MeSH 
****** 10027499
----K E
----T End-point interpretation in clinical trials: the case for discipline.
----A The recent submission of a new drug application to the federal Food and Drug Administration (FDA) has led to vigorous discussion concerning the rules of clinical trial conduct. The regulatory importance of prospectively defined end points, long held as a fundamental tenet of well-designed research efforts, and the proper role of alpha-spending functions in clinical trials are current foci of attention. Sound public policy requires that the highest research standards govern statistical analyses to support a new drug application. These research standards should be rooted in the fundamentals of epidemiology and biostatistics, long accepted by clinical trial workers. Also, because the physician-scientists whose research results are disseminated to the community bear considerable responsibility for both that community's protection and the protection of the individual patient, these investigators must provide unambiguous interpretations of type I and type II error rates. This obligation includes clear prospective statements of analysis plans and complete reporting of findings for the prospectively defined endpoints in presentations and in manuscripts. The public health is best served if regulatory agencies continue to join clinical trial workers in repudiating the philosophy of "sound methodology or a small p-value" in judging research efforts. Reviewers of new drug applications might best take the tack "judge first what the investigators set out to do, then judge what else was discovered in an 'exploratory light.'"
----P Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Drug_Approval_MeSH S_methods_MeSH Drug_Approval_methods_MeSH S_statistics_&_numerical_data_MeSH Drug_Approval_statistics_&_numerical_data_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_United_States_MeSH 
****** 10068356
----K E
----T Medical therapy after successful percutaneous coronary revascularization.
----A BACKGROUND: Percutaneous coronary revascularization frequently relieves angina in patients with ischemic heart disease and may obviate the need for antianginal medications. OBJECTIVE: To examine the use of antianginal medications after successful percutaneous coronary revascularization. DESIGN: Retrospective cohort study of the Mayo Clinic PTCA [percutaneous transluminal coronary angioplasty] Registry. SETTING: Tertiary care center. PATIENTS: 3831 patients who underwent successful percutaneous coronary revascularization from September 1979 through August 1997 and had not had myocardial infarction within the year before the intervention. MEASUREMENTS: Use of antianginal medications (beta-adrenergic blockers, nitrates, and calcium-channel blockers) before the intervention, at hospital discharge, and 6 months after the intervention. RESULTS: 99% of patients reported improvement in their symptoms at hospital discharge. At 6 months, 87% of patients were free of myocardial infarction, coronary bypass surgery, or additional percutaneous intervention. Compared with 66% of patients before the index intervention, only 12% of patients had severe angina at 6 months and 69% were completely free of angina. Nonetheless, at 6 months, 39% of patients were receiving beta-adrenergic blockers (preprocedure proportion, 43%; P < 0.001), 36% were receiving nitrates (preprocedure proportion, 41%; P < 0.001), and 57% were receiving calcium-channel blockers (preprocedure proportion, 50%; P < 0.001). These trends persisted for patients without hypertension and those who had complete revascularization. CONCLUSIONS: Successful percutaneous coronary revascularization did not substantially supplant the use of antianginal medications, which were commonly used despite the marked improvement in anginal status. This may reflect reluctance to alter therapy once symptoms of angina subside. Guidelines on continued medical therapy after percutaneous coronary revascularization are needed.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_classification_MeSH Coronary_Disease_classification_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Postoperative_Period_MeSH M_Retrospective_Studies_MeSH 
****** 10028936
----K E
----T Total arterial compliance in ambulatory hypertension during selective beta1-adrenergic receptor blockade and angiotensin-converting enzyme inhibition.
----A Aortic root flow and pressure estimates were obtained noninvasively with Doppler echocardiography and calibrated subclavian artery pulse tracing in 30 subjects with ambulatory hypertension in a randomized, crossover study with 4 weeks' treatment and washout periods. Total arterial compliance, assessed by use of a three-element Windkessel model of the arterial tree, increased 42% with atenolol (50-100 mg once daily), and 7% (p = NS) with captopril (25-50 mg twice daily). Atenolol reduced mean arterial pressure by 15%, heart rate by 22%, and cardiac output by 14%, and increased acceleration time of aortic root flow by 17% and stroke volume and ejection time each by 11%. Captopril reduced mean arterial pressure and total peripheral resistance each by 7%. Acceleration time of aortic root flow, ejection time, heart rate, stroke volume, and cardiac output were not significantly changed by captopril. We conclude that total arterial compliance, at the operational blood pressure, increases during selective beta1-adrenergic receptor blockade in subjects with ambulatory hypertension. Although the main mechanism may be a reduction in mean arterial pressure, it should be considered whether reduced heart rate may play an additional role. The nonsignificant increase in total arterial compliance during angiotensin-converting enzyme inhibition may primarily be a consequence of a modest reduction of the mean arterial pressure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_Antagonists_MeSH S_pharmacology_MeSH Adrenergic_Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Aorta_MeSH S_drug_effects_MeSH Aorta_drug_effects_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH 
****** 10026356
----K E
----T QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion.
----A OBJECTIVE: To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function. DESIGN: A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment. SETTING: A regional cardiology centre and a university teaching hospital. PATIENTS: 25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function. MAIN OUTCOME MEASURES: QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion. RESULTS: All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01). CONCLUSIONS: QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Case-Control_Studies_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Echocardiography__Doppler__Color_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_ultrasonography_MeSH Ventricular_Dysfunction__Left_ultrasonography_MeSH 
****** 10030320
----K I
----T Which drug for treatment of hypertension?
----A BACKGROUND: Angiotensin-converting-enzyme (ACE) inhibitors have been used for more than a decade to treat high blood pressure, despite the lack of data from randomised intervention trials to show that such treatment affects cardiovascular morbidity and mortality. The Captopril Prevention Project (CAPPP) is a randomised intervention trial to compare the effects of ACE inhibition and conventional therapy on cardiovascular morbidity and mortality in patients with hypertension. METHODS: CAPPP was a prospective, randomised, open trial with blinded endpoint evaluation. 10,985 patients were enrolled at 536 health centres in Sweden and Finland. Patients aged 25-66 years with a measured diastolic blood pressure of 100 mm Hg or more on two occasions were randomly assigned captopril or conventional antihypertensive treatment (diuretics, beta-blockers). Analysis was by intention-to-treat. The primary endpoint was a composite of fatal and non-fatal myocardial infarction, stroke, and other cardiovascular deaths. FINDINGS: Of 5492 patients assigned captopril and 5493 assigned conventional therapy, 14 and 13, respectively, were lost to follow-up. Primary endpoint events occurred in 363 patients in the captopril group (11.1 per 1000 patient-years) and 335 in the conventional-treatment group (10.2 per 1000 patient-years; relative risk 1.05 [95% CI 0.90-1.22], p=0-52). Cardiovascular mortality was lower with captopril than with conventional treatment (76 vs 95 events; relative risk 0.77 [0.57-1-04], p=0.092), the rate of fatal and non-fatal myocardial infarction was similar (162 vs 161), but fatal and non-fatal stroke was more common with captopril (189 vs 148; 1.25 [1-01-1-55]. p=0.044). INTERPRETATION: Captopril and conventional treatment did not differ in efficacy in preventing cardiovascular morbidity and mortality. The difference in stroke risk is probably due to the lower levels of blood pressure obtained initially in previously treated patients randomised to conventional therapy.
----P Comment Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Multicenter_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 10030325
----K E
----T Effect of angiotensin-converting-enzyme inhibition compared with conventional therapy on cardiovascular morbidity and mortality in hypertension: the Captopril Prevention Project (CAPPP) randomised trial.
----A BACKGROUND: Angiotensin-converting-enzyme (ACE) inhibitors have been used for more than a decade to treat high blood pressure, despite the lack of data from randomised intervention trials to show that such treatment affects cardiovascular morbidity and mortality. The Captopril Prevention Project (CAPPP) is a randomised intervention trial to compare the effects of ACE inhibition and conventional therapy on cardiovascular morbidity and mortality in patients with hypertension. METHODS: CAPPP was a prospective, randomised, open trial with blinded endpoint evaluation. 10,985 patients were enrolled at 536 health centres in Sweden and Finland. Patients aged 25-66 years with a measured diastolic blood pressure of 100 mm Hg or more on two occasions were randomly assigned captopril or conventional antihypertensive treatment (diuretics, beta-blockers). Analysis was by intention-to-treat. The primary endpoint was a composite of fatal and non-fatal myocardial infarction, stroke, and other cardiovascular deaths. FINDINGS: Of 5492 patients assigned captopril and 5493 assigned conventional therapy, 14 and 13, respectively, were lost to follow-up. Primary endpoint events occurred in 363 patients in the captopril group (11.1 per 1000 patient-years) and 335 in the conventional-treatment group (10.2 per 1000 patient-years; relative risk 1.05 [95% CI 0.90-1.22], p=0-52). Cardiovascular mortality was lower with captopril than with conventional treatment (76 vs 95 events; relative risk 0.77 [0.57-1-04], p=0.092), the rate of fatal and non-fatal myocardial infarction was similar (162 vs 161), but fatal and non-fatal stroke was more common with captopril (189 vs 148; 1.25 [1-01-1-55]. p=0.044). INTERPRETATION: Captopril and conventional treatment did not differ in efficacy in preventing cardiovascular morbidity and mortality. The difference in stroke risk is probably due to the lower levels of blood pressure obtained initially in previously treated patients randomised to conventional therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Cerebrovascular_Disorders_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Confidence_Intervals_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Diseases_MeSH S_etiology_MeSH Heart_Diseases_etiology_MeSH S_prevention_&_control_MeSH Heart_Diseases_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Intervention_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 10030088
----K 1
----T [Predictors of readmission in patients with congestive heart failure]
----A Repeated hospitalizations among patients (pts) with congestive heart failure (CHF) are common. PURPOSE: This retrospective study was designed to determine predictors of readmission. METHODS: Inclusion criteria: admitted to University Hospital with a primary diagnosis of CHF between 10/1/94-9/30/95: lived in Jefferson county. Exclusions: cardiac transplant during study period; major comorbidity (e.g. malignancy, advanced renal failure). Predictors of readmission were determined by stepwise logistic regression analysis and predictor of time to readmission with Cox Proportionate Hazards modeling p < 0.05 was considered statistically significant. RESULTS: Mean age of the 237 pts was 66.5 yrs; 56% women. Mean left ventricular ejection fraction (LVEF) was 29%; 96% were in NYHA class III/IV. Mean length of stay was 5 days; 52 pts (22%) had > 1 admission. CHF etiologies: Ischemic (42%), hypertensive (37%), idiopathic (12%). Demographic characteristics and insurance status did not predict readmission risk. Predictors of readmission in the logistic and Cox models were similar. Increased risk of readmission was associated with myocardial ischemia (logistic OR 42.7), past NYHA Class III and IV (OR 32.8), plasmatic creatinine at discharge (OR 1.9) and continued smoking (OR 3.26). History of CABG was associated with a decreased risk of rehospitalization (OR 0.12). Beta-blocker use was associated with decreased risk, but did not achieve statistical significance. ACE-I use (prescribed in 78% of pts), did not contribute to the model. Diabetes Mellitus and a lower LVEF were more frequent in the readmitted group, but they did not predict readmission. CONCLUSION: CHF pts who have evidence of ischemia, advanced symptoms, renal dysfunction, and who continue to smoke are at increased risk for hospital readmission. Pts with these characteristics should be identified prior to hospital discharge and considered for intensive outpatient intervention.
----P Journal_Article 
----M M_Aged_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Incidence_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH M_Patient_Readmission_MeSH S_statistics_&_numerical_data_MeSH Patient_Readmission_statistics_&_numerical_data_MeSH M_Recurrence_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH 
****** 10030097
----K I
----T [New multicentric studies in hypertension]
----A Prospective, randomized and long term multicentric studies, published since 1988, on the effects of pharmacological or non pharmacological treatment of hypertension are analyzed. Former studies, performed between 1967 and 1987, are devoted, in chronological order, to special populations or to forms of hypertension not sufficiently studied previously (elders and isolated systolic hypertension), using classical pharmacological treatments such as diuretics and beta blockers. Their results confirm the reduction in mortality obtained using such therapies. Ensuing studies, focused on the analysis of new drugs such as calcium antagonists and angiotensin converting enzyme inhibitors, also demonstrated a reduction in cardiovascular risk, even in severely damaged populations. Thereafter, meta analysis of new pharmacological treatments and of non pharmacological therapies such as sodium restriction, weight reduction, avoidance of alcohol intake, calcium and potassium supplementation have appeared. These studies have emphasized the importance of prevention through changes in lifestyles. Their positive, although modest results, encourage the assessment of long term preventive and therapeutic measures in hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Multicenter_Studies_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10047618
----K E
----T Sotalol: An important new antiarrhythmic.
----A Sotalol, the most recently approved oral antiarrhythmic drug, has a unique pharmacologic profile. Its electrophysiology is explained by nonselective beta-blocking action as well as class III antiarrhythmic activity (including fast-activating cardiac membrane-delayed rectifier current blockade), which leads to increases in action potential duration and refractory period throughout the heart and in QT interval on the surface electrocardiogram. Its better hemodynamic tolerance than other beta-blockers may be a result of enhanced inotropy associated with class III activity. Sotalol's ability to suppress ventricular ectopy is similar to that of class I agents and better than that of standard beta-blockers. Unlike class I agents, its use in a postinfarction trial was not associated with increased mortality rate. Therapeutically, it has shown superior efficacy for prevention of recurrent ventricular tachycardia and ventricular fibrillation, which was the basis for its approval. In a randomized study, the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial, sotalol was associated with an increased in-hospital efficacy prediction rate (by Holter monitor or electrophysiologic study), reduced long-term arrhythmic recurrence rate with superior tolerance, and lower mortality rate than class I ("standard") antiarrhythmic drugs. Sotalol was 1 of 2 drugs selected for comparison with implantable defibrillators in the recent National Institutes of Health Antiarrhythmics versus Implantable Defibrillator (AVID) study. Sotalol appears to be a preferred drug for use with implantable defibrillators; unlike some other agents (eg, amiodarone) it does not elevate and, indeed, may lower defibrillation threshold. Although unapproved for this use, sotalol is active against atrial arrhythmias. It has shown efficacy equivalent to propafenone and quinidine in preventing atrial fibrillation recurrence, but it is better tolerated than quinidine and provides excellent rate control during recurrence. Sotalol's major side effects are related to beta-blockade and the risk of torsades de pointes (acceptably small if appropriate precautions are taken). Unlike several other antiarrhythmics (eg, amiodarone), it has no pharmacokinetic drug-drug interactions, is not metabolized, and is entirely renally excreted. Initial dose is 80 mg twice daily, with gradual titration to 240 to 360 mg/day as needed. The daily dose must be reduced in renal failure. On the basis of favorable clinical trials and practice experience, sotalol has shown a steadily growing impact on the treatment of arrhythmias during its 5 years of market availability, a trend that is likely to continue.
----P Journal_Article Review Review__Tutorial 
----M M_Action_Potentials_MeSH S_drug_effects_MeSH Action_Potentials_drug_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Defibrillators__Implantable_MeSH M_Drug_Interactions_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Refractory_Period__Neurologic_MeSH S_drug_effects_MeSH Refractory_Period__Neurologic_drug_effects_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH S_adverse_effects_MeSH Sotalol_adverse_effects_MeSH S_pharmacology_MeSH Sotalol_pharmacology_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Ventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Ventricular_prevention_&_control_MeSH M_Torsades_de_Pointes_MeSH S_chemically_induced_MeSH Torsades_de_Pointes_chemically_induced_MeSH M_Ventricular_Fibrillation_MeSH S_prevention_&_control_MeSH Ventricular_Fibrillation_prevention_&_control_MeSH M_Ventricular_Premature_Complexes_MeSH S_prevention_&_control_MeSH Ventricular_Premature_Complexes_prevention_&_control_MeSH 
****** 10063787
----K I
----T Low-dose combination therapy as first-line hypertension treatment for blacks and nonblacks.
----A To assess the efficacy and safety of bisoprolol/6.25-mg hydrochlorothiazide (HCTZ), amlodipine, and enalapril in black and nonblack patients, data from two comparative studies were pooled and subgroup analyses performed. Both studies had similar designs and included all three active treatments. The second study also included a placebo group. Subjects (n = 541) with a sitting diastolic blood pressure of 95-114 mmHg were titrated to achieve a diastolic blood pressure < or = 90 mmHg. The studies included 114 blacks and 427 nonblacks. Results of an intention-to-treat analysis of mean change from baseline after 12 weeks of treatment showed the following: 1) blood pressure was significantly lowered by all three active drugs compared with baseline or placebo; 2) in blacks, bisoprolol/6.25-mg HCTZ resulted in significantly greater reductions of systolic and diastolic blood pressure than enalapril or placebo, but was not significantly different from amlodipine; 3) in nonblacks, bisoprolol/6.25-mg HCTZ resulted in significantly greater reduction of diastolic blood pressure than amlodipine, enalapril, or placebo. The placebo-corrected change in blood pressure was greater for blacks than whites on the bisoprolol/6.25-mg HCTZ combination, but this was not statistically significant. Bisoprolol/6.25-mg HCTZ controlled diastolic blood pressure to < or = 90 mmHg in significantly more patients than enalapril or placebo in blacks and nonblacks. The difference in control rates was not significant versus amlodipine. The incidence of drug-related adverse events was similar between treatments; however, bisoprolol/6.25-mg HCTZ had a lower discontinuation rate due to lack of blood pressure control or adverse experiences in both blacks and nonblacks.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 10073788
----K I
----T Jeffrey Michael Isner, MD: a conversation with the editor. Interview by William Clifford Roberts.
----A 
----P Interview 
----M P_Cardiology_MeSH M_Germany_MeSH M_Human_MeSH M_Jews_MeSH M_Portraits_MeSH M_Support__Non-U_S__Gov't_MeSH M_United_States_MeSH 
****** 10073847
----K E
----T Support for the open-artery hypothesis in survivors of acute myocardial infarction: analysis of 11,228 patients treated with thrombolytic therapy.
----A We examined the possible benefits of achieving and maintaining infarct-related artery potency beyond the time when preservation of left ventricular function would be expected. The open-artery hypothesis suggests that a patent infarct-related artery confers a survival benefit greater than that expected from myocardial salvage alone, which extends beyond the time when preservation of left ventricular function is expected. We examined the survival experience of patients undergoing thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO-I) trial for whom data on the potency of the infarct artery were available. Univariable analysis was used to determine the unadjusted relations of angiographic variables and revascularization procedures to both 30-day and 1-year mortality in 30-day survivors. Multivariable analysis was used to test for interactions between patency and each characteristic and to adjust both for all other variables and for baseline characteristics known to predict mortality. In both univariable and multivariable analysis, patients with an open rather than a closed infarct-related artery had significantly lower 30-day mortality (p <0.001). This benefit cannot be accounted for by myocardial salvage alone, because it remained after adjustment for left ventricular ejection fraction. Patency was also associated with lower 1-year mortality in 30-day survivors, but not after adjustment for other variables affecting late mortality. Having an open infarct-related artery at the time of first catheterization confers a survival advantage that extends beyond the benefit of myocardial salvage from thrombolytic therapy, and is independent of ejection fraction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Algorithms_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Survivors_MeSH P_Thrombolytic_Therapy_MeSH M_Treatment_Outcome_MeSH P_Vascular_Patency_MeSH 
****** 10073852
----K E
----T Comparison of controlled-onset, extended-release verapamil with amlodipine and amlodipine plus atenolol on exercise performance and ambulatory ischemia in patients with chronic stable angina pectoris.
----A This multicenter, randomized, double-blind, parallel group, placebo lead-in, placebo-controlled study compared the antianginal and anti-ischemic effects of once-daily bedtime dosing of controlled-onset extended-release (COER-24) verapamil to a once-daily morning dosing of amlodipine +/- atenolol in patients with chronic stable angina. A total of 551 patients with exercise-induced myocardial ischemia and evidence of coronary artery disease were randomized to a 4-week, forced-dose titration treatment period with (1) COER-24 verapamil 240 mg titrated to 480 mg at bedtime (n = 173), (2) amlodipine 5 mg titrated to 10 mg/day (n = 149), (3) amlodipine 5 mg (titrated to 10 mg) plus atenolol 50 mg/day in the A.M. (n = 154), or (4) placebo (n = 75). Treadmill exercise tolerance testing (standard Bruce protocol), and 48-hour ambulatory electrocardiographic (Holter) monitoring were performed at the end of placebo lead-in and double-blind treatment. Each active treatment significantly improved symptom-limited exercise duration and time to moderate angina (p < or = 0.01 vs placebo). For patients with baseline ischemia, amlodipine resulted in a statistically significant increase in total duration of ischemic episodes compared with placebo, whereas COER-24 verapamil and amlodipine plus atenolol resulted in statistically significant decreases compared with placebo and amlodipine. Heart rate at onset of ischemic episodes and ST product were also significantly increased with amlodipine (p < 0.05) compared with either COER-24 or amlodipine plus atenolol. COER-24 and amlodipine alone or in combination with atenolol improved exercise capacity in patients with angina pectoris. COER-24 verapamil monotherapy or amlodipine plus atenolol combination therapy were more effective than amlodipine monotherapy in decreasing ambulatory myocardial ischemia, especially during the hours of 6 A.M. to 12 noon.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10075136
----K E
----T Hotline sessions at the 20th European Congress of Cardiology.
----A 
----P Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_mortality_MeSH Arrhythmia_mortality_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH P_Cardiology_MeSH P_Congresses_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Europe_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_mortality_MeSH Myocardial_Ischemia_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10075137
----K E
----T Treatment with beta-blockers for the primary prevention of the cardiovascular complications of hypertension.
----A 
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH P_Primary_Prevention_MeSH S_methods_MeSH Primary_Prevention_methods_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH 
****** 10075140
----K E
----T Heart rate variability and ischaemia in patients with coronary heart disease and stable angina pectoris; influence of drug therapy and prognostic value. TIBBS Investigators Group. Total Ischemic Burden Bisoprolol Study.
----A AIMS: Determination of the influence of therapy with bisoprolol and nifedipine on the heart rate variability of patients from the Total Ischemic Burden Bisoprolol Study and examination of the prognostic value. METHODS AND RESULTS: Four hundred and twenty-two patients with stable angina were included. The heart rate variability was determined over a period of 24 h. Parameters determined: standard deviation of the mean of all corrected RR intervals, standard deviation of all 5 min mean cycle lengths, square root of the mean of the squared differences of successive corrected RR intervals. Nifedipine reduced the mean values of all heart rate variability parameters tested. Square root of the mean of the square differences of successive corrected RR intervals increased under bisoprolol. Standard deviation of the mean of all corrected RR intervals and standard deviation of all 5 min mean cycle lengths increased from low baseline values and declined from higher baseline values. The increase in heart rate variability under therapy was accompanied by a tendency towards a better prognosis. Patients with an increase in heart rate variability and simultaneous complete suppression of ischaemia under therapy displayed no serious events in the course of one year. CONCLUSIONS: The increase in the heart rate variability, which can be regarded as prognostically favourable, was predominantly observed under bisoprolol. The parameter constellation of an increase in heart rate variability and complete ischaemia suppression on the 48-h Holter ECG was associated with the greatest benefit.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography__Ambulatory_MeSH M_Europe_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Prognosis_MeSH M_Reproducibility_of_Results_MeSH M_Retrospective_Studies_MeSH 
****** 10080412
----K I
----T Comparison of safety and efficacy of carvedilol and metoprolol in stable angina pectoris.
----A In a double-blind, randomized, 3-month multicenter study, the safety and tolerability and the antianginal and anti-ischemic efficacy of carvedilol 25 to 50 mg twice daily were assessed in comparison with metoprolol 50 to 100 mg twice daily in younger and elderly patients with stable angina. After a 7-day placebo run-in at the end of which a symptom-limited bicycle ergometric exercise was performed, 368 patients were randomly allocated to the parallel treatment groups. After 4 weeks of therapy with a low dose, a further exercise test was performed and patients were titrated in single-blind fashion to the higher dose if the increase in total exercise time was < 1 minute, and there was no safety concern. After a further 8 weeks of treatment a third exercise test was performed. Carvedilol low dose/high dose was shown to be at least as safe and well tolerated as metoprolol low dose/high dose both in younger and elderly patients. There were no hitherto unknown adverse events and no marked change in the types of events after increase of the doses. Early adverse events after treatment initiation or uptitration were equal with both medications, indicating no particular risk associated with carvedilol's vasodilatory action. No rebound phenomena were observed. Both drugs showed good antianginal and anti-ischemic efficacy, with marked increases on uptitration including patients > or = 65 years of age. However, in the doses selected, which appeared equipotent with respect to beta blockade, carvedilol's improvement of time to 1-mm ST-segment depression was statistically significantly greater than that of metoprolol. This could be due to its additional vasodilatory or antioxidative actions. Based on the safety and efficacy data of the present study, use of the higher of the 2 recommended doses of carvedilol and metoprolol appears justified in younger and elderly patients without adequate therapeutic control at lower doses.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Antioxidants_MeSH S_administration_&_dosage_MeSH Antioxidants_administration_&_dosage_MeSH S_adverse_effects_MeSH Antioxidants_adverse_effects_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH M_Placebos_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10081339
----K 1
----T [Heart failure and treatment of ventricular arrhythmias]
----A Chronic heart failure (CHF) is generally associated with a poor prognosis with an annual mortality rate ranging between 15-50% depending on the severity of cardiac dysfunction thus presenting a major health problem in our society. Drugs for the treatment of CHF include vasodilators (ACE-inhibitors, angiotensin II receptor blockers), diuretics, digoxin and beta-blockers. However, antiarrhythmic drugs are not currently recommended in the management of CHF with the exception of beta-blockers for which a favorable effect on the prognosis could be shown. Amiodarone is effective in the suppression of ventricular arrhythmias without a significant effect on total mortality. Implanted defibrillators are superior to antiarrhythmic drug therapy in prolonging survival among survivors of sudden cardiac death. They should be offered as firstline therapy in case of life-threatening ventricular tachy-arrhythmias.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Survival_Rate_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH 
****** 10081516
----K E
----T A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction--the MEMO study.
----A OBJECTIVES: To compare the analgesic effect of metoprolol and morphine in patients with chest pain due to suspected or definite acute myocardial infarction after initial treatment with intravenous metoprolol. DESIGN: All patients, regardless of age, admitted to the coronary care unit at Uddevalla Central Hospital due to suspected acute myocardial infarction were evaluated for inclusion in the MEMO study (metoprolol-morphine). The effects on chest pain and side-effects of the two treatments were followed during 24 h. Pain was assessed by a numerical rating scale. RESULTS: A total of 265 patients were randomized in this prospective double-blind study and 59% developed a confirmed acute myocardial infarction. In both treatment groups, there were rapid reductions of pain intensity. However, in the patient group treated with morphine, there was a more pronounced pain relief during the first 80 min after start of double-blind treatment. The side-effects were few and were those expected from each therapeutic regimen. During the first 24 h, nausea requiring anti-emetics was more common in the morphine-treated patients. CONCLUSION: In suspected acute myocardial infarction, if chest pain persists after intravenous beta-adrenergic blockade treatment, standard doses of an opioid analgesic such as morphine will offer better pain relief than increased dosages of metoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Analgesics__Opioid_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH M_Comparative_Study_MeSH M_Diagnosis__Differential_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Morphine_MeSH S_therapeutic_use_MeSH Morphine_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Pain_Measurement_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10081517
----K E
----T Factors associated with the use of various medications amongst patients with severe coronary artery disease. SECOR/SBU Project Group.
----A AIM: To describe variations by age, sex, symptom severity and hospital region in the use of various medications amongst patients with stable angina pectoris who are candidates for coronary revascularization. PATIENTS: Patients (n = 2030) with chronic stable angina pectoris participating in a national survey evaluating the appropriateness of the use of percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG). METHODS: As part of a national study of the appropriateness of coronary revascularization, data were prospectively collected on patients referred for consideration of coronary revascularization to seven of the eight public Swedish heart centres that performed approximately 92% of all bypass operations in Sweden in 1994. RESULTS: Amongst all patients 76% were treated with beta blockers, 41% with calcium antagonists and 71% with long-acting nitrates and 70% were treated with at least two of these three drugs. Eighty-two per cent of the patients used aspirin and 14% lipid-lowering drugs. According to logistic regression analysis, with medication as the dependent variable and independent variables of age, sex, angina functional class, findings at exercise test, history of various diseases and region in Sweden where the investigation took place, the most consistent factor explaining the use of various medications was found to be geographical region. A previous history of acute myocardial infarction (AMI) was also associated with the use of all drugs and age was associated with all with the exception of beta blockers. Sex was not an independent factor explaining the use of any of the drugs. CONCLUSION: In a national survey including patients with stable angina pectoris who are potential candidates for coronary revascularization, the most important predictor for the use of various medications was the geographical region in which the investigation took place.
----P Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH S_surgery_MeSH Angina_Pectoris_surgery_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Coronary_Artery_Bypass_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_surgery_MeSH Coronary_Disease_surgery_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Severity_of_Illness_Index_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH 
****** 10099140
----K I
----T Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding.
----A BACKGROUND AND METHODS: We compared propranolol therapy and endoscopic ligation for the primary prevention of bleeding from esophageal varices. This prospective, controlled trial included consecutive eligible patients who had large varices (>5 mm in diameter) that were at high risk for bleeding. The patients were assigned to either propranolol therapy, at a dose sufficient to decrease the base-line heart rate by 25 percent, or variceal ligation, to be performed weekly until the varices were obliterated or so reduced in size that it was not possible to continue treatment. RESULTS: Of the 89 patients, 82 of whom had cirrhosis of the liver, 44 received propranolol and 45 underwent variceal ligation. The mean (+/-SD) duration of follow-up in each group was 14+/-9 and 13+/-10 months, respectively. The mean time required to achieve an adequate reduction in the heart rate was 2.5+/-1.7 days; the mean number of sessions needed to complete variceal ligation was 3.2+/-1.1. After 18 months, the actuarial probability of bleeding was 43 percent in the propranolol group and 15 percent in the ligation group (P=0.04). Twelve patients in the propranolol group and four in the ligation group had bleeding. Three of the four in the ligation group had bleeding before their varices had been obliterated. Nine patients in the ligation group had recurrent varices, a mean of 3.7 months after the initial treatment. Five patients in each group died; bleeding from the varices was the cause of death of four patients in the propranolol group and of three in the ligation group. There were no serious complications of variceal ligation; in the propranolol group, treatment was stopped in two patients because of side effects. CONCLUSIONS: In patients with high-risk esophageal varices, endoscopic ligation of the varices is safe and more effective than propranolol for the primary prevention of variceal bleeding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Comparative_Study_MeSH P_Endoscopy_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_surgery_MeSH Esophageal_and_Gastric_Varices_surgery_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_etiology_MeSH Gastrointestinal_Hemorrhage_etiology_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Ligation_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Postoperative_Complications_MeSH M_Probability_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Treatment_Outcome_MeSH 
****** 10082500
----K E
----T ACE inhibitor versus beta-blocker for the treatment of hypertension in renal allograft recipients.
----A Angiotensin-converting enzyme (ACE) inhibitors have been shown to slow the progression of chronic renal failure. However, the value of ACE inhibitors for the treatment of hypertension in renal allograft recipients has not been established. ACE inhibitors dilate the efferent glomerular arteriole, an effect that may aggravate the decrease in glomerular filtration rate resulting from cyclosporine-induced vasoconstriction at the afferent glomerular arteriole. Therefore, the goal of this double-blind, randomized study was to compare the antihypertensive and renal effects of the ACE inhibitor quinapril with those of the beta-blocker atenolol in renal allograft recipients in whom hypertension developed 6 to 12 weeks after transplantation. All patients received cyclosporine as an immunosuppressant and had stable graft function (serum creatinine concentration, <220 micromol/L) at entry into the study. Twenty-nine patients who received quinapril (daily dose titrated between 2.5 and 20 mg) and 30 patients who received atenolol (daily dose titrated between 12.5 and 100 mg) completed the 24-month study. The two groups did not differ in age, sex ratio, height, and weight before entry into the study. Quinapril decreased diastolic blood pressure from 96+/-1 to 84+/-1 mm Hg (average throughout treatment period), and atenolol decreased diastolic blood pressure from 96+/-1 to 83+/-1 mm Hg. The serum creatinine concentration did not change significantly in either group after 24 months (129+/-8 micromol/L at entry and 148+/-19 micromol/L after 24 months in the quinapril group and 131+/-6 micromol/L at entry and 152+/-15 micromol/L after 24 months in the atenolol group; P=NS for both groups). After 24 months, the change in urinary albumin excretion from baseline was -10+/-15 mg/d in the quinapril group and 52+/-32 mg/d in the atenolol group (P=0.03). These results show that quinapril and atenolol are effective antihypertensive drugs when used after renal transplantation. Moreover, compared with atenolol, quinapril has no adverse effects on graft function. The relative reduction in albuminuria observed with quinapril as compared with atenolol could indicate a beneficial effect of quinapril on long-term graft function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Cyclosporine_MeSH S_therapeutic_use_MeSH Cyclosporine_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Immunosuppressive_Agents_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH M_Isoquinolines_MeSH S_therapeutic_use_MeSH Isoquinolines_therapeutic_use_MeSH M_Kidney_Transplantation_MeSH S_adverse_effects_MeSH Kidney_Transplantation_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Proteinuria_MeSH S_urine_MeSH Proteinuria_urine_MeSH M_Support__Non-U_S__Gov't_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 10088066
----K E
----T Effects of early treatment with captopril and metoprolol singly or together on six-month mortality and morbidity after acute myocardial infarction. Results of the RIMA (Rimodellamento Infarto Miocardico Acuto) study. The RIMA researchers.
----A The RIMA (Rimodellamento Infarto Miocardico Acuto) study was designed to assess the relative effects of angiotensin-converting enzyme (ACE) inhibition by captopril, beta-blocker therapy by metoprolol, and their combination in patients with a first acute myocardial infarction on: 1. echocardiographically detected left ventricular remodeling; 2. prognosis. The second goal will be the argument of the present paper. Two-hundred fifty < or = 75 years consecutive patients (mean age: 58 yrs, males = 203) with acute myocardial infarction were randomly allocated to receive for > or = 3 months captopril (up to 75 mg/day, Group 1), metoprolol (up to 200 mg/day, Group 2) or captopril + metoprolol (Group 3) starting in the first 24 hours after the onset of symptoms. Intravenous beta-blockers in the acute phase of myocardial infarction and all other cardioactive drugs were allowed. The effect of the randomized therapy at six months from admission to the coronary care unit was considered in relation to: 1. recurrence of spontaneous cardiac events and of elective revascularization procedures; 2. adverse reactions (hypotension, atrioventricular block, cough, allergy, need of beta-blockers in Group 1, need for ACE inhibition in Group 2) requiring treatment modification based on physician's decision. RESULTS: Definite follow-up data were available in 226 patients and 195/226 patients (86%) had a complete treatment period. In these patients (per protocol analysis), 37 spontaneous cardiac events occurred: cardiac death = 6, non-fatal reinfarction = 9, unstable angina requiring hospitalization = 16, congestive heart failure = 6. Moreover, seven patients received a coronary revascularization procedure. Events occurred in 11/67 patients from Group 1, 16/63 patients from Group 2, 10/65 patients from Group 3 (16% vs 25% vs 15%, p = 0.28). The multiple logistic regression analysis demonstrated an increased odds ratio (OR) for spontaneous cardiac events in patients from Group 2 (OR = 2.82, 95% Cl: 1.16-6.87: p < 0.05). Elective revascularization procedures were statistically less frequent in patients treated with metoprolol (Group 1 = 9%, Group 2 = 1.6%, Group 3 = 0%; Group 1 vs Groups 2 and 3; p = 0.03). The intention-to-treat analysis on the overall population (226 patients) confirmed the presence of a trend towards a higher risk in patients from Group 2 (OR = 2.1, 95% Cl: 0.96-4.59; p = 0.06). Adverse reactions were observed in 16 patients from Group 1, 6 patients from Group 2 and 15 patients from Group 3 (22% vs 10% vs 23%; Group 2 vs Groups 1 and 3; p = 0.08). At the multivariate regression analysis, a trend towards less adverse reactions in patients assigned to the beta-blocker therapy alone was confirmed (OR = 0.41, 95% Cl: 0.15-1.13; p = 0.07). CONCLUSIONS: In a randomized early post-infarction treatment strategy, ACE inhibition with captopril alone or in combination with metoprolol demonstrated an increased protection against spontaneous cardiac events at six months in comparison with metoprolol alone. On the other hand, the beta-blocker treatment was associated with a lower number of elective revascularization procedures and appeared better tolerated than ACE inhibition.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Disease-Free_Survival_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10090111
----K I
----T Diuretics and beta-blockers do not have adverse effects at 1 year on plasma lipid and lipoprotein profiles in men with hypertension. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.
----A BACKGROUND: Concern based on the reported short-term adverse effects of antihypertensive agents on plasma lipid and lipoprotein profiles (PLPPs) has complicated the therapy for hypertension. OBJECTIVE: To compare the long-term (1-year) effects of 6 different antihypertensive drugs and placebo on PLPPs in a multicenter, randomized, double-blind, parallel-group clinical trial in 15 US Veterans Affairs medical centers. PATIENTS AND METHODS: A total of 1292 ambulatory men, 21 years or older, with diastolic blood pressures (DBPs) ranging from 95 to 109 mm Hg taking placebo were randomized to receive placebo or 1 of 6 antihypertensive drugs: hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem, or prazosin. After drug titration, patients with a DBP of less than 90 mm Hg were followed up for 1 year. Plasma lipids and lipoprotein profiles were determined at baseline, after initial titration, and at 1 year. RESULTS: After 8 weeks on a regimen of hydrochlorothiazide, increases of 3.3 mg/dL (0.09 mmol/L) in total cholesterol and 2.7 mg/dL in apolipoprotein B were significantly different (P< or =.05) from decreases of 9.3 mg/dL in total cholesterol and 5.4 mg/dL in ApoB levels while receiving prazosin but not from placebo. Patients achieving positive DBP control using hydrochlorothiazide (responders) showed no adverse changes in PLPPs, whereas nonresponders exhibited increases in triglycerides, total cholesterol, and low-density lipoprotein cholesterol levels. Plasma lipids and lipoprotein profiles did not change significantly among treatment groups after 1 year except for minor decreases in high-density lipoprotein 2 levels using hydrochlorothiazide, clonidine, and atenolol. CONCLUSIONS: None of these 6 antihypertensive drugs has any long-term adverse effects on PLPPs and, therefore, may be safely prescribed. Previously reported short-term adverse effects from using hydrochlorothiazide are limited to nonresponders.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH M_Clonidine_MeSH S_adverse_effects_MeSH Clonidine_adverse_effects_MeSH M_Comparative_Study_MeSH M_Diltiazem_MeSH S_adverse_effects_MeSH Diltiazem_adverse_effects_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH M_Double-Blind_Method_MeSH M_Hospitals__Veterans_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins_MeSH S_blood_MeSH Lipoproteins_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Prazosin_MeSH S_adverse_effects_MeSH Prazosin_adverse_effects_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH 
****** 10091817
----K E
----T Tolerability and efficacy of carvedilol in patients with New York Heart Association class IV heart failure.
----A OBJECTIVES: The purpose of this study was to assess the tolerability and efficacy of carvedilol in patients with New York Heart Association (NYHA) functional class IV symptoms. BACKGROUND: Carvedilol, a nonselective beta-adrenergic blocking drug with alpha-adrenergic blocking and antioxidant properties, has been shown to improve left ventricular function and clinical outcome in patients with mild to moderate chronic heart failure. METHODS: We retrospectively analyzed the outcomes of 230 patients with heart failure treated with carvedilol who were stratified according to baseline functional class: 63 patients were NYHA class IV and 167 were NYHA class I, II or III. Carvedilol was commenced at 3.125 mg b.i.d. and titrated to 25 mg b.i.d. as tolerated. Patients with class IV symptoms were older (p = 0.03), had lower left ventricular fractional shortening (p < 0.001), had lower six-min walk distance (p < 0.001) and were receiving more heart failure medications at baseline compared with less symptomatic patients. RESULTS: Nonfatal adverse events while taking carvedilol occurred more frequently in class IV patients (43% vs. 24%, p < 0.0001), and more often resulted in permanent withdrawal of the drug (25% vs. 13%, p < 0.01). Thirty-seven (59%) patients who were NYHA class IV at baseline had improved by one or more functional class at 3 months, 8 (13%) were unchanged and 18 (29%) had deteriorated or died. Among the less symptomatic group, 62 (37%) patients had improved their NYHA status at 3 months, 73 (44%) were unchanged and 32 (19%) had deteriorated or died. The differences in symptomatic outcome at three months between the two groups were statistically significant (p = 0.001, chi-square analysis). Both groups demonstrated similar significant improvements in left ventricular dimensions and systolic function. CONCLUSIONS: Patients with chronic NYHA class IV heart failure are more likely to develop adverse events during initiation and dose titration when compared with less symptomatic patients but are more likely to show symptomatic improvement in the long term. We conclude that carvedilol is a useful adjunctive therapy for patients with NYHA class IV heart failure; however, they require close observation during initiation and titration of the drug.
----P Journal_Article 
----M M_Actuarial_Analysis_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Adverse_Drug_Reaction_Reporting_Systems_MeSH M_Aged_MeSH M_Australia_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10095796
----K E
----T Comparison of effects of quinapril and metoprolol on glycaemic control, serum lipids, blood pressure, albuminuria and quality of life in non-insulin-dependent diabetes mellitus patients with hypertension. Swedish Quinapril Group.
----A OBJECTIVE: To compare the long-term effects of the angiotensin-converting enzyme (ACE)-inhibitor quinapril and the cardioselective beta-adrenergic blocking agent metoprolol on glycaemic control, with glycosylated haemoglobin (HbA1c) as the principal variable, in non-insulin-dependent diabetes mellitus (NIDDM) patients with hypertension. DESIGN: A randomized, double-blind, double-dummy, multicentre study during 6 months preceded by a 4 week wash-out and a 3 week run-in placebo period. Quinapril (20 mg) and metoprolol (100 mg, conventional tablets) were given once daily. No change was made in the treatment of diabetes (diet and hypoglycaemic agents). SUBJECTS: Seventy-two patients fulfilling the criteria were randomized and entered the double-blind period. Twelve patients did not complete the study. Sixty patients, 26 on quinapril and 34 on metoprolol, were available for the final analysis. MAIN OUTCOME MEASURES: The effect was assessed by changes in HbA1c, the fasting serum glucose and the post-load serum glucose, C-peptide and insulin levels during the oral glucose tolerance test. RESULTS: In the quinapril group, the fasting serum glucose, oral glucose tolerance and the C-peptide and insulin responses, determined as the incremental area under the curves (AUC), showed no change, but the mean HbA1c level increased from 6.2 +/- 1.1% to 6.5 +/- 1.3% (P < 0.05). In the metoprolol group, the rise in the mean level of HbA1c, from 6.3 +/- 1.0% to 6.8 +/- 1.3% (P < 0.01), tended to be more marked than after quinapril, although there was no significant difference between the increments. The mean fasting serum glucose showed an increase from 9.1 +/- 1.9 mM to 10.1 +/- 2.8 mM (P < 0.01) which correlated significantly with the duration of diabetes (P < 0.01) and the increase in fasting serum triglycerides (P < 0.001). Moreover, in the metoprolol group we found significant decreases in the oral glucose tolerance as well as C-peptide and insulin responses to the glucose load. CONCLUSIONS: Treatment with quinapril for 6 months appears to have advantages over metoprolol in NIDDM patients with hypertension. Although treatment with quinapril or metoprolol over 6 months was concomitant with a rise in the HbA1c, increased fasting blood glucose, decreased oral glucose tolerance and decreased C-peptide and insulin responses to a glucose challenge were observed only in patients treated with metoprolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Aged_MeSH M_Albuminuria_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_C-Peptide_MeSH S_blood_MeSH C-Peptide_blood_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Hemoglobin_A_MeSH S_drug_effects_MeSH Hemoglobin_A_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH M_Isoquinolines_MeSH S_pharmacology_MeSH Isoquinolines_pharmacology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH P_Tetrahydroisoquinolines_MeSH 
****** 10097224
----K E
----T Carvedilol prevents remodeling in patients with left ventricular dysfunction after acute myocardial infarction.
----A OBJECTIVE: The aim of the study was to assess the effects of carvedilol, a vasodilating nonselective beta-blocker, on the indexes of left ventricular remodeling after acute myocardial infarction in those with left ventricular dysfunction. METHODS AND RESULTS: Forty-nine patients with predischarge left ventricular ejection fraction <45% after acute myocardial infarction were evaluated in a double-blind, randomized, placebo-controlled, parallel group study (selected from the database of the Carvedilol Heart Attack Pilot Study: CHAPS). Patients received medication after thrombolysis and continued to do so for 6 months. Two-dimensional echocardiography was performed before discharge (7 to 10 days after admission) and at 3 months after acute myocardial infarction. Analysis of variance showed that wall thickness opposite the site of infarction decreased from (mean +/- SD) 12.3 +/- 2.1 mm to 11.0 +/- 2.4 mm with carvedilol compared with 11.6 +/- 1.9 mm to 12.2 +/- 1.9 mm with placebo (P =.01). Left ventricular mass changed from 235 +/- 74 g to 217 +/- 64 g with carvedilol compared with 227 +/- 80 g to 252 +/- 85 g with placebo ( P =.02). Carvedilol prevented alteration of sphericity index (ratio of long and short axis of left ventricle) that changed from 1.65 +/- 0.29 to 1.66 +/- 20 with carvedilol compared with 1.58 +/- 0.33 to 1.39 +/- 0.19 with placebo (P =.02); alteration was also prevented of wall thickening abnormality at infarct site, which changed from 9.2 +/- 3.1 cm2 to 9.1 +/- 3.5 cm 2 with carvedilol compared with 10.3 +/- 3.3 cm2 to 13.5 +/- 4.6 cm2 with placebo (P =.002). CONCLUSION: Carvedilol administered early after acute myocardial infarction results in attenuation of left ventricular remodeling in patients with persistent left ventricular dysfunction before discharge.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_ultrasonography_MeSH Ventricular_Dysfunction__Left_ultrasonography_MeSH P_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 10097226
----K E
----T Long-term beta-blocker therapy improves autonomic nervous regulation in advanced congestive heart failure: a longitudinal heart rate variability study.
----A BACKGROUND: beta-Blocker therapy is believed to modulate the detrimental effect of overcompensating neurohormonal activation in chronic heart failure. However, clinical doubts remain, particularly the physiologic sympathovagal balance. METHODS: To respond to clinical concern about worsening autonomic nervous perturbation in beta-blocker therapy of advanced congestive heart failure, 15 consecutive patients were longitudinally studied to elucidate the evolution of cardiac function versus 24-hour heart rate variability (HRV) before and after 1, 3, and 6 to 9 months of atenolol-combined therapy. RESULTS: Two patients died prematurely within 1 month. All 13 surviving patients showed improvement in New York Heart Association functional class, with decrease in left ventricular end-systolic and end-diastolic dimensions and increase in fraction shortening and ejection fraction by echocardiography after at least 3 months of atenolol use. The retarded therapeutic effect was accompanied by a general rise of total, very low, low-, and high-frequency components (9.0 +/- 0.5, 8.8 +/- 0.5, 6.2 +/- 0.6, and 6.1 +/- 0.5 vs 10.9 +/- 0.3, 10.7 +/- 0.4, 8.6 +/- 0.3, and 7.8 +/- 0.3; all P <.02) of daily HRV. This implied recovery of parasympathetic and baroreceptor function. Return of sympathovagal interaction was further supported by the suppression of Cheyne-Stokes type HRV as detected by Wigner-Ville distribution. CONCLUSIONS: Long-term beta-blocker therapy for advanced congestive heart failure upwardly regulates the autonomic nervous interaction in synchrony with the evolution of cardiac function performance.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Function_Tests_MeSH S_drug_effects_MeSH Heart_Function_Tests_drug_effects_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 10100068
----K E
----T Association of arginine vasopressin and arterial blood pressure in a population-based sample.
----A BACKGROUND: The role of arginine vasopressin (AVP) in the development and maintenance of arterial hypertension is controversial. Furthermore, it remains unclear whether chronic treatment with antihypertensive agents modulates levels of AVP, with potential secondary effects on vascular tone and fluid homeostasis. OBJECTIVE: To investigate the relation between plasma AVP and arterial blood pressure in a population-based sample of 534 middle-aged subjects. RESULTS: Overall, levels of AVP were higher in hypertensive subjects (2.15 +/- 0.26 pg/ml; n = 289) than in normotensive subjects (1.45 +/- 0.15 pg/ml; n = 245; P < 0.05). (Hypertension was defined as systolic blood pressure > 160 mmHg and/or diastolic blood pressure > 95 mmHg, or receiving antihypertensive medication.) In untreated individuals, plasma levels of AVP were found to be correlated with both systolic (r = 0.15, P = 0.002) and diastolic (r = 0.14, P = 0.005) blood pressure. The differences between the lowest and highest quartile of AVP levels were 5.1 mmHg (P = 0.03) and 2.6 mmHg (NS) for systolic and diastolic blood pressure, respectively, after adjustment for age and sex. Moreover, it appeared that the relation between AVP and blood pressure was particularly strong in subjects with low levels of renin (< 10 mU/l; n = 118; systolic blood pressure r = 0.24, P = 0.007; diastolic blood pressure r = 0.19, P = 0.03). Specifically, patients receiving monotherapy with diuretics (n = 39) or beta-blockers (n = 54) displayed elevated plasma levels of AVP (2.93 +/- 0.98 pg/ml and 2.74 +/- 0.74 pg/ml respectively); however, only in patients taking diuretics was this finding apparently independent of confounding variables. Other monotherapies with angiotensin-converting enzyme inhibitors (n = 9) or Ca(2+)-antagonists (n = 19) were not associated with levels of AVP. CONCLUSION: The data suggest that plasma levels of AVP display a discernible relationship with arterial blood pressure and hypertension, particularly when renin levels are low. In addition, with the exception of diuretics, no modulation of AVP levels is attributable to the intake of antihypertensive agents as it occurs in a population-based sample.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Argipressin_MeSH S_blood_MeSH Argipressin_blood_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH P_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Radioimmunoassay_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10189005
----K E
----T Potential risk of beta-blockade withdrawal in congestive heart failure due to abrupt autonomic changes.
----A Beta-Blockers reduce mortality in patients with congestive heart failure and a proposed mechanism has been changes of autonomic tone. Heart rate variability is a non-invasive tool to estimate cardiac autonomic tone. The aim was to study changes of heart rate variability in patients with congestive heart failure on placebo, on the beta1-selective antagonist metoprolol or 24 h after metoprolol withdrawal. Forty-five patients with congestive heart failure were studied with Holter recordings. Heart rate variability measurements were performed before, after 6-12 months of treatment with 150 mg metoprolol/placebo, or 24 h after discontinued metoprolol. After treatment, patients on beta-blockade had a significantly longer mean RR interval and changes of heart rate variability, suggesting elevated vagal tone. Patients monitored in the rebound phase of beta-blocker withdrawal had a significant vagal reduction to the level of the placebo group. There was also a nonsignificant trend towards increased sympathetic tone (LF/HF over 24 h), compared with the beta-blockade group. Heart rate variability indicates an elevated vagal tone during treatment with metoprolol but beta-blockade withdrawal shifts the autonomic balance towards lower vagal and higher sympathetic tone within 24 h. These results could imply a potential risk when abruptly discontinuing beta-blockade medication in these patients.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Comparative_Study_MeSH M_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_chemically_induced_MeSH Myocardial_Ischemia_chemically_induced_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Substance_Withdrawal_Syndrome_MeSH S_physiopathology_MeSH Substance_Withdrawal_Syndrome_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vagus_Nerve_MeSH S_drug_effects_MeSH Vagus_Nerve_drug_effects_MeSH S_physiopathology_MeSH Vagus_Nerve_physiopathology_MeSH M_Ventricular_Fibrillation_MeSH S_chemically_induced_MeSH Ventricular_Fibrillation_chemically_induced_MeSH S_physiopathology_MeSH Ventricular_Fibrillation_physiopathology_MeSH 
****** 10190404
----K E
----T Effects of combination antihypertensive therapy on baroreflex sensitivity and heart rate variability in systemic hypertension.
----A Earlier studies have shown that cardiovascular autonomic regulation is impaired in untreated or poorly controlled systemic hypertension. The purpose of this double-blind, randomized parallel trial was to evaluate whether improved blood pressure (BP) control can reverse this impairment. The study group consisted of 33 patients (age 45 to 63 years) with poor BP control who received randomized metoprolol or enalapril monotherapy. Baroreflex sensitivity (BRS) was assessed by phenylephrine test and time- and frequency-domain measurements of heart rate variability (HRV) were analyzed from 24-hour ambulatory electrocardiographic recordings during monotherapy and after 10 weeks of combination therapy with metoprolol + felodipine or enalaril + hydrochlorothiazide to lower casual BP to < 140/90 mm Hg. Intensified treatment decreased 24-hour systolic and diastolic BP from 139 +/- 12/86 +/- 8 mm Hg to 126 +/- 8/80 +/- 7 mm Hg (p <0.0001). BRS improved from 6.2 +/- 3.2 ms/mm Hg to 8.9 +/- 4.1 ms/mm Hg (p <0.0001) and measurements of HRV (e.g., SD of all RR intervals from 128 +/- 45 ms to 145 +/- 46 ms, p <0.001) improved significantly during the combination therapy. Changes in BRS and HRV were similar in magnitude in both treatment arms. Mean RR intervals were comparable before and after intensive antihypertensive therapy (850 +/- 124 ms vs 937 +/- 279 ms, p = NS). These data indicate that adequate BP control with modem antihypertensive combination therapy can improve cardiovascular autonomic function, which may partially explain the reduced cardiac mortality observed in patients with intensified antihypertensive therapy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler__Color_MeSH M_Electrocardiography__Ambulatory_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Phenylephrine_MeSH S_diagnostic_use_MeSH Phenylephrine_diagnostic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10190405
----K E
----T Cost effectiveness of carvedilol for heart failure.
----A In this study, we examine the cost effectiveness of carvedilol for the treatment of chronic heart failure (CHF). We use a Markov model to project life expectancy and lifetime medical care costs for a hypothetical cohort of patients with CHF who were assumed alternatively to receive carvedilol plus conventional therapy (digoxin, diuretics, and angiotensin-converting enzyme inhibitors) or conventional therapy alone. Patients on carvedilol were assumed to experience a reduced risk of death and hospitalization for CHF, which is consistent with findings from the US Carvedilol Heart Failure Trials Program. The benefits of carvedilol were projected under 2 alternative scenarios. In the first ("limited benefits"), benefits were conservatively assumed to persist for 6 months, the average duration of follow-up in these clinical trials, and then end abruptly. In the other ("extended benefits"), they were arbitrarily assumed to persist for 6 months and then decline gradually over time, vanishing by the end of 3 years. We estimated our model using data from the US Carvedilol Heart Failure Trials Program and other sources. For patients receiving conventional therapy alone, estimated life expectancy was 6.67 years; corresponding figures for those also receiving carvedilol were 6.98 and 7.62 years under the limited and extended benefits scenarios, respectively. Expected lifetime costs of CHF-related care were estimated to be $28,756 for conventional therapy, and $36,420 and $38,867 for carvedilol (limited and extended benefits, respectively). Cost per life-year saved for carvedilol was $29,477 and $12,799 under limited and extended benefits assumptions, respectively. The cost effectiveness of carvedilol for CHF compares favorably to that of other generally accepted medical interventions, even under conservative assumptions regarding the duration of therapeutic benefit.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH M_Carbazoles_MeSH S_economics_MeSH Carbazoles_economics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_economics_MeSH Cardiotonic_Agents_economics_MeSH M_Cost-Benefit_Analysis_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH S_economics_MeSH Digoxin_economics_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH S_economics_MeSH Diuretics_economics_MeSH M_Drug_Therapy__Combination_MeSH M_Health_Care_Costs_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_economics_MeSH Heart_Failure__Congestive_economics_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Life_Expectancy_MeSH M_Markov_Chains_MeSH M_Propanolamines_MeSH S_economics_MeSH Propanolamines_economics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Vasodilator_Agents_MeSH S_economics_MeSH Vasodilator_Agents_economics_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10193670
----K E
----T Effects on plasma angiotensin-converting enzyme activity and circulating renin of lisinopril and enalapril alone and in combination with propranolol in healthy volunteers.
----A The effects on plasma angiotensin-converting enzyme activity and renin activity of the two long-acting angiotensin-converting enzyme inhibitors, lisinopril and enalapril, alone and in combination with propranolol were studied. In an open, randomised, cross-over design 12 healthy volunteers received orally enalapril 20 mg alone, enalapril 20 mg in combination with propranolol 80 mg, lisinopril 20 mg alone, and lisinopril 20 mg in combination with propranolol 80 mg. Plasma angiotensin-converting enzyme activity and plasma renin activity were measured for 24 h after each treatment period. Lisinopril and enalapril reduced plasma angiotensin converting enzyme activity substantially and equally at six hr (-70%, P<0.05) and 12 hr (-65%, P<0.05), irrespective of combination with propranolol. At 24 hr plasma angiotensin-converting enzyme activity remained significantly suppressed only after lisinopril (-60%, P<0.05). Plasma renin activity increased almost ten times after ingestion of both angiotensin-converting enzyme inhibitors, but the effect lasted significantly longer after lisinopril than after enalapril. Beta-Adrenergic blockade blunted the effect on the increase in plasma renin activity induced by both angiotensin-converting enzyme inhibitors. Our results show that the effect of lisinopril on plasma angiotensin-converting enzyme activity and plasma renin activity lasted longer than that of enalapril. beta-Adrenergic blockade suppressed the effect on elevated plasma renin activity, but did not influence the effect of angiotensin-converting enzyme inhibitors on plasma angiotensin-converting enzyme activity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Interactions_MeSH M_Enalapril_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Lisinopril_MeSH S_pharmacology_MeSH Lisinopril_pharmacology_MeSH M_Male_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Time_Factors_MeSH 
****** 10192973
----K E
----T Nebivolol versus enalapril in essential hypertension: a long-term double-blind comparative trial.
----A Nebivolol was compared in a dose of 5 mg once daily with enalapril 10 mg once daily over 7 months in a double-blind randomised trial in essential hypertension. The two drugs had very similar sustained effects in lowering both systolic and diastolic pressures; neither had an orthostatic component. Both drugs were well-tolerated. No haematological, biochemical, or urinary abnormalities were seen.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzopyrans_MeSH S_administration_&_dosage_MeSH Benzopyrans_administration_&_dosage_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Ethanolamines_MeSH S_administration_&_dosage_MeSH Ethanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypotension__Orthostatic_MeSH S_prevention_&_control_MeSH Hypotension__Orthostatic_prevention_&_control_MeSH M_Longitudinal_Studies_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Satisfaction_MeSH M_Placebos_MeSH 
****** 10193451
----K I
----T Carvedilol for heart failure: more than just a beta-blocker?
----A Carvedilol is a non-selective beta-blocker, and the only one, in recent clinical trials, to have shown a clear reduction in mortality. It is suggested that, compared with other beta-blockers, carvedilol has additional advantageous effects in heart failure, and should be considered as part of the routine treatment of heart failure.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Morbidity_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH 
****** 10197196
----K E
----T Recent advances in the drug treatment of heart failure.
----A A number of important questions surrounding the treatment of systolic congestive heart failure have been answered by randomised clinical trials completed within the past 2 years. In particular, these studies have established that high-dose angiotensin-converting enzyme (ACE) inhibition is more beneficial than low dose therapy, and that angiotensin II receptor antagonists are an acceptable alternative in patients unable to tolerate ACE inhibitors. Digoxin has been shown to be the only inotropic agent not associated with increased mortality, while amiodarone exerts a modest survival benefit in arrhythmiaprone patients. Beta-blockers appear to be beneficial for selected patients although their precise role remains to be defined by ongoing studies.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10204815
----K E
----T Baroreflex sensitivity and the blood pressure response to beta-blockade.
----A The objective of this analysis was to determine whether changes in baroreflex sensitivity (BRS) within 35 hypertensive patients (25 M, 10 F, mean age 47 years) treated with beta-blockade as monotherapy relate to reductions in ambulatory blood pressure (BP) or its variability. BP was recorded intra-arterially directly from the brachial artery before and during submaximal exercise. BRS was determined by the phenylephrine injection technique. MAP and its variability were determined for the awake period of 24-h BP monitoring. Subjects were randomised to one of atenolol, metoprolol, pindolol, or propranolol, and restudied after a mean of 5 months. Beta-blockade increased BRS in 24 patients and decreased BRS in 11. BRS increased from 6.53+/-4.94 to 9.40+/-8.62 ms/mm Hg (mean +/- s.d.) (P<0.01). Waking ambulatory MAP decreased from 125.8+/-15.8 to 106.4+/-16.2 mm Hg (P<0.0001), but its variability did not change. Higher BRS after chronic beta-blockade was associated with a decrease in waking ambulatory MAP (r = -0.55, P<0.001), but not with its variability (r = -0.08). Beta-blockade attenuated the pressor response to exercise, but there was a positive relationship between the effect of beta-blockade on BRS, and on the rise in systolic BP during bicycling (r = 0.63; P<0.001). Any dampening effect of beta-blockade on BP variability at rest in hypertensive patients with the greatest increase in BRS may be offset by increased pressor responses to physical activity such as exercise. Consequently, BP variability is unaffected, even though reductions in ambulatory BP during chronic beta-blockade are inversely related to changes in BRS. BP responses to beta-blockade may be a function of the action of this class of drugs on BRS. However, there is considerable variation, between subjects, in their effect on BRS. This may have implications for other conditions, such as dilated cardiomyopathy, or following myocardial infarction, in which improvement in BRS is one mechanism by which beta-adrenoceptor blockade could improve survival.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_alpha-Agonists_MeSH S_diagnostic_use_MeSH Adrenergic_alpha-Agonists_diagnostic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Baroreflex_MeSH S_drug_effects_MeSH Baroreflex_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH 
****** 10206383
----K E
----T Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease.
----A AIM: To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias. METHODS: Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia. RESULTS: At 36 months. 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0.05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5.9 times higher (P=0.008) than that for patients on sotalol. CONCLUSION: Sotalol is superior to amiodarone for long-term treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Cross-Over_Studies_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Retrospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia__Ventricular_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_physiopathology_MeSH Tachycardia__Ventricular_physiopathology_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10208787
----K E
----T Differences in drug treatment of chronic heart failure between European countries.
----A AIMS: A large number of drugs are currently used for the treatment of chronic heart failure. Treatment for other cardiovascular disorders has been shown to differ between countries. In this study we examined whether this would also be true in heart failure. METHODS AND RESULTS: We studied patients with moderate to severe heart failure, who were enrolled in an international survival study, and compared patterns of drug use between the nine countries that each included >50 patients in the study. The results were analysed to determine whether observed differences between countries could be explained by differences in the patients recruited. 1825 patients were studied (range 81-427 per country). By trial protocol, most patients were treated with angiotensin converting enzyme (ACE) inhibitors (92%) and all with diuretics, but the proportion of patients taking high doses of these drugs was markedly different between countries. Large differences were also observed in the use of digoxin (overall 64%, 39% in the U.K. to 87% in Germany) and antiarrhythmics (overall 25%, with the highest use 44% in France). The use of beta-blockers and calcium antagonists was low (overall 6% and 8%, respectively), but also different between countries. Anticoagulants (overall 43%) were used in many patients in the Netherlands and Switzerland (around 70%), while antiplatelets (overall use 30%) were most often prescribed in Denmark (51%). CONCLUSIONS: Large differences in drug use and dosing for patients with advanced heart failure are observed between (European) countries. None of these differences could be explained by differences in patient characteristics, and whether they are related to factors such as tradition, economic circumstances and national guidelines, etc. is unknown.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH M_Anticoagulants_MeSH S_administration_&_dosage_MeSH Anticoagulants_administration_&_dosage_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Europe_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Physician's_Practice_Patterns_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_administration_&_dosage_MeSH Platelet_Aggregation_Inhibitors_administration_&_dosage_MeSH M_Prospective_Studies_MeSH 
****** 10215284
----K E
----T Effects of carvedilol on left ventricular mass, chamber geometry, and mitral regurgitation in chronic heart failure.
----A We and others have previously shown that carvedilol improves left ventricular (LV) function and symptoms in chronic heart failure. This improvement in LV function has also been shown to be associated with an improvement in survival. This study evaluates the effect of carvedilol on LV mass, geometry, and degree of mitral regurgitation (MR). In 59 patients with symptomatic heart failure and LV ejection fraction <0.35, previously randomized to either treatment with carvedilol or placebo, we evaluated LV mass, geometry, and degree of MR over the time period of carvedilol treatment. LV mass decreased as early as 4 months into the treatment protocol and continued to decrease over a period of 1 year. LV geometry, defined by the length/diameter ratio, and severity of MR also improved with 4 months of therapy. Thus, compared with placebo treatment, carvedilol decreases LV mass while improving cardiac geometry and decreasing MR in patients with chronic heart failure. These changes occur in association with an improvement in LV systolic function. This process begins by 4 months of treatment and continues for 12 months.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Ventricles_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_radionuclide_imaging_MeSH Heart_Ventricles_radionuclide_imaging_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Mitral_Valve_Insufficiency_MeSH S_complications_MeSH Mitral_Valve_Insufficiency_complications_MeSH S_diagnosis_MeSH Mitral_Valve_Insufficiency_diagnosis_MeSH S_drug_therapy_MeSH Mitral_Valve_Insufficiency_drug_therapy_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 10215303
----K E
----T Different effects of bisoprolol on heart rate in patients with ischemic or idiopathic dilated cardiomyopathy (a 24-hour Holter substudy of the Cardiac Insufficiency Bisoprolol Study [CIBIS]).
----A The effect of beta blockade on heart rate in patients with either idiopathic or ischemic cardiomyopathy was studied. It was found that beta blockade reduced the early morning increase in heart rate to a greater extent in patients with idiopathic dilated cardiomyopathy than in those with ischemic dilated cardiomyopathy.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH P_Electrocardiography__Ambulatory_MeSH S_drug_effects_MeSH Electrocardiography__Ambulatory_drug_effects_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10212156
----K E
----T Introducing new treatments in clinical practice: the Italian approach to beta blockers in heart failure.
----A 
----P Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Multicenter_Studies_MeSH M_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10218722
----K I
----T Beta-blocker effects on plasma lipids during prolonged treatment of hypertensive patients with hypercholesterolemia.
----A The aim of this study was to compare the effects of long-term monotherapy with four different beta-blockers on plasma lipids in hypercholesterolemic hypertensive patients. We studied 152 subjects with essential hypertension [diastolic blood pressure (DBP) >90 mm Hg], total cholesterol (TC) >240 and <330 mg/dl, and triglycerides (TGs) <300 mg/dl. After a 4-week washout period with placebo, patients were randomized to receive propranolol, 160 mg/day (n = 37), atenolol, 100 mg/day (n = 38), bisoprolol, 10 mg/day (n = 39), or celiprolol, 400 mg/day (n = 38), for 18 months. No cholesterol-reducing drug was allowed. Blood samples for evaluation of TC, low-density lipoprotein cholesterol (LDL-C), HDL cholesterol (HDL-C), and TGs were taken before and after the placebo period and subsequently every 6 months. No beta-blocker worsened TC or LDL-C. Nonselective propranolol caused the most pronounced changes in HDL-C and TGs. Beta1-Selective atenolol produced the same qualitative effects, but to a lesser extent. The more beta1-selective bisoprolol did not affect HDL-C and TGs. Celiprolol significantly improved the lipid profile by significantly decreasing TC, LDL-C, and TGs, and increasing HDL-C. These findings suggest that in hypercholesterolemic hypertensive patients, (a) beta1-selective beta-blockers are likely to adversely affect plasma lipids to a lesser extent than nonselective ones; and (b) celiprolol is able to improve the lipid pattern, which could be because of its peculiar ancillary properties.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Agonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Celiprolol_MeSH S_pharmacology_MeSH Celiprolol_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH 
****** 10220102
----K E
----T Drugs, heart failure and quality of life: what are we achieving? What should we be trying to achieve?
----A This article is a review of chronic compensated congestive heart failure (CHF), with special reference to its clinical features and pathophysiology and recent advances in pharmacotherapy, including beta-blockers, loop diuretics, ACE inhibitors and angiotensin II receptor antagonists. Clinical problems related to elderly patients and multifaceted aspects of multidisciplinary approaches of medical care to these particular patients are also discussed with special emphasis on the aspect of improved quality of life associated with reduced mortality. Concepts of CHF have greatly changed over the past decades with regard to its pathophysiology, natural progression, mechanisms, causes of death, arrhythmias and treatment goals. Although the current most frequent aetiologies of CHF include coronary heart disease and dilated cardiomyopathy, hypertension has been revisited in a different way, and has been considered of pivotal importance in most recent trends and possibly in future perspectives. Nowadays, however, with the results of improved survival, alleviation of symptoms, improvement in functional capacity and prevention of associated complications including even left ventricular remodelling through various appropriate pharmacotherapies, patients with CHF are used to being physically and psychosocially more active than ever before. Thus, improvement of patients' quality of life and reduction of mortality have become of prime importance in achieving treatment goals. Another emerging aspect of CHF is aging itself, and special features in the medical care of elderly patients with CHF always have to be taken into consideration in reduction of hospital readmission along with improvement of morbidity and mortality. Despite advances in the treatment of CHF, it remains a common disease with a poor prognosis. Therefore, this review focuses on what we should be trying to achieve in reaching goals to reduce repeated hospital readmission and mortality, and increase social activity and quality of life, especially in elderly patients with CHF. In these clinical settings, educational strategies for patients and their family members should be emphasised. Multidisciplinary interventions by nurses and possibly other contributions from a widely available social support system might be effective in preventing repeated hospital readmissions of elderly patients with CHF. In this regard, special precautions have to be paid in the management of elderly patients to achieve effective treatment goals, and any treatment strategy has to be appropriately determined through a comprehensive assessment of patient clinical profiles. Multidisciplinary approaches to these problems have to be effectively utilised to improve patients' quality of life, while possibly reducing medical expenses.
----P Journal_Article Review Review_Literature 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH P_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Education_MeSH P_Quality_of_Life_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Retrospective_Studies_MeSH 
****** 10220232
----K E
----T An economic evaluation of the JNC hypertension guidelines using data from a randomized controlled trial. Joint National Committee.
----A BACKGROUND: We wanted to determine the clinical cost of managing hypertension when following the Joint National Committee on Hypertension (JNC) guidelines, including drug therapy, the cost of monitoring for and treating side effects, compliance, and the cost of switching after therapeutic failures. METHODS: The base-case analysis considers antihypertensive agents from four therapeutic classes that were recently evaluated in a large randomized trial: enalapril, amlodipine, acebutolol, and chlorthalidone. Clinical evaluation, therapy, and monitoring for hypertension are modeled with an incidence-based Markov model. Clinical inputs include agent efficacy, side effects, and compliance with dosing schedules. JNC-recommended clinical and laboratory monitoring schedules are followed for each agent. Switches between classes occur for therapeutic failures. Drug and medical care costs are valued in 1995 US dollars. RESULTS: Although patients whose hypertension was initially treated with amlodipine achieved control more readily than patients who were given the other agents, the initial costs to achieve and maintain hypertension control were lowest for chlorthalidone ($641), followed by acebutolol ($920), amlodipine ($946), and enalapril ($948). Maintenance costs were lowest for chlorthalidone. For all agents except chlorthalidone, drug costs were the largest component of overall costs, followed by the costs of office visits, laboratory monitoring, and switching between classes for therapeutic failures. CONCLUSIONS: By following JNC guidelines, a slightly higher percentage of patients will achieve hypertension control with a newer class calcium channel blocker (amlodipine) but at a substantially higher cost than with a generic diuretic (chlorthalidone).
----P Journal_Article 
----M M_Acebutolol_MeSH S_economics_MeSH Acebutolol_economics_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Amlodipine_MeSH S_economics_MeSH Amlodipine_economics_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_economics_MeSH Calcium_Channel_Blockers_economics_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_economics_MeSH Chlorthalidone_economics_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Decision_Making_MeSH M_Decision_Support_Techniques_MeSH M_Diuretics__Sulfamyl_MeSH S_economics_MeSH Diuretics__Sulfamyl_economics_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Enalapril_MeSH S_economics_MeSH Enalapril_economics_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH P_Health_Care_Costs_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_economics_MeSH Hypertension_economics_MeSH P_Practice_Guidelines_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10221068
----K 1
----T [Clinical trial of the month. The CIBIS-II study]
----A CIBIS-II was a multicentre bouble-blind randomized placebo-controlled trial which enrolled 2,647 class III-IV heart failure patients, with a left ventricular ejection fraction < or = 35%, receiving standard therapy with a diuretic and ACEI and randomly assigned to placebo (n = 1,320) or to bisoprolol (n = 1,327) 1.25 mg/day, progressively increased to a maximum of 10 mg/day. Mean follow-up was 1.3 years. The study was stopped early because the 2nd interim analysis showed a significant mortality benefit in the treated group. All cause mortality was significantly lower in the bisoprolol group (156 [11.8%] vs 228 [17.3%]; p < 0.0001). Sudden deaths were fewer among patients on bisoprolol and treatment effects were independent on severity and aetiology of heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 10220630
----K E
----T Effect of intravenous metoprolol before hospital admission on chest pain in suspected acute myocardial infarction.
----A BACKGROUND: The aim of this study was to describe the effect of intravenous metoprolol on the intensity of chest pain before hospital admission in patients with suspected acute myocardial infarction AMI). METHODS AND RESULTS: Two hundred sixty-two patients with acute chest pain and suspected AMI were randomly assigned before hospital admission to either 5 mg morphine plus metoprolol 5 mg x 3 intravenously or 5 mg morphine plus intravenous placebo. Chest pain was evaluated on a 10-grade scale before and for 60 minutes after intravenous injection. One hundred thirty-four patients were randomly assigned to metoprolol and 128 to placebo. Among all patients randomized to metoprolol, the mean chest pain score was reduced by 3.0 +/- 1.9 arbitrary units AU) from before to after intravenous injection compared with 2.6 +/- 2.1 AU for placebo not significant). Among patients with an initially confirmed or strong suspicion of AMI, the corresponding figures were 3.1 +/- 1.8 AU for metoprolol and 2.2 +/- 1.6 AU for placebo P =.02). Among patients with only a vague or moderate suspicion of AMI, there was no difference. The treatment was well tolerated. CONCLUSIONS: When all patients were included in the analyses, there was no significant difference with regard to reduction of chest pain in the patients randomly assigned to metoprolol compared with placebo. A retrospective subgroup analysis indicated a beneficial effect of metoprolol among patients with an initially strong suspicion of or confirmed AMI. Further investigations are warranted to confirm this finding.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analgesics__Opioid_MeSH S_administration_&_dosage_MeSH Analgesics__Opioid_administration_&_dosage_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Chest_Pain_MeSH S_diagnosis_MeSH Chest_Pain_diagnosis_MeSH S_drug_therapy_MeSH Chest_Pain_drug_therapy_MeSH S_etiology_MeSH Chest_Pain_etiology_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Diagnosis__Differential_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH P_Emergency_Medical_Services_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Morphine_MeSH S_administration_&_dosage_MeSH Morphine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Morphine_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH M_Prognosis_MeSH M_Retrospective_Studies_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10220634
----K E
----T Antianginal efficacy of the combination of felodipine-metoprolol 10/100 mg compared with each drug alone in patients with stable effort-induced angina pectoris: a multicenter parallel group study. The TRAFFIC Study Group.
----A OBJECTIVE: The primary objective of this randomized, double-blind, parallel group trial was to compare the antianginal and antiischemic efficacy of a combination tablet of felodipine-metoprolol 10/100 mg once daily with both drugs given separately once daily in patients with stable effort-induced angina pectoris. The secondary objective was to compare the tolerability of the 3 treatments. METHODS: The main criteria for inclusion were stable effort-induced angina pectoris for at least 2 months before the enrollment and a positive bicycle exercise test result. Patients were allocated to once-daily treatment with either felodipine-metoprolol 10/100 mg, felodipine 10 mg, or metoprolol 100 mg. The duration of active double-blind treatment was 4 weeks. There were 3 primary efficacy variables in the study; time until end of exercise, time until onset of chest discomfort, and time until 1-mm ST depression during a standardized exercise test. RESULTS: The number of patients randomized was 397. There was a statistically significant improvement in time until end of exercise with felodipine-metoprolol 10/100 mg compared with metoprolol 100 mg (P =.04) and felodipine 10 mg compared with metoprolol 100 mg ( P =.03). However, for time until onset of pain or time until 1-mm ST-depression there were no significant differences among the treatment groups. At highest comparable workload, ST depression was less pronounced with felodipine-metoprolol than with metoprolol alone (P =.04), and the rate-pressure product was significantly lower in the groups receiving felodipine-metoprolol and metoprolol than in the group receiving felodipine alone. The combination and metoprolol were better tolerated than felodipine alone. CONCLUSIONS: In stable angina pectoris, the combination felodipine-metoprolol 10/100 mg and felodipine 10 mg alone increased exercise time compared with metoprolol 100 mg. The combination tablet and metoprolol 100 mg alone showed a more favorable tolerability profile than felodipine 10 mg alone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_etiology_MeSH Angina_Pectoris_etiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Exercise_Test_MeSH S_adverse_effects_MeSH Exercise_Test_adverse_effects_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10220639
----K E
----T Cardioprotection for Duchenne's muscular dystrophy.
----A PURPOSE: To explore the use of neuroendocrine monitoring for more timely diagnosis of dilated cardiomyopathy (DCM) in Duchenne's muscular dystrophy (DMD) and to determine the effects of angiotensin-converting enzyme inhibitors (ACEI) and beta-blockers on neuroendocrine levels, left ventricular diastolic diameter (LVDd), ejection fraction, and mortality rate on DMD. METHODS: Eighty-five patients with DMD underwent yearly cardiac monitoring including neuroendocrine screening. Eleven patients had symptoms of DCM develop once plasma neuroendocrine levels increased. At this point the patients received ACEI for 9 to 62 months (35.8 +/- 18.4 months) and beta-blockers for 7 to 60 months (31.6 +/- 20.1 months). RESULTS: The combination of ACEI and beta-blockers relieved symptoms and signs of heart failure in all 11 patients and significantly reduced atrial natriuretic protein (ANP) levels from 197.5 +/- 152.1 pg/mL to 25.5 +/- 16.2 pg/mL ( P <.002) at 15.5 +/- 8.2 months, brain natriuretic protein from 523.8 +/- 434.8 pg/mL to 59.3 +/- 24. 2 pg/mL ( P <.05) at 12.2 +/- 3.1 months (data complete for 5 patients), norepinephrine levels from 1114 +/- 689 pg/mL to 360 +/- 257 pg/mL at 20.5 +/- 9.6 months for 11 patients (P =.001), and LVDd from 65.9 +/- 9.2 mm to 63.3 +/- 6.3 mm (P =.15) at 15.0 +/- 7.4 months for 10 patients, including 3 for whom the LVDd increased by 2 to 6 mm. The combination increased left ventricular ejection fraction (LVEF) from 25.1% +/- 9.2% to 36.5% +/- 5.8% (P <.001) at 17.1 +/- 11.0 months for 10 patients. For 9 of the patients ANP levels remained lower throughout the 36.8 +/- 20.1 month course of the follow-up. Two patients had sudden severe re-elevations of ANP levels just before death from congestive heart failure after 44 and 23 months of therapy, respectively. CONCLUSION: Neuroendocrine level monitoring can assist in the diagnosis of DCM in patients with DMD. Combination therapy with ACEI and beta-blockers can significantly decrease neuroendocrine activation and LVDd and reverse symptoms and signs of congestive heart failure for patients with DMD.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Child_MeSH M_Comparative_Study_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Heart_Ventricles_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Muscular_Dystrophies_MeSH S_blood_MeSH Muscular_Dystrophies_blood_MeSH S_complications_MeSH Muscular_Dystrophies_complications_MeSH S_mortality_MeSH Muscular_Dystrophies_mortality_MeSH M_Natriuretic_Peptide__Brain_MeSH S_blood_MeSH Natriuretic_Peptide__Brain_blood_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 10220541
----K E
----T beta blocker treatment and other prognostic variables in patients with clinical evidence of heart failure after acute myocardial infarction: evidence from the AIRE study.
----A OBJECTIVES: To examine clinical outcomes associated with optional beta blockade in a population of patients with evidence of heart failure after myocardial infarction. DESIGN AND PATIENTS: Data from the acute infarction ramipril efficacy (AIRE) study were analysed retrospectively. At baseline 22.3% of the patients were receiving a beta blocker. To minimise confounding, beta blocker and diuretic treatments, presence of clinical signs of heart failure, left ventricular ejection fraction, and 16 other baseline clinical variables were simultaneously entered in a multivariate Cox regression model. In addition, the same analysis was repeated separately within a high and a low risk group of patients, as defined according to the need for diuretic treatment. RESULTS: beta Blocker treatment was an independent predictor of reduced risk of total mortality (hazard ratio 0.66, 95% confidence interval (CI) 0. 48 to 0.90) and progression to severe heart failure (0.58, 95% CI 0.40 to 0.83) for the entire study population. There were similar findings in high risk patients requiring diuretics (0.59, 95% CI 0.40 to 0.86; and 0.58, 95% CI 0.38 to 0.89). CONCLUSIONS: beta Blocker treatment is associated with improved outcomes in patients with clinical evidence of mild to moderate heart failure after myocardial infarction. Most importantly, high risk patients with persistent heart failure appear to benefit at least as much as lower risk patients with transient heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Regression_Analysis_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10229240
----K I
----T Beta-blockers for the treatment of congestive heart failure.
----A 
----P Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Reproducibility_of_Results_MeSH 
****** 10235094
----K E
----T Gender differences and practice implications of risk factors for frequent hospitalization for heart failure in an urban center serving predominantly African-American patients.
----A To identify the clinical correlates of recurrent heart failure hospitalization in a large urban hospital serving predominately African-American patients, and to provide further insight into modifiable risks for heart failure readmissions, a retrospective period prevalence review of the records of all adult patients admitted with a primary diagnosis of heart failure (International Classification of Diseases-9 code 428.0) between January and December 1995 was performed.The main outcome was the number of heart failure hospitalizations over 12 months. Twelve hundred patients were identified. Mean age was 64 +/- 16 years, 94% were black, 57% were women, and 40% were > or = 65 years old. Ninety-eight percent had a history of systemic hypertension and 55% had uncontrolled hypertension. Other comorbidities were left ventricular (LV) hypertrophy (64%), coronary artery disease (52%), and tobacco abuse (28%). Sixty-five percent of patients were on angiotensin-converting enzyme (ACE) inhibitors, 51% on calcium antagonists, and 8% on beta blockers. Most patients had suboptimal dosing of ACE inhibitors and there was inappropriate use of calcium antagonists in 56% of patients with moderate or severe systolic dysfunction. Diabetes mellitus and echocardiographic wall motion abnormality were independently associated with frequent admissions for women but not for men. Medication-related increase in heart failure hospitalization was seen for calcium antagonists in patients with severe LV dysfunction (odds ratio 2.24, 95% confidence intervals 1.0 to 5.03; p <0.03). Uncontrolled hypertension, underdosing of ACE inhibitors, and overuse of calcium antagonists in patients with significant LV dysfunction are potential targets for intervention.
----P Journal_Article 
----M M_Adult_MeSH M_African_Americans_MeSH S_statistics_&_numerical_data_MeSH African_Americans_statistics_&_numerical_data_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Comorbidity_MeSH M_Cross-Sectional_Studies_MeSH M_Female_MeSH M_Georgia_MeSH S_epidemiology_MeSH Georgia_epidemiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Sex_Distribution_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Urban_Population_MeSH 
****** 10235696
----K E
----T Nebivolol in the management of essential hypertension: a review.
----A Nebivolol is a lipophilic beta1-blocker. It is devoid of intrinsic sympathomimetic or membrane stabilising activity but appears to have nitric oxide-mediated vasodilatory effects. Nebivolol is administered as a racemic mixture of equal proportions of d- and l-enantiomers. The drug does not significantly influence glucose or plasma lipid metabolism and appears to have a protective effect on left ventricular function. At the recommended dosage (5 mg once daily) nebivolol reduces resting diastolic blood pressure as effectively as standard therapeutic dosages of atenolol, metoprolol, lisinopril and nifedipine, as shown in comparative trials. Nebivolol reduced blood pressure significantly more than enalapril 10 mg daily in the short but not the long term, although the enalapril dose may not have been optimal. Nebivolol has an additive effect in combination with hydrochlorothiazide. Standing blood pressure and/or mean 24-hour ambulatory blood pressure is significantly and similarly reduced with nebivolol, atenolol or nifedipine. Nebivolol tended to prevent increases in early morning blood pressure better than nifedipine. Overall response rates to nebivolol therapy (a decrease in sitting/supine diastolic blood pressure to < or = 90 mm Hg or a 10% or > or = 10 mm Hg fall in diastolic blood pressure) ranged from 58 to 81% after 4 to 52 weeks' treatment. In comparative studies, response rates were greater in nebivolol than in enalapril or metoprolol recipients, but not significantly different from those in atenolol or nifedipine recipients. Nebivolol 5 mg once daily is well tolerated in patients with hypertension. Adverse events are infrequent, transient and mild to moderate. Those reported most often include headache, fatigue, paraesthesias and dizziness. Several studies reported no signs of orthostatic hypotension with nebivolol. Comparative trials revealed no significant differences between the frequency and severity of adverse events in patients receiving nebivolol, atenolol, enalapril or placebo; however, the overall incidence of adverse events was greater with nifedipine or metoprolol. Some atenolol or enalapril, but not nebivolol, recipients reported impotence or decreased libido during therapy. CONCLUSION: Current evidence indicates that nebivolol 5 mg once daily is a well tolerated beta-blocker, which is as effective as once daily atenolol and other classes of antihypertensive agents. It may therefore be recommended as a useful alternative first-line treatment option for the management of patients with mild to moderate uncomplicated essential hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzopyrans_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_pharmacokinetics_MeSH Benzopyrans_pharmacokinetics_MeSH S_pharmacology_MeSH Benzopyrans_pharmacology_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Ethanolamines_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_pharmacokinetics_MeSH Ethanolamines_pharmacokinetics_MeSH S_pharmacology_MeSH Ethanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 10321444
----K E
----T Combination therapy with felodipine and metoprolol compared with captopril and hydrochlorothiazide. German MC Study Group.
----A This study compared the antihypertensive efficacy and tolerability of a combination tablet containing the vascular-selective calcium antagonist felodipine and the beta1-selective adrenergic antagonist metoprolol, with a combination tablet of captopril-hydrochlorothiazide in a randomized, double-blind trial involving 109 patients with mild to moderate hypertension. After 2 weeks on placebo, patients with a supine diastolic blood pressure of 95-115 mm Hg were randomized to felodipine-metoprolol, 5/50 mg o.d. (Logimax) or captopril-hydrochlorothiazide, 25/25 mg o.d. (Capozide). After a further 4 weeks, there was a mandatory dose increase to felodipine-metoprolol 10/100 mg o.d., and captopril-hydrochlorothiazide, 50/25 mg o.d., and treatment then continued for a another 4 weeks. At the end of the study, felodipine-metoprolol reduced supine blood pressure significantly more than captopril-hydrochlorothiazide. The mean differences in change in supine systolic and diastolic blood pressure between treatments after 8 weeks were 5.2 and 3.4 mm Hg, respectively, in favour of felodipine-metoprolol (p<0.05). Standing blood pressure also showed trends in favour of felodipine-metoprolol. The proportion of responders was similar in both groups. Both treatments were well tolerated. Two patients treated with felodipine-metoprolol and 5 with captopril-hydrochlorothiazide discontinued treatment due to adverse events. Felodipine-metoprolol combination reduced supine blood pressure significantly more than captopril-hydrochlorothiazide with maintained tolerability.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Captopril_MeSH S_adverse_effects_MeSH Captopril_adverse_effects_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_adverse_effects_MeSH Felodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_adverse_effects_MeSH Hydrochlorothiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 10321112
----K 1
----T [Clinical study of the month. The CAPPP study: "The Captopril Prevention Project"]
----A The Captopril Prevention Project (CAPPP) was a prospective, randomized, open trial which aimed at comparing the prevention by captopril (n = 5492) or by a conventional treatment (n = 5493; diuretics or beta-blockers) of cardiovascular morbidity and mortality in patients with hypertension (diastolic blood pressure > 100 mmHg). After a mean follow-up of 6.1 years, the results regarding the primary endpoint and most secondary endpoints were not significantly different between the two therapeutic modalities. The only differences (perhaps due to a randomisation bias) were a slightly higher incidence of stroke, but a lower risk of diabetes mellitus, in the captopril group than in the group receiving conventional treatment. In conclusion, the CAPPP study demonstrates, for the first time, that captopril, an angiotensin-converting-enzyme inhibitor, is as effective as conventional treatment with diuretics or beta-blockers, two drugs whose efficacy has already been demonstrated when compared to placebo, in the prevention of cardiovascular morbidity and mortality in hypertensive patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Disorders_MeSH M_Diabetes_Mellitus_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus_prevention_&_control_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 10323654
----K E
----T Drug treatment of hypertension in older persons in an academic hospital-based geriatrics practice.
----A OBJECTIVE: To investigate the prevalence of hypertension in older persons, the prevalence of the different antihypertensive drugs used to treat hypertension, the prevalence of the different antihypertensive drugs used to treat hypertension in persons with prior myocardial infarction (MI) or congestive heart failure (CHF), and the prevalence of lowering the blood pressure to <140/90 mm Hg with therapy. DESIGN: A retrospective analysis of charts from all older patients seen from December 1, 1997, through August 31, 1998, at an academic, hospital-based geriatrics practice was performed to investigate the prevalence of hypertension in older persons, the prevalence of different antihypertensive drugs used to treat hypertension, the prevalence of different antihypertensive drugs used to treat hypertension in persons with prior MI or CHF, and the prevalence of lowering the blood pressure to <140/90 mm Hg with therapy. SETTING: An academic hospital-based geriatrics practice staffed by fellows in a geriatrics training program and fulltime faculty geriatricians. PATIENTS: A total of 459 men and 1360 women, mean age 80 +/- 8 years (range 59 to 101 years), were included in the study. MEASUREMENTS AND MAIN RESULTS: Hypertension was present in 1051 of the 1819 persons in the study (58%). Target organ damage, clinical cardiovascular disease, or diabetes mellitus was present in 738 (70%) of these 1051 persons. Of the 1051 persons with hypertension, 520 (49%) were treated with diuretics, 297 (28%) with beta-blockers, 445 (42%) with angiotensin-converting enzyme (ACE) inhibitors, 171 (16%) with calcium channel blockers, and 13 (1%) with other antihypertensive drugs; 41 (4%) received no antihypertensive therapy. The last blood pressure recorded on the chart was <140/90 mm Hg for 735 of the 1051 persons (70%) with hypertension. Of 306 persons with hypertension and prior MI, 182 (59%) were treated with beta-blockers, 146 (48%) with ACE inhibitors, 96 (31%) with diuretics, and 29 (9%) with calcium channel blockers. Of 103 persons with hypertension and CHF, 103 (100%) were treated with diuretics, 94 (91%) with ACE inhibitors, 22 (21%) with beta-blockers, and 3 (3%) with calcium channel blockers. CONCLUSIONS: The prevalence of hypertension in the 1819 older persons seen in an academic, hospital-based geriatrics practice was 58%. Educational efforts led to increased use of diuretics and beta-blockers and decreased use of calcium channel blockers in treating hypertension. The last blood pressure recorded on the chart was <140/90 mm Hg in 70% of older persons with hypertension in the study.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Drug_Utilization_MeSH M_Female_MeSH M_Geriatrics_MeSH M_Hospitals__Teaching_MeSH S_statistics_&_numerical_data_MeSH Hospitals__Teaching_statistics_&_numerical_data_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Retrospective_Studies_MeSH M_United_States_MeSH 
****** 10327727
----K E
----T Long-term preservation of left ventricular function in medically treated patients with coronary artery disease and persistent exercise-induced ischemia.
----A Little information is available on the long-term evolution of left ventricular function of medically treated patients with coronary artery disease and gross limitation of coronary flow reserve. The aim of this study was to assess the long-term evolution of effort tolerance and left ventricular function and their relation to the control of ischemic events in patients with coronary artery disease and prolonged inducible exercise-induced myocardial dysfunction who either declined or were ineligible for cardiac revascularization.
----P Journal_Article 
----M M_Aged_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Data_Interpretation__Statistical_MeSH M_Diastole_MeSH M_Diltiazem_MeSH S_administration_&_dosage_MeSH Diltiazem_administration_&_dosage_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Nitrates_MeSH S_administration_&_dosage_MeSH Nitrates_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Stroke_Volume_MeSH M_Systole_MeSH M_Time_Factors_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH P_Ventricular_Function__Left_MeSH 
****** 10331109
----K E
----T The use of pindolol with fluoxetine in the treatment of major depression: final results from a double-blind, placebo-controlled trial.
----A BACKGROUND: Preliminary reports have suggested that concomitant institution of pindolol and serotonin reuptake inhibitors robustly hastens clinical response; however, contradictory evidence from a randomized double-blind, controlled trial was recently reported by this group in a population of depressed patients who were prescribed fluoxetine and pindolol. Herein, we report final results from an extended sample size. METHODS: Drug-free outpatients with a major depressive episode were randomized in a double-blind manner to one of two treatment conditions: fluoxetine (20 mg daily) with pindolol (7.5 to 10 mg daily) or fluoxetine (20 mg daily) with placebo. After 6 weeks, patients were followed for 3 more weeks in a single-blind manner, on fluoxetine and placebo pindolol. RESULTS: Eighty-six patients completed at least 1 or more weeks on protocol, with 45 and 41 patients randomized to the pindolol and placebo groups respectively. After 2 weeks on protocol, partial remission (i.e., at least 50% decrease in depression rating scores from baseline) rates for pindolol (16%) and placebo (19%) groups were comparable. By the study's end, a partial remission was achieved, at least transiently, for 67% of the pindolol group and 80% of the placebo group. Pindolol treatment was associated with statistically significant reduction in blood pressure and pulse as compared to the control group. The two groups did not have overall differences in rates of attrition, time to response, and side effects. CONCLUSIONS: In accord with our previously published findings, these extended results do not support the efficacy of pindolol in hastening clinical response to fluoxetine in a patient population with predominantly chronic and recurrent depression.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Depressive_Disorder_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fluoxetine_MeSH S_adverse_effects_MeSH Fluoxetine_adverse_effects_MeSH S_therapeutic_use_MeSH Fluoxetine_therapeutic_use_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pindolol_MeSH S_adverse_effects_MeSH Pindolol_adverse_effects_MeSH S_therapeutic_use_MeSH Pindolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 10329091
----K E
----T Treatment of congestive heart failure. Has the time come for decreased complexity?
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_pathology_MeSH Heart_Failure__Congestive_pathology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Ventricles_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH M_Human_MeSH M_Myocardium_MeSH S_pathology_MeSH Myocardium_pathology_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Ventricular_Remodeling_MeSH 
****** 10335420
----K E
----T Propranolol in hypoglycaemia unawareness.
----A The effect of propranolol on the occurrence of hypoglycaemic symptoms was assessed in insulin-dependent diabetic patients with hypoglycaemia unawareness. A double-blind, randomised parallel group study (2:1 fashion) was conducted over 4-week period. The propranolol group (n = 9) received 20 mg (week 1 and 2) and 30 mg (week 3 and 4) twice daily, and the other group (n = 5) a matched placebo for 4 weeks. Patients included had experienced at least two severe hypoglycaemic episodes (coma or seizures) during the previous year, which were characterised by a lack of adrenergic symptoms and required the assistance of another person. The mean number of hypoglycaemias during the study period was similar in both groups (placebo: 13 +/- 2 propranolol: 11 +/- 1), whereas the number of totally asymptomatic hypoglycaemias (< 0.6 g/l) was lower on propranolol than on placebo (3 +/- 1 vs 8 +/- 3, NS) and the number of symptomatic hypoglycaemias was higher (7.2 +/- 2 vs 4.6 +/- 1, NS). Subjective evaluation of treatment by the investigators showed 0/5 successes in the placebo group and 5/9 in the propranolol group (chi2 = 4.32, p = 0.038). The main advantage of propranolol over placebo was an increased incidence of sweating. The ratio [number of hypoglycaemias with sweating/total number of hypoglycaemias] being higher with propranolol (0.28 +/- 0.08 vs 0.06 +/- 0.02, p = 0.06). This pilot study suggests that beta-blockers may be useful in restoring adrenergic symptoms during hypoglycaemia in insulin-dependent diabetic patients without warning symptoms of hypoglycaemia. This beneficial effect seems to be predominantly related to an increase in hypoglycaemia-induced sweating. A larger study is needed to confirm or invalidate these preliminary results.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_diagnostic_use_MeSH Adrenergic_beta-Antagonists_diagnostic_use_MeSH M_Adult_MeSH M_Diabetes_Mellitus__Type_I_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_I_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypoglycemia_MeSH S_chemically_induced_MeSH Hypoglycemia_chemically_induced_MeSH S_diagnosis_MeSH Hypoglycemia_diagnosis_MeSH S_physiopathology_MeSH Hypoglycemia_physiopathology_MeSH M_Insulin_MeSH S_adverse_effects_MeSH Insulin_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_diagnostic_use_MeSH Propranolol_diagnostic_use_MeSH M_Questionnaires_MeSH M_Sweating_MeSH 
****** 10337449
----K I
----T Betaxolol versus carvedilol in chronic heart failure (BETACAR study). Rationale and design.
----A The use of beta-blockers in heart failure for a long time was regarded as contra-indicated because of their negative inotropic effects. Nevertheless, there is growing evidence that beta-blockers slow down the progression of left ventricular dilatation that characterizes heart failure. In addition changes in left ventricular ejection fraction after several months of beta-blocker treatment appears to have predictive value for survival. This beneficial effect of beta-blockade in chronic heart failure needs to be assessed further. The presumed benefit of beta-blockade with betaxolol (CAS 63659-18-7), a highly selective beta-blocker with long duration of action in chronic heart failure (CHF) will be assessed in BETACAR, a comparative study versus carvedilol (CAS 72956-09-3). The design of this study is provided in this article.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Betaxolol_adverse_effects_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10337539
----K E
----T Beta-blockers for heart failure: is slowing of heart rate essential?
----A 
----P Comment Editorial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 10337542
----K E
----T Heart rate dependency of cardiac performance in heart failure patients treated with metoprolol.
----A AIMS: To investigate whether a low heart rate is necessary to maintain improvement in myocardial function after long-term treatment with a beta-blocker in patients with heart failure. METHODS AND RESULTS: Forty-eight patients with congestive heart failure were investigated: 30 patients with dilated cardiomyopathy participating in a placebo-controlled trial (15 on placebo, 15 on metoprolol), and 18 patients treated by metoprolol in an open protocol. Investigations of spontaneous heart rate and of matched paced heart rates were performed at baseline and after 3, 6 and 12 months of follow-up by radionuclide angiography. There were significant signs of improvement in systolic indices of the spontaneous heart rate in the metoprolol-treated group (peak ejection rate: 0.98 to 1.32 end-diastolic volume.s-1, P = 0.015) as compared to placebo (1.14 to 1.19 end-diastolic volume.s-1, not significant). Similar effects were observed during the matched paced heart rate (peak ejection rate: metoprolol 0.91 to 1.38 end-diastolic volume.s-1, P = 0.037; placebo 1.22 to 1.12 end-diastolic volume.s-1, not significant). No effects were observed in the early peak filling rate. Left ventricular volumes decreased during metoprolol treatment, both for the spontaneous heart rate and during matched pacing. CONCLUSIONS: These data imply that beta-blocker treatment improves the force-frequency relationship of myocardial performance. A lower heart rate is not necessary to maintain cardiac function on a short-term basis, once myocardial recovery has occurred.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Cardiac_Output_MeSH S_drug_effects_MeSH Cardiac_Output_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10338457
----K I
----T Prospective, randomized comparison of effect of long-term treatment with metoprolol or carvedilol on symptoms, exercise, ejection fraction, and oxidative stress in heart failure.
----A BACKGROUND: With beta-blocker use becoming more prevalent in treating chronic heart failure (CHF), the choice of drugs raises important theoretical and practical questions. Although the second-generation compound metoprolol is beta1-selective, the third-generation compound carvedilol is beta-nonselective, with ancillary pharmacological properties including alpha-blockade and antioxidant effects. A prospective comparison of these 2 agents can address the issue of optimal adrenergic blockade in selecting agents for therapy in CHF. METHODS AND RESULTS: Sixty-seven patients with symptomatic stable heart failure were randomly assigned to receive either carvedilol or metoprolol in addition to standard therapy for CHF. Measured variables included symptoms, exercise, ejection fraction, and thiobarbituric acid-reactive substances (TBARS) as an indirect marker of free radical activity. Metoprolol and carvedilol were well tolerated, and both patient groups showed beneficial effects of beta-blocker therapy in each of the measured parameters, with no between-group differences. Ejection fraction increased over 6 months from 18+/-6.3% to 23+/-8.7% (P<0.005) with metoprolol and from 19+/-8.5% to 25+/-9.9% (P<0.0005) with carvedilol (P=NS between groups). With metoprolol, TBARS values decreased from 4.7+/-0.9 nmol/mL at baseline to 4.2+/-1.5 nmol/mL at month 4 to 3.9+/-1.0 nmol/mL at month 6 (P<0.0001). With carvedilol, there was a parallel decline from 4.7+/-1.4 to 4.2+/-1.3 to 4.1+/-1.2 nmol/mL over the same time frame (P<0.025), with no between-group difference in these changes. CONCLUSIONS: Carvedilol and metoprolol showed parallel beneficial effects in the measured parameters over 6 months, with no relevant between-group differences in this heart failure population.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiac_Output__Low_MeSH S_drug_therapy_MeSH Cardiac_Output__Low_drug_therapy_MeSH S_metabolism_MeSH Cardiac_Output__Low_metabolism_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH P_Exercise_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Oxidative_Stress_MeSH S_drug_effects_MeSH Oxidative_Stress_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiobarbituric_Acid_Reactive_Substances_MeSH S_metabolism_MeSH Thiobarbituric_Acid_Reactive_Substances_metabolism_MeSH 
****** 10342782
----K E
----T Beta-adrenergic receptor blockade as a therapeutic approach for suppressing the renin-angiotensin-aldosterone system in normotensive and hypertensive subjects.
----A Although beta-adrenergic-blocking drugs suppress the renin system (RAAS), plasma angiotensin II (Ang II) responses during beta-blockade have not been defined. This study quantifies the effects of beta-blockade on the RAAS and examines its impact on prorenin processing by measuring changes in the ratio of plasma renin activity (PRA) to total renin. In normotensive (N = 14) and hypertensive (N = 16) subjects, blood pressure (BP), heart rate, PRA, plasma prorenin, plasma total renin (prorenin + PRA), ratio of PRA to total renin (%PRA), plasma Ang II, and urinary aldosterone were measured before and after 1 week of beta-blockade. Plasma renin activity, Ang II, and urinary aldosterone levels were similar for normotensive and hypertensive subjects. Plasma renin activity correlated with Ang II. Total renin, which is proportional to (pro)renin gene expression, was lower in hypertensive subjects and was inversely related to BP. Beta-blockade decreased BP and heart rate in both groups, with medium- and high-renin hypertensive subjects responding more frequently than those with low renin. Beta-blockade consistently suppressed PRA, Ang II, and aldosterone. Total renin was unchanged, thus, %PRA fell. These results indicate that beta-blockers suppress plasma angiotensin II levels, in parallel with the marked reductions in PRA and urinary aldosterone levels in normotensive and hypertensive subjects. The suppression of Ang II levels was comparable to that produced during angiotensin converting enzyme (ACE) inhibition. However, by reducing prorenin processing to renin, beta-blockers do not stimulate renin secretion, unlike ACE inhibitors and Ang II receptor antagonists. This unique action of beta-blockers has important implications for the treatment of cardiovascular disease.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aldosterone_MeSH S_urine_MeSH Aldosterone_urine_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH S_blood_MeSH Angiotensin_II_blood_MeSH S_genetics_MeSH Angiotensin_II_genetics_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Enzyme_Precursors_MeSH S_blood_MeSH Enzyme_Precursors_blood_MeSH S_genetics_MeSH Enzyme_Precursors_genetics_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gene_Expression_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH S_drug_effects_MeSH Peptidyl-Dipeptidase_A_drug_effects_MeSH M_Renin_MeSH S_antagonists_&_inhibitors_MeSH Renin_antagonists_&_inhibitors_MeSH S_blood_MeSH Renin_blood_MeSH S_genetics_MeSH Renin_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH 
****** 10347937
----K 1
----T [Efficacy and tolerance of the bisoprolol/hydrochlorothiazide combination in arterial hypertension]
----A PURPOSE: Multicenter, open and non-controlled study to evaluated the efficacy and the tolerability of a low-dose combination of two anti-hypertensive agents: a cardioselective beta-blocker, bisoprolol (2.5 and 5.0 mg) with 6.25 mg of hydrochlorothiazide. METHODS: One hundred and six patients in the stage I and stage II of the systemic hypertension (mild to moderate) were given the bisoprolol/hydrochlorothiazide combination once daily and the diastolic and systolic blood pressures were monitored during the 8-week trial. RESULTS: The bisoprolol/hydrochlorothiazide combination reduced the initial mean values of systolic and diastolic blood pressures, respectively, from the 157.4 mmHg and 98.8 mmHg to 137.3 mmHg and 87.4 mmHg. At the end of the treatment period, 61% of the patients normalized blood pressure values (< 90 mmHg) and 22.9% of them had responded to the treatment, resulting in a total response rate (normalized + responsive) of 83.9% of cases. Adverse events were described only in 18.9% of the patients and dizziness and headache were the most common. There were no clinically significant changes on plasma levels of potassium, uric acid, glucose, or in the lipid profile. CONCLUSION: The combination of low dosages of bisoprolol and hydrochlorothiazide may be considered an effective, well tolerated and rational alternative for the initial treatment of the patients with mild to moderate hypertension.
----P Clinical_Trial Clinical_Trial__Phase_IV Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 10349897
----K I
----T Meta-analysis of trials comparing beta-blockers, calcium antagonists, and nitrates for stable angina.
----A CONTEXT: Which drug is most effective as a first-line treatment for stable angina is not known. OBJECTIVE: To compare the relative efficacy and tolerability of treatment with beta-blockers, calcium antagonists, and long-acting nitrates for patients who have stable angina. DATA SOURCES: We identified English-language studies published between 1966 and 1997 by searching the MEDLINE and EMBASE databases and reviewing the bibliographies of identified articles to locate additional relevant studies. STUDY SELECTION: Randomized or crossover studies comparing antianginal drugs from 2 or 3 different classes (beta-blockers, calcium antagonists, and long-acting nitrates) lasting at least 1 week were reviewed. Studies were selected if they reported at least 1 of the following outcomes: cardiac death, myocardial infarction, study withdrawal due to adverse events, angina frequency, nitroglycerin use, or exercise duration. Ninety (63%) of 143 identified studies met the inclusion criteria. DATA EXTRACTION: Two independent reviewers extracted data from selected articles, settling any differences by consensus. Outcome data were extracted a third time by 1 of the investigators. We combined results using odds ratios (ORs) for discrete data and mean differences for continuous data. Studies of calcium antagonists were grouped by duration and type of drug (nifedipine vs nonnifedipine). DATA SYNTHESIS: Rates of cardiac death and myocardial infarction were not significantly different for treatment with beta-blockers vs calcium antagonists (OR, 0.97; 95% confidence interval [CI], 0.67-1.38; P = .79). There were 0.31 (95% CI, 0.00-0.62; P = .05) fewer episodes of angina per week with beta-blockers than with calcium antagonists. beta-Blockers were discontinued because of adverse events less often than were calcium antagonists (OR, 0.72; 95% CI, 0.60-0.86; P<.001). The differences between beta-blockers and calcium antagonists were most striking for nifedipine (OR for adverse events with beta-blockers vs nifedipine, 0.60; 95% CI, 0.47-0.77). Too few trials compared nitrates with calcium antagonists or beta-blockers to draw firm conclusions about relative efficacy. CONCLUSIONS: beta-Blockers provide similar clinical outcomes and are associated with fewer adverse events than calcium antagonists in randomized trials of patients who have stable angina.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 10349064
----K I
----T Carvedilol.
----A Carvedilol is the first beta-blocker to obtain approval for treatment of heart failure. Improvement in hemodynamic parameters was initially documented in three methodologically sound studies involving 156 patients. Follow up was limited to 16 weeks. A placebo-controlled, double-blind trial involving 1094 patients showed beneficial effects on overall mortality of 4.6% in absolute terms after a median follow up of 6.5 months. This benefit was not found in another trial involving 415 patients followed on average for 19 months. Results for symptom-based criteria conflict. When treatment is introduced very gradually, adverse effects (malaise) seem to be minor and infrequent. Carvedilol's place in the treatment of heart failure is not yet precisely documented.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Evaluation_Studies_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10356008
----K E
----T Effect of postal prompts to patients and general practitioners on the quality of primary care after a coronary event (POST): randomised controlled trial.
----A OBJECTIVES: To determine whether postal prompts to patients who have survived an acute coronary event and to their general practitioners improve secondary prevention of coronary heart disease. DESIGN: Randomised controlled trial. Setting: 52 general practices in east London, 44 of which had received facilitation of local guidelines for coronary heart disease. Participants: 328 patients admitted to hospital for myocardial infarction or unstable angina. Interventions: Postal prompts sent 2 weeks and 3 months after discharge from hospital. The prompts contained recommendations for lowering the risk of another coronary event, including changes to lifestyle, drug treatment, and making an appointment to discuss these issues with the general practitioner or practice nurse. MAIN OUTCOME MEASURES: Proportion of patients in whom serum cholesterol concentrations were measured; proportion of patients prescribed beta blockers (6 months after discharge); and proportion of patients prescribed cholesterol lowering drugs (1 year after discharge). RESULTS: Prescribing of beta bockers (odds ratio 1.7, 95% confidence interval 0.8 to 3.0, P>0.05) and cholesterol lowering drugs (1.7, 0. 8 to 3.4, P>0.05) did not differ between intervention and control groups. A higher proportion of patients in the intervention group (64%) than in the control group (38%) had their serum cholesterol concentrations measured (2.9, 1.5 to 5.5, P<0.001). Secondary outcomes were significantly improved for consultations for coronary heart disease, the recording of risk factors, and advice given. There were no significant differences in patients' self reported changes to lifestyle or to the belief that it is possible to modify the risk of another coronary event. CONCLUSIONS: Postal prompts to patients who had had acute coronary events and to their general practitioners in a locality where guidelines for coronary heart disease had been disseminated did not improve prescribing of effective drugs for secondary prevention or self reported changes to lifestyle. The prompts did increase consultation rates related to coronary heart disease and the recording of risk factors in the practices. Effective secondary prevention of coronary heart disease requires more than postal prompts and the dissemination of guidelines.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Family_Practice_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Guideline_Adherence_MeSH M_Health_Promotion_MeSH S_methods_MeSH Health_Promotion_methods_MeSH S_standards_MeSH Health_Promotion_standards_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_prevention_&_control_MeSH Hypercholesterolemia_prevention_&_control_MeSH M_Information_Services_MeSH M_Male_MeSH M_Mass_Screening_MeSH S_methods_MeSH Mass_Screening_methods_MeSH M_Middle_Aged_MeSH M_Patient_Education_MeSH S_methods_MeSH Patient_Education_methods_MeSH M_Practice_Guidelines_MeSH M_Quality_of_Health_Care_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 10362195
----K E
----T Long-term effects of carvedilol in idiopathic dilated cardiomyopathy with persistent left ventricular dysfunction despite chronic metoprolol. The Heart-Muscle Disease Study Group.
----A OBJECTIVES: The purpose of this study was to analyze whether long-term treatment with the nonselective beta-adrenergic blocking agent carvedilol may have beneficial effects in patients with dilated cardiomyopathy (DCM), who are poor responders in terms of left ventricular (LV) function and exercise tolerance to chronic treatment with the selective beta-blocker metoprolol. BACKGROUND: Although metoprolol has been proven to be beneficial in the majority of patients with heart failure, a subset of the remaining patients shows long-term survival without satisfactory clinical improvement. METHODS: Thirty consecutive DCM patients with persistent LV dysfunction (ejection fraction < or =40%) and reduced exercise tolerance (peak oxygen consumption <25 ml/kg/min) despite chronic (>1 year) tailored treatment with metoprolol and angiotensin-converting enzyme inhibitors were enrolled in a 12-month, open-label, parallel trial and were randomized either to continue on metoprolol (n = 16, mean dosage 142+/-44 mg/day) or to cross over to maximum tolerated dosage of carvedilol (n = 14, mean dosage 74+/-23 mg/day). RESULTS: At 12 months, patients on carvedilol, compared with those continuing on metoprolol, showed a decrease in LV dimensions (end-diastolic volume -8+/-7 vs. +7+/-6 ml/m2, p = 0.053; end-systolic volume -7+/-5 vs. +6+/-4 ml/m2, p = 0.047), an improvement in LV ejection fraction (+7+/-3% vs. -1+/-2%, p = 0.045), a reduction in ventricular ectopic beats (-12+/-9 vs. +62+/-50 n/h, p = 0.05) and couplets (-0.5+/-0.4 vs. +1.5+/-0.6 n/h, p = 0.048), no significant benefit on symptoms and quality of life and a negative effect on peak oxygen consumption (-0.6+/-0.6 vs. +1.3+/-0.5 ml/kg/min, p = 0.03). CONCLUSIONS: In DCM patients who were poor responders to chronic metoprolol, carvedilol treatment was associated with favorable effects on LV systolic function and remodeling as well as on ventricular arrhythmias, whereas it had a negative effect on peak oxygen consumption.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Follow-Up_Studies_MeSH M_Heart_Ventricles_MeSH S_metabolism_MeSH Heart_Ventricles_metabolism_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Oxygen_Consumption_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Quality_of_Life_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 10368586
----K 1
----T [The therapeutic focus in severe hypertrophic obstructive cardiomyopathy with multivessel coronary disease]
----A The association of severe hypertrophic obstructive cardiomyopathy and coronary artery disease increases surgical morbimortality, even more in patients over 65 years. We describe a combined therapeutic approach to these diseases. A 68-year-old woman with a diagnosis of hypertrophic obstructive cardiomyopathy was in functional class IV for angina and dyspnea despite 360 mg of propranolol a day. An echocardiogram and a complete cardiac catheterization were performed under betablocker therapy, confirming a severe hypertrophic obstructive cardiomyopathy and revealing severe stenosis in the proximal left circumflex and the proximal right coronary arteries, and a moderate lesion in the mid-left anterior descendent. They were both treated with balloon PTCA, and a 3 x 15 mm stent was placed in the circumflex and a 3.5 x 20 mm stent in the right coronary, with an excellent angiographic result. A basal hemodynamic study was then performed and A-V sequential pacing was attempted, achieving a significant decrease in the left ventricle outflow tract gradient. A DDD-R pacemaker was implanted. Echocardiographic study was performed post-implantation, and follow-up was made six months later with a new coronary angiography, hemodynamic study and a Doppler echocardiogram. At the present time A-V sequential pacing as a therapeutic option for hypertrophic obstructive cardiomyopathy and coronary angioplasty and stenting for the treatment of coronary artery disease are sufficiently established and supported to be offered as a combined therapy to patients suffering from both diseases, specially those with a higher surgical risk.
----P Case_Reports Journal_Article Review Review_of_Reported_Cases 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Cardiomyopathy__Hypertrophic_MeSH S_diagnosis_MeSH Cardiomyopathy__Hypertrophic_diagnosis_MeSH S_physiopathology_MeSH Cardiomyopathy__Hypertrophic_physiopathology_MeSH S_therapy_MeSH Cardiomyopathy__Hypertrophic_therapy_MeSH M_Combined_Modality_Therapy_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Echocardiography__Doppler_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Pacemaker__Artificial_MeSH M_Stents_MeSH 
****** 10371362
----K E
----T Atenolol and fetal growth in pregnancies complicated by hypertension.
----A Atenolol use may be associated with growth retardation when given in pregnancy, although the relationship to trimester of initiation, duration of treatment, and its use as monotherapy is still uncertain. To compare the obstetric and fetal outcome between women receiving atenolol (as monotherapy) and other antihypertensive drug monotherapies, and also to investigate the effect of duration of treatment on fetal growth, we performed a retrospective cohort study of 312 pregnancies in 223 women attending an Antenatal Hypertension Clinic. Atenolol (as monotherapy) was given in 78 pregnancies (25.0%), other types of antihypertensive drugs as monotherapy were given in 53 pregnancies (17.0%), and multiple drug combinations were given in 90 pregnancies (28.8%). In 91 pregnancies (29.2%) no antihypertensive drugs were given. Atenolol was found to be associated with lower birth weight and ponderal index values, with a trend toward a higher prevalence of preterm (<37 weeks) delivery and small-for-gestational-age babies when compared to other antihypertensive drugs as monotherapy, or to no treatment. The adverse effect of atenolol was more pronounced in women receiving the drug earlier in their pregnancy, and continuing the drug for a longer duration. In conclusion, atenolol should be avoided in the early stages of pregnancy and given with caution at the later stages, as it is associated with fetal growth retardation, which is related to duration of treatment.
----P Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Embryo_and_Fetal_Development_MeSH S_drug_effects_MeSH Embryo_and_Fetal_Development_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Infant__Newborn_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_drug_therapy_MeSH Pregnancy_Complications__Cardiovascular_drug_therapy_MeSH M_Pregnancy_Outcome_MeSH M_Retrospective_Studies_MeSH 
****** 10376609
----K I
----T Benefit of beta-blockers for heart failure: proven in 1999.
----A BACKGROUND: We have shown previously that lumpectomy with radiation therapy was more effective than lumpectomy alone for the treatment of ductal carcinoma in situ (DCIS). We did a double-blind randomised controlled trial to find out whether lumpectomy, radiation therapy, and tamoxifen was of more benefit than lumpectomy and radiation therapy alone for DCIS. METHODS: 1804 women with DCIS, including those whose resected sample margins were involved with tumour, were randomly assigned lumpectomy, radiation therapy (50 Gy), and placebo (n=902), or lumpectomy, radiation therapy, and tamoxifen (20 mg daily for 5 years, n=902). Median follow-up was 74 months (range 57-93). We compared annual event rates and cumulative probability of invasive or non-invasive ipsilateral and contralateral tumours over 5 years. FINDINGS: Women in the tamoxifen group had fewer breast-cancer events at 5 years than did those on placebo (8.2 vs 13.4%, p=0.0009). The cumulative incidence of all invasive breast-cancer events in the tamoxifen group was 4.1% at 5 years: 2.1% in the ipsilateral breast, 1.8% in the contralateral breast, and 0.2% at regional or distant sites. The risk of ipsilateral-breast cancer was lower in the tamoxifen group even when sample margins contained tumour and when DCIS was associated with comedonecrosis. INTERPRETATION: The combination of lumpectomy, radiation therapy, and tamoxifen was effective in the prevention of invasive cancer.
----P Comment Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH 
****** 10376614
----K I
----T Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)
----A BACKGROUND: Metoprolol can improve haemodynamics in chronic heart failure, but survival benefit has not been proven. We investigated whether metoprolol controlled release/extended release (CR/XL) once daily, in addition to standard therapy, would lower mortality in patients with decreased ejection fraction and symptoms of heart failure. METHODS: We enrolled 3991 patients with chronic heart failure in New York Heart Association (NYHA) functional class II-IV and with ejection fraction of 0.40 or less, stabilised with optimum standard therapy, in a double-blind randomised controlled study. Randomisation was preceded by a 2-week single-blind placebo run-in period. 1990 patients were randomly assigned metoprolol CR/XL 12.5 mg (NYHA III-IV) or 25.0 mg once daily (NYHA II) and 2001 were assigned placebo. The target dose was 200 mg once daily and doses were up-titrated over 8 weeks. Our primary endpoint was all-cause mortality, analysed by intention to treat. FINDINGS: The study was stopped early on the recommendation of the independent safety committee. Mean follow-up time was 1 year. All-cause mortality was lower in the metoprolol CR/XL group than in the placebo group (145 [7.2%, per patient-year of follow-up]) vs 217 deaths [11.0%], relative risk 0.66 [95% CI 0.53-0.81]; p=0.00009 or adjusted for interim analyses p=0.0062). There were fewer sudden deaths in the metoprolol CR/XL group than in the placebo group (79 vs 132, 0.59 [0.45-0.78]; p=0.0002) and deaths from worsening heart failure (30 vs 58, 0.51 [0.33-0.79]; p=0.0023). INTERPRETATION: Metoprolol CR/XL once daily in addition to optimum standard therapy improved survival. The drug was well tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Death__Sudden_MeSH M_Delayed-Action_Preparations_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 10376615
----K E
----T Optimisation of antihypertensive treatment by crossover rotation of four major classes.
----A BACKGROUND: Most comparisons of antihypertensive drugs are undertaken in parallel groups. We undertook a crossover rotation of the four main classes of antihypertensive drugs, in untreated young hypertensive patients, to assess the response rate with monotherapy achieved by a systematic rotation. METHODS: 56 patients, mean blood pressure 161/98 mm Hg, entered the rotation, of whom 36 received all four monthly cycles of treatment with an angiotensin-converting-enzyme (ACE) inhibitor (A), beta-blocker (B), calcium-channel blocker (C), and diuretic (D). Each patient's best drug was then repeated to assess repeatability. Two measures of individual variability in response were used. First, the value of rotation was measured by the increased proportion of patients reaching target blood pressure on their best drug versus their first drug. Second, we assessed whether the responses to each drug were correlated with each other. FINDINGS: Significant variability in response was found. 20 of the 41 patients reaching target blood pressure (< or =140/90 mm Hg) failed to achieve this target on their first drug. Rotation increased from 22/56 (39%) to 41/56 (73%) the success of monotherapy (p=0.0001); in half the patients, blood-pressure on the best treatment was 135/85 mm Hg or less. There were significant correlations between the blood pressure responses to A and B (r=0.5, p<0.01), and C and D (r=0.6, p<0.001), but not between the other four pairings of treatments. The responses to the AB pair were, on average, at least 50% higher than those to the CD pair; this difference was highly significant by multivariate repeated-measures ANOVA. INTERPRETATION: There is a marked variability in hypertensive patients' response to different antihypertensive drugs. The basis may be underlying variability in types of essential hypertension. Optimisation of treatment requires systematic rotation through several therapies; however, an "AB/CD" rule is proposed in which one of each of the two pairs of treatments is initially selected to abbreviate the rotation in routine practice.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Middle_Aged_MeSH 
****** 10376178
----K E
----T The effects of metoprolol and captopril on heart rate variability in patients with idiopathic dilated cardiomyopathy.
----A BACKGROUND: The effects of treatment with captopril or metoprolol on heart rate variability (HRV) were investigated in 38 patients (29 men and 9 women) with mild to moderate symptoms of heart failure due to idiopathic dilated cardiomyopathy (DCM). HYPOTHESIS: The aim of the study was to investigate and compare the effects of the angiotensin-converting enzyme inhibitor captopril with those of the selective beta-adrenergic receptor blocker metoprolol on HRV in patients with idiopathic DCM. METHODS: Heart rate variability was analyzed in the time and frequency domains from 18th of Holter monitoring before randomized treatment was started, after 6 months of therapy, and 1 month after therapy was stopped. RESULTS: Captopril treatment increased HRV expressed as total power and low-frequency power in the frequency domain. There was no change in the time domain. In the metoprolol group, there was a pronounced increase in both time- and frequency-domain indices of HRV. The increase in total power was partly maintained 1 month after therapy was stopped in both treatment groups. CONCLUSION: Treatment with captopril and metoprolol increases HRV in patients with DCM. This effect seems to be maintained for at least 1 month after therapy is stopped. The increase in HRV seems to be more pronounced with metoprolol, and the two different pharmacologic approaches may have additive effects that are of prognostic importance in patients with heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_pharmacology_MeSH Captopril_pharmacology_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH 
****** 10379634
----K E
----T The effect of four different antihypertensive medications on cardiovascular regulation in hypertensive sleep apneic patients--assessment by spectral analysis of heart rate and blood pressure variability.
----A OBJECTIVE: To study the effect of antihypertensive medications on autonomic nervous system in patients with hypertension and sleep apnea syndrome using frequency domain measures of heart rate and blood pressure variabilities. METHODS: The beta-receptor blocking agent atenolol (50 mg), the calcium antagonist isradipine SRO (2.5 mg), the diuretic hydrochlorothiazide (25 mg) and the ACE inhibitor spirapril (6 mg) once daily were given in a double-blind crossover schedule for 8 weeks. Cardiovascular autonomic control was assessed using frequency domain measures of heart rate variability during the spontaneous and controlled breathing tests. During orthostatic maneuver and cold pressor test the blood pressure variability analysis also was performed. RESULTS: In general, the responses of heart rate and blood pressure variabilities were abnormal in the patients with arterial hypertension and sleep apnea syndrome compared to reference data. Of the four drugs, only atenolol effected heart rate and blood pressure variabilities as it shifted the autonomic regulation to the vagal direction. Other antihypertensive drugs did not change any parameter of heart rate or blood pressure variabilities. CONCLUSION: The short-term treatment with atenolol in patients with arterial hypertension and sleep apnea syndrome is associated with normalization of autonomic nervous control judged by heart rate and blood pressure variability. Thus, beta-receptor blockade may have adjunctive beneficial effects beyond blood pressure reduction in these patients. However, the long-term effects of blood pressure reduction on autonomic nervous control remain to be studied.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Diuretics__Thiazide_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_analogs_&_derivatives_MeSH Enalapril_analogs_&_derivatives_MeSH S_pharmacology_MeSH Enalapril_pharmacology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Isradipine_MeSH S_pharmacology_MeSH Isradipine_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Sleep_Apnea_Syndromes_MeSH S_complications_MeSH Sleep_Apnea_Syndromes_complications_MeSH S_physiopathology_MeSH Sleep_Apnea_Syndromes_physiopathology_MeSH 
****** 10377294
----K E
----T Misuse of "coronary heart disease".
----A 
----P Editorial 
----M M_Coronary_Arteriosclerosis_MeSH S_classification_MeSH Coronary_Arteriosclerosis_classification_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH M_Coronary_Disease_MeSH S_classification_MeSH Coronary_Disease_classification_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH M_Human_MeSH M_Incidence_MeSH M_Myocardial_Ischemia_MeSH S_classification_MeSH Myocardial_Ischemia_classification_MeSH S_epidemiology_MeSH Myocardial_Ischemia_epidemiology_MeSH M_Support__Non-U_S__Gov't_MeSH P_Terminology_MeSH 
****** 10381708
----K I
----T beta Blockade after myocardial infarction: systematic review and meta regression analysis.
----A OBJECTIVES: To assess the effectiveness of beta blockers in short term treatment for acute myocardial infarction and in longer term secondary prevention; to examine predictive factors that may influence outcome and therefore choice of drug; and to examine the clinical importance of the results in the light of current treatment. DESIGN: Systematic review of randomised controlled trials. SETTING: Randomised controlled trials. SUBJECTS: Patients with acute or past myocardial infarction. Intervention: beta Blockers compared with control. MAIN OUTCOME MEASURES: All cause mortality and non-fatal reinfarction. RESULTS: Overall, 5477 of 54 234 patients (10.1%) randomised to beta blockers or control died. We identified a 23% reduction in the odds of death in long term trials (95% confidence interval 15% to 31%), but only a 4% reduction in the odds of death in short term trials (-8% to 15%). Meta regression in long term trials did not identify a significant reduction in effectiveness in drugs with cardioselectivity but did identify a near significant trend towards decreased benefit in drugs with intrinsic sympathomimetic activity. Most evidence is available for propranolol, timolol, and metoprolol. In long term trials, the number needed to treat for 2 years to avoid a death is 42, which compares favourably with other treatments for patients with acute or past myocardial infarction. CONCLUSIONS: beta Blockers are effective in long term secondary prevention after myocardial infarction, but they are underused in such cases and lead to avoidable mortality and morbidity.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Regression_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10382332
----K E
----T [An overview of hypertension studies with calcium antagonists]
----A Calcium antagonists are widely used in the treatment of hypertension. However, few endpoint studies with calcium antagonists have been done to prove reduction in hypertensive complications. Results of the STONE, SYST-EUR and SYST-CHINA studies show that long-acting calcium antagonists are effective compared to placebo, especially in patients with isolated systolic hypertension and diabetes. Ongoing prospective and randomized trials like STOP II, INSIGHT, NORDIL, ALLHAT and ASCOT will clarify whether calcium antagonists are more effective than well-proven diuretics and betablockers. ASCOT will test the hypothesis that amlodipine is more efficacious than atenolol in preventing cardiac complications in 18,000 hypertensive patients with high coronary risk including diabetes (among them, 2,000 in Norway). The study is also randomizing the patients in a factorial design to either atorvastatin or placebo, testing the so-called lipid hypothesis.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Controlled_Clinical_Trials_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_English_Abstract_MeSH M_Europe_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Multicenter_Studies_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10386477
----K E
----T The effect of ACE inhibitors on cardiovascular morbidity and mortality.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_complications_MeSH Cardiovascular_Diseases_complications_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Prospective_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Reproducibility_of_Results_MeSH 
****** 10385721
----K E
----T Use of color Doppler EUS in assessing azygos blood flow for patients with portal hypertension.
----A BACKGROUND: Azygos blood flow is an index of blood flow through gastroesophageal collateral vessels and varices in portal hypertension. Conventional measurement of azygos blood flow involves catheterization of the azygos vein. We studied the feasibility of assessing azygos blood flow with color Doppler endosonography and of monitoring the effects of vasoactive agents on azygos blood flow. METHODS: Patients with portal hypertension were examined by means of linear array color Doppler endoscopic ultrasonography (EUS). Patients who had taken propranolol or nitrates in the 4 weeks before the day of measurement of azygos blood flow were excluded. After identification of the azygos vein and recording of baseline readings of mean arterial blood pressure, pulse rate, and azygos blood flow, patients were selected in a random manner to receive a bolus injection of 2 mg terlipressin, 250 microg somatostatin, or saline solution (control). Azygos blood flow was measured 1, 5, and 10 minutes after injection (AzBF-1, AzBF-5, AzBF-10). RESULTS: Six patients were recruited in each treatment group. Basal azygos blood flow showed a positive association with the Child-Pugh grade of cirrhosis (p < 0.005). After bolus injection of terlipressin and somatostatin, there was a marked decrease in AzBF-1 (24% and 37%), AzBF-5 (42% and 19%), and AzBF-10 (40% both) compared with baseline. The control group showed no significant change in azygos blood flow. CONCLUSIONS: Color Doppler EUS is useful in assessing azygos blood flow in portal hypertension and in monitoring the effects of vasoactive agents.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_diagnostic_use_MeSH Antihypertensive_Agents_diagnostic_use_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Azygos_Vein_MeSH S_drug_effects_MeSH Azygos_Vein_drug_effects_MeSH S_physiopathology_MeSH Azygos_Vein_physiopathology_MeSH S_ultrasonography_MeSH Azygos_Vein_ultrasonography_MeSH M_Comparative_Study_MeSH P_Endosonography_MeSH S_drug_effects_MeSH Endosonography_drug_effects_MeSH S_instrumentation_MeSH Endosonography_instrumentation_MeSH S_methods_MeSH Endosonography_methods_MeSH S_statistics_&_numerical_data_MeSH Endosonography_statistics_&_numerical_data_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH S_ultrasonography_MeSH Hypertension__Portal_ultrasonography_MeSH M_Lypressin_MeSH S_analogs_&_derivatives_MeSH Lypressin_analogs_&_derivatives_MeSH S_diagnostic_use_MeSH Lypressin_diagnostic_use_MeSH S_pharmacology_MeSH Lypressin_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Somatostatin_MeSH S_diagnostic_use_MeSH Somatostatin_diagnostic_use_MeSH S_pharmacology_MeSH Somatostatin_pharmacology_MeSH M_Statistics__Nonparametric_MeSH M_Time_Factors_MeSH M_Ultrasonography__Doppler__Color_MeSH S_drug_effects_MeSH Ultrasonography__Doppler__Color_drug_effects_MeSH S_instrumentation_MeSH Ultrasonography__Doppler__Color_instrumentation_MeSH S_methods_MeSH Ultrasonography__Doppler__Color_methods_MeSH S_statistics_&_numerical_data_MeSH Ultrasonography__Doppler__Color_statistics_&_numerical_data_MeSH 
****** 10385642
----K E
----T Carvedilol, a new nonselective beta-blocker with intrinsic anti- Alpha1-adrenergic activity, has a greater portal hypotensive effect than propranolol in patients with cirrhosis.
----A Only some patients show a substantial hepatic venous pressure gradient (HVPG) reduction after propranolol, which makes it desirable to investigate drugs with greater portal hypotensive effect. The aim of this study was to investigate whether carvedilol, a nonselective beta-blocker with anti-alpha1-adrenergic activity, may cause a greater HVPG reduction than propranolol. Thirty-five cirrhotic patients had hemodynamic measurements before and after the random administration of carvedilol (n = 14), propranolol (n = 14), or placebo (n = 7). Carvedilol markedly reduced HVPG, from 19.5 +/- 1.3 to 15.4 +/- 1 mm Hg (P <.0001). This HVPG reduction was greater than after propranolol (-20.4 +/- 2 vs. -12.7 +/- 2%, P <.05). Moreover, carvedilol decreased HVPG greater than 20% of baseline values or to </=12 mm Hg in a greater proportion of patients (64% vs. 14%, P <.05). Both drugs caused similar reductions in hepatic and azygos blood flows, suggesting that the greater HVPG decrease by carvedilol was because of reduced hepatic and portocollateral resistance. Propranolol caused greater reductions in heart rate and cardiac output than carvedilol, whereas carvedilol caused a greater decrease in mean arterial pressure (-23.1 vs. -11%, P <.05). Thus, carvedilol has a greater portal hypotensive effect than propranolol in patients with cirrhosis, suggesting a greater therapeutic potential. However, it causes arterial hypotension, which calls for careful evaluation before its long-term use.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Portal_Pressure_MeSH S_drug_effects_MeSH Portal_Pressure_drug_effects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 10389533
----K 1
----T [Glycemic regulation and management of essential hypertension in diabetics with type 2 diabetes mellitus; the 'United Kingdom prospective diabetes study' of diabetic complications]
----A Patients with type 2 diabetes mellitus often develop micro- and macrovascular complications. In 25% of them, complications are already present at the time of diagnosis. The principal objective of the United Kingdom prospective diabetes study was to determine if good blood glucose control and adequate treatment of hypertension in patients with type 2 diabetes mellitus can prevent development of diabetes-related complications. The question was also studied if they way in which this blood glucose control was achieved and the way of treating the blood pressure affected the prognosis. Blood glucose control was found to reduce the incidence of--especially--microvascular complications. Oral hypoglycaemic agents and insulin both play an important part in achieving good control. Treatment with metformin reduced mortality due to cardiovascular disease in obese patients. Strict control of the blood pressure reduced development of micro- and macrovascular complications; the mortality from diabetes-related disorders and the numbers of patients suffering a stroke or heart failure. Non of the antihypertensive drugs used (an ACE inhibitor and a beta-blocking agent) offered any advantages over the other.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cerebral_Infarction_MeSH S_prevention_&_control_MeSH Cerebral_Infarction_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_mortality_MeSH Diabetes_Mellitus__Type_II_mortality_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Great_Britain_MeSH M_Human_MeSH M_Hyperglycemia_MeSH S_prevention_&_control_MeSH Hyperglycemia_prevention_&_control_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Insulin_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Male_MeSH M_Metformin_MeSH S_therapeutic_use_MeSH Metformin_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Peripheral_Vascular_Diseases_MeSH S_prevention_&_control_MeSH Peripheral_Vascular_Diseases_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Survival_Rate_MeSH 
****** 10392481
----K E
----T Impaired results of a randomised double blinded clinical trial of propranolol versus placebo on the expansion rate of small abdominal aortic aneurysms.
----A BACKGROUND: To study the propranolol treatment of small abdominal aortic aneurysms (AAA) concerning intention to treat, side effects, and inhibition of expansion. METHODS: DESIGN: Two-year lasting prospective randomised double-blinded intervention trial. SETTING: Hospital-based mass screening for AAA with annual ambulatory control of small AAA. PARTICIPANTS: Of 122 screening-diagnosed small AAA, 51 (42%) were excluded because of contraindications or present beta-blockage, and 17 refused participation. Thus, 54 (44.3%) were included. INTERVENTION: Participants were randomised to 40 mg propranolol twice a day or placebo. MEASURES: The same observed was used to follow-up AAA-expansion, side effects, quality of life (QL), branchial and ankle blood pressure (ABI), and pulmonary function (FEV1 and FVC). RESULTS: Sixty percent in the propranolol group, and 25% in the placebo group dropped out, mainly caused by dyspnoea in the propranolol group (RR=1.74, 95% C.I.: 1.06-2.86). Five (16.7%) died in the propranolol group, while 1 (4.2%) died in the placebo group (RR=1.6 (1.02-2.51)). Furthermore, decreased pulmonary function, ABI, and QL was noticed in the propranolol group. Consequently, the trial was stopped after two years. Ninety-five percent of the measurements of the AAA were measured within 2 mm variation. If expansion was defined as above 2 mm annually, the relative risk of expansion in the placebo group was 1.17 (0.74-1.85), and 2.44 (0.88-6.77) among the non-drop-outs. CONCLUSIONS: Only 22% of small screenings-diagnosed AAA were treatable with propranolol for two years. Consequently, only large scale studies are capable of showing potential minor inhibition of expansion by propranolol. However, whether such treatment ever becomes ethically acceptable is debatable.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aortic_Aneurysm__Abdominal_MeSH S_drug_therapy_MeSH Aortic_Aneurysm__Abdominal_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_Dyspnea_MeSH S_chemically_induced_MeSH Dyspnea_chemically_induced_MeSH M_Human_MeSH M_Male_MeSH M_Patient_Dropouts_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10394257
----K 1
----T Comparison of bisoprolol and verapamil in hypertension: influence on left ventricular mass and function--a pilot study.
----A The objective of this study was to test the influence of bisoprolol and verapamil on left ventricular filling in hypertensive patients in a 6 month randomized, double-blind trial in 54 hypertensive patients not previously treated with beta-blockers or calcium inhibitors. After administration of placebo for 14 days, an M echocardiogram of the left ventricle was recorded to determine left ventricular mass. Blood flow was evaluated by pulsed Doppler sonography. After randomization into two groups, one group received 10 mg of bisoprolol and the other 240 mg of verapamil LP in a single dose in the morning. After 2 months' treatment, the patients whose blood pressure was not well controlled were given a diuretic. Echo-Doppler was performed again by the same operator after 4-10 days on active treatment, after 6 months and after a subsequent 2 weeks of placebo for the patients treated with a single drug. The reduction in blood pressure was comparable in the two treated groups, but there was no significant decrease in left ventricular mass. Left ventricular filling was improved only in the patients receiving bisoprolol. The effect was observed immediately after the first administration and throughout the 6 months' treatment period declining slowly during the placebo wash-out. This effect appeared to be independent of any alteration in heart rate and was thought to be a specific action of this drug.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography__Doppler_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_pathology_MeSH Heart_Ventricles_pathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Pilot_Projects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10404854
----K I
----T Comparison of acebutolol with and without hydrochlorothiazide versus carvedilol with and without hydrochlorothiazide in black patients with mild to moderate systemic hypertension.
----A In the present study, we assessed the antihypertensive efficacy of acebutolol 200 mg versus carvedilol 25 mg once daily, given as monotherapy for 3 months to 40 black patients (20 patients in each group, mean age 53+/-10 years, 24 women) with mean blood pressure (BP) during the day >90 and <110 mm Hg. Patients in whom blood pressure could not be controlled took medication, which was increased at 3-month intervals as follows: step 2, acebutolol 200 mg or carvedilol 25 mg plus hydrochlorothiazide 12.5 mg once daily; step 3, acebutolol 400 mg or carvedilol 50 mg plus hydrochlorothiazide 25 mg once daily. Overall, significant but modest BP reduction was achieved with both beta blockers at 3 months. In the acebutolol group, 24-hour BP decreased from 142+/-15/94+/-7 mm Hg to 138+/-16/89+/-8 mm Hg (p<0.005 for diastolic BP at 3 months vs baseline). Mean day BP decreased from 145+/-15/98+/-5 mm Hg to 140+/-14/93+/-7 mm Hg (p<0.05 for systolic BP and p<0.0005 for diastolic BP at 3 months vs. baseline). In the carvedilol group, 24-hour BP decreased from 145+/-11/93+/-6 to 138+/-16/87+/-9 mm Hg (p<0.05 for systolic BP and p<0.005 for diastolic BP at 3 months vs baseline). Mean day BP decreased from 149+/-10/99+/-5 to 141+/-16/91+/-87 mm Hg (p<0.05 for systolic BP and p<0.0005 for diastolic BP at 3 months vs baseline). At 12 months, most patients required combination therapy to achieve BP control. The control (mean day diastolic BP <90 mm Hg) and response (mean day diastolic BP decrease > or =10 mm Hg) rates at 12 months were 59% and 82% in the acebutolol and 78% and 78% in the carvedilol groups, respectively. In conclusion, acebutolol or carvedilol in combination with hydrochlorothiazide, rather than acebutolol or carvedilol alone, should be considered as first-line antihypertensive therapy in black patients with mild to moderate hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acebutolol_MeSH S_therapeutic_use_MeSH Acebutolol_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_African_Continental_Ancestry_Group_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH 
****** 10404924
----K E
----T The treatment and prevention of coronary heart disease in Canada: do older patients receive efficacious therapies? The Clinical Quality Improvement Network (CQIN) Investigators.
----A OBJECTIVES: To review the evidence for clinical efficacy and cost-effectiveness of proven medications in the treatment and prevention of myocardial infarction (MI) in older patients; to summarize Canadian data on treatment patterns and clinical outcomes for younger and older patients with coronary heart disease; to explore the reasons for gaps between best care, based on the evidence of efficacy from trials, and usual care, based on the population effectiveness audits; and to explore potential approaches to closing the care gaps. DESIGN: Review of the recent clinical trial literature on the management of MI, highlighting results in older patients. Review of medication utilization and outcomes data from a series of large, consecutively enrolled patient cohorts with acute MI (N = 7070) in a variety of cardiac care settings (10 centers in five Canadian provinces, including university-based teaching hospitals, community hospitals, cardiologist and family physician out-patient clinics) from 1987 to 1996. RESULTS: There is no qualitative interaction of cardiac therapies: thrombolytics, beta-blockers, acetylsalicylic acid (ASA), and statins are efficacious in all clinically relevant patient subgroups, including older people. However, there are consistent gaps between usual care and best care, particularly among older patients (in whom there is also a concomitantly higher mortality risk). Repeated multivariate analyses confirm older age to be an independent contributor to increased risk. Use of efficacious medications is, in contrast, consistently associated with increased survival. Analysis of temporal trends suggests beneficial changes in practice patterns and outcomes are possible to achieve. However, "best care" has not been rapidly or completely achieved. Review of strategies to close these care gaps suggests that audit and feedback, critical pathways, and multifactorial interventions involving patients and other members of the healthcare team as well as physicians may be the most efficacious strategies for change. CONCLUSIONS: Despite equal or enhanced efficacy, there is consistently less prescription of proven drugs among older cardiac patients. These care patterns may contribute to their enhanced risk. The causes underlying these practice patterns are complex, and their population impact may be undervalued by clinicians and managers. Improvement of these patterns is difficult, but ultimately it would be beneficial for this presently disadvantaged, readily identified, high risk patient population.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Benchmarking_MeSH M_Canada_MeSH S_epidemiology_MeSH Canada_epidemiology_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_mortality_MeSH Coronary_Disease_mortality_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Cost-Benefit_Analysis_MeSH M_Evidence-Based_Medicine_MeSH M_Health_Services_for_the_Aged_MeSH S_standards_MeSH Health_Services_for_the_Aged_standards_MeSH M_Human_MeSH M_Multivariate_Analysis_MeSH M_Physician's_Practice_Patterns_MeSH S_economics_MeSH Physician's_Practice_Patterns_economics_MeSH S_standards_MeSH Physician's_Practice_Patterns_standards_MeSH P_Quality_of_Health_Care_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10404937
----K I
----T Management of the older person with ventricular arrhythmias.
----A OBJECTIVE: To review the prognosis and management of ventricular arrhythmias (VA) in persons with and without heart disease, with emphasis on older adults. DATA SOURCES: A computer-assisted search of the English language literature (MEDLINE database) followed by a manual search of the bibliographies of pertinent articles. STUDY SELECTION: Studies on the prognosis and management of VA in persons with and without heart disease were screened for review. Studies in older persons and recent studies were emphasized. DATA EXTRACTION: Pertinent data were extracted from the reviewed articles. Emphasis was placed on studies involving older persons. Relevant articles were reviewed in depth. DATA SYNTHESIS: Available data on the prognosis and management of VA in persons with and without heart disease, with emphasis on studies in older persons, were summarized. CONCLUSIONS: Ventricular arrhythmias in older persons without heart disease should not be treated with antiarrhythmic drugs, nor should Class I antiarrhythmic drugs be used to treat VA in older persons with heart disease. Beta-blockers should be used to treat complex VA in older persons with ischemic or nonischemic heart disease without contraindications to beta-blockers. Amiodarone should be reserved for life-threatening ventricular tachyarrhythmias in older persons who cannot tolerate or who do not respond to beta-blockers. Angiotensin-converting enzyme inhibitors should be used to treat older persons with heart failure, an anterior myocardial infarction, or a left ventricular ejection fraction < or = 40%. If older persons have life-threatening recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) resistant to antiarrhythmic drugs, invasive intervention should be performed. The automatic implantable cardioverter-defibrillator is recommended in older persons who have medically refractory sustained VT or VF.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_classification_MeSH Anti-Arrhythmia_Agents_classification_MeSH S_contraindications_MeSH Anti-Arrhythmia_Agents_contraindications_MeSH M_Defibrillators__Implantable_MeSH M_Electrocardiography_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH M_Human_MeSH P_Patient_Selection_MeSH M_Prevalence_MeSH M_Prognosis_MeSH M_Tachycardia__Ventricular_MeSH S_diagnosis_MeSH Tachycardia__Ventricular_diagnosis_MeSH S_drug_therapy_MeSH Tachycardia__Ventricular_drug_therapy_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH S_mortality_MeSH Tachycardia__Ventricular_mortality_MeSH M_Treatment_Outcome_MeSH 
****** 10404354
----K E
----T Effects of losartan versus captopril on mortality in patients with symptomatic heart failure: rationale, design, and baseline characteristics of patients in the Losartan Heart Failure Survival Study--ELITE II.
----A BACKGROUND: In the Evaluation of Losartan in the Elderly (ELITE) heart failure study, a survival benefit (primarily because of a reduction in sudden deaths) was observed in symptomatic patients treated with losartan compared with captopril. METHODS AND RESULTS: The Losartan Heart Failure Survival Study--ELITE II (currently ongoing) is a double-blind, randomized clinical trial being conducted in 45 countries at 288 sites. ELITE II formally tests the hypotheses that losartan, compared with captopril, will reduce all-cause mortality (primary end point) and sudden cardiac death and/or resuscitated cardiac arrest (secondary end point). In addition, all-cause mortality and/or hospitalizations and cardiovascular mortality and/or hospitalizations will be evaluated. The trial has 90% power to detect a 25% treatment difference in all-cause mortality (event driven, 510 deaths). Substudies are examining quality of life, health care resource utilization, and mechanisms related to the reduction in sudden death. During recruitment (June 1997 to May 1998), 3,152 patients aged 60 years or older (mean age, 71.6 years), with New York Heart Association classes II (51%), III (44%), and IV (5%), and left ventricular ejection fraction of 40% or less (mean, 31%) were randomized to receive either 12.5 mg of losartan, titrated as tolerated to 50 mg once daily, or 12.5 mg of captopril, titrated as tolerated to 50 mg thrice daily. Randomization was stratified by clinical site and for baseline beta-blocker use. CONCLUSION: The ELITE II study will further define the role of losartan in the treatment of patients with symptomatic heart failure relative to the angiotensin-converting enzyme inhibitor captopril, an agent from a class currently considered standard treatment for this disease.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH P_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Research_Design_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 10406816
----K E
----T Association of the G(s)alpha gene with essential hypertension and response to beta-blockade.
----A We examined whether the GNAS1 locus, encoding the G(s) protein alpha-subunit (G(s)alpha), is implicated in the genetic causes of essential hypertension. A common silent polymorphism (ATT-->ATC, Ile(131)) was identified in exon 5 of the G(s)alpha gene by single-strand conformation polymorphism analysis and DNA sequencing. This polymorphism consists of the presence (+) or absence (-) of a restriction site for FokI. Only 1 other rare allele was found in the coding region; the high GC content of the 5' noncoding sequence prevented mutation scanning of the promoter region of the gene. There was a significant difference in frequency of the FokI alleles between 268 white hypertensives (FokI+:FokI-, 51%:49%) and a matched group of 231 control subjects (FokI+:FokI-, 58%:42%) (P=0.02). Multiple regression analysis showed that the FokI genotype was independently related to the level of untreated systolic blood pressure in 294 well-characterized white hypertensives (P=0.01) but not in normotensives. The influence of the FokI allele on blood pressure (BP) response to beta-blockade was examined in 114 of the patients randomly assigned to this class of drug. Significant differences in frequency of the FokI allele were observed in the good responders (FokI+:FokI-, 62.5%:37.5%, n=36) versus the poor responders (FokI+:FokI-, 41.7%:58.3%, n=30) after beta-blocker therapy (P=0.02). In a multiple regression analysis, the G(s)alpha genotype was the only independent predictor of BP response. These results suggest that the GNAS1 locus might carry a functional variant that influences BP variation and response to beta-blockade in essential hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cohort_Studies_MeSH M_Exons_MeSH S_genetics_MeSH Exons_genetics_MeSH M_Female_MeSH M_GTP-Binding_Protein_alpha_Subunits__Gs_MeSH S_genetics_MeSH GTP-Binding_Protein_alpha_Subunits__Gs_genetics_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Polymorphism__Single-Stranded_Conformational_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10411364
----K E
----T Effect of hypertension and its treatment on lipid, lipoprotein(a), fibrinogen, and bilirubin levels in patients referred for dyslipidemia.
----A We measured the serum lipid profile, together with plasma fibrinogen and serum lipoprotein(a) (Lp[a]), glucose, bilirubin, and albumin levels in 491 patients (310 men) who were referred for the management of primary dyslipidemia. All these variables have been shown to predict vascular events. The patients were not taking lipid-lowering drugs; hypertension was present in 156 (31.7%) of them. Of the hypertensive patients, 52 (33%) were not receiving any treatment to control their blood pressure. This omission was not due to a lower prevalence of established vascular disease. The treated hypertensives were divided into three groups according to their treatment: 62 were taking lipid-hostile antihypertensives (beta-blockers, thiazides), 37 were taking lipid-neutral antihypertensives (angiotensin converting enzyme inhibitors, Ca-channel blockers, angiotensin II receptor blockers, indapamide sustained release), and five were taking lipid-friendly antihypertensives (doxazosin). Lipid-hostile antihypertensive drugs were associated with a significantly higher fibrinogen concentration when compared with untreated hypertensives or those taking lipid-neutral/lipid-friendly drugs (median values: 383, 353, and 336 mg/dL, respectively; P < .01). Lipid-neutral/lipid-friendly antihypertensive drugs were associated with lower Lp(a) levels when compared with untreated hypertensives (median values: 22 and 45 mg/dL, respectively; P < .05). The serum bilirubin level was significantly lower in the untreated hypertensives when compared with normotensives or the treated hypertensives. There were no significant differences in lipids, glucose, or albumin among the groups of hypertensives or normotensives. The influence of antihypertensive drugs on additional cardiovascular risk factors should be considered when selecting medication to reduce blood pressure.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bilirubin_MeSH S_blood_MeSH Bilirubin_blood_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Fibrinogen_MeSH S_metabolism_MeSH Fibrinogen_metabolism_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_blood_MeSH Hyperlipidemia_blood_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoprotein(a)_MeSH S_blood_MeSH Lipoprotein(a)_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Prognosis_MeSH M_Referral_and_Consultation_MeSH M_Retrospective_Studies_MeSH M_Risk_Factors_MeSH M_Serum_Albumin_MeSH S_metabolism_MeSH Serum_Albumin_metabolism_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH 
****** 10412878
----K E
----T Skeletal muscle angiotensin-converting enzyme and its relationship to blood pressure in primary hypertension and healthy elderly men.
----A The aim of this study was to investigate the relationships between angiotensin-converting enzyme (ACE) activity in serum and skeletal muscle to blood pressure and the long-term antihypertensive effects of fosinopril and atenolol. We examined 50 hypertensive patients randomized to receive 20 mg fosinopril or 50 mg atenolol daily for 16 weeks. ACE activity was measured in biopsy specimens from skeletal muscle. Measurements of office and ambulatory blood pressure, serum ACE, and left ventricular wall thickness were also performed. The same investigations were performed in a cross-sectional study of 50 healthy elderly men. Muscle ACE correlated inversely to blood pressure in cross-sectional analyses in both populations (p < 0.05). During atenolol treatment muscle ACE activity tended to increase (14%, p = 0.059), and this increase correlated inversely to the changes in standing systolic and diastolic blood pressure (r = -0.62, p = 0.0044, and r = 0.54, p = 0.016, respectively). Muscle ACE was also inversely correlated to left ventricular wall thickness when the two populations were pooled (r =-0.29, p = 0.0053). In the fosinopril group, muscle ACE activity was not different during treatment than at baseline (-2. 1%, p = 0.68). The inverse relationship between blood pressure and muscle ACE levels in this study indicate that muscle tissue ACE levels are influenced by haemodynamic factors in humans.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Cross-Sectional_Studies_MeSH M_Double-Blind_Method_MeSH M_Feedback_MeSH M_Female_MeSH M_Fosinopril_MeSH S_therapeutic_use_MeSH Fosinopril_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Muscle__Skeletal_MeSH S_enzymology_MeSH Muscle__Skeletal_enzymology_MeSH M_Peptidyl-Dipeptidase_A_MeSH S_blood_MeSH Peptidyl-Dipeptidase_A_blood_MeSH S_metabolism_MeSH Peptidyl-Dipeptidase_A_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10409530
----K I
----T An open label, randomised, crossover study comparing sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation.
----A OBJECTIVE: To compare sotalol and atenolol in the treatment of symptomatic paroxysmal atrial fibrillation. DESIGN: Prospective, randomised, open label, crossover study. SETTING: University hospital. PATIENTS: 47 subjects aged over 50 years were recruited from the hospital outpatient department following ECG documentation of paroxysmal atrial fibrillation that coincided with symptoms. Six patients withdrew and 41 completed the trial. INTERVENTIONS: Patients were randomised to one month's treatment with sotalol 80 mg twice daily or atenolol 50 mg once daily. Treatment arms were then crossed over. Patients underwent 72 hour Holter monitoring before randomisation and repeat studies were carried out at the end of both treatment periods. Symptom assessments were completed using linear analogue scales and the Nottingham health profile. MAIN OUTCOME MEASURE: Frequency of paroxysmal atrial fibrillation; secondary outcome measures included average and total duration of paroxysmal atrial fibrillation, total ectopic count, and symptom assessments. RESULTS: A reduction in the number and duration of episodes of paroxysmal atrial fibrillation was noted following treatment with sotalol and atenolol. There was no difference in frequency of paroxysmal atrial fibrillation during treatment with sotalol or atenolol (median difference 0; 95% confidence interval (CI) 0 to 1; p = 0.47). There was no difference in total duration of paroxysmal atrial fibrillation (median difference 0 min; 95% CI -1 to 2; p = 0. 51) or in average duration (median difference 0 min; 95% CI 0 to 1; p = 0.31). No difference was found in total ectopic count between sotalol and atenolol (median difference -123; 95% CI -362 to 135; p = 0.14). Treatments were equally tolerated with no difference in linear analogue scores for symptoms of paroxysmal atrial fibrillation (median difference -5; 95% CI -20 to 5; p = 0.26) or in all categories of the Nottingham health profile. CONCLUSIONS: No difference was found in terms of ECG or symptomatic control of paroxysmal atrial fibrillation between prescribing sotalol 80 mg twice daily and atenolol 50 mg once daily. There was an improvement in paroxysmal atrial fibrillation from baseline following treatment with either sotalol or atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Administration_Schedule_MeSH M_Electrocardiography__Ambulatory_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_administration_&_dosage_MeSH Sotalol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH 
****** 10411851
----K E
----T Role of bradykinin in the vasodilator effects of losartan and enalapril in patients with heart failure.
----A BACKGROUND: ACE inhibitors have been shown to potentiate the effects of exogenous bradykinin by inhibition of its breakdown. Despite this, there is little evidence that inhibition of endogenous bradykinin breakdown actually contributes to the effects of ACE inhibitors, or indeed, other inhibitors of the renin-angiotensin system, such as angiotensin II type I receptor (AT(1)) antagonists, and no evidence at all that it does so in patients with heart failure. METHODS AND RESULTS: Twelve patients with heart failure (11 male, 1 female, ages 59 to 81 years) were randomized to double-blind crossover treatment with enalapril 10 mg BID followed by losartan 25 mg BID, or the reverse, each for 5 weeks. At the end of each treatment period, forearm blood flow was measured by venous occlusion plethysmography during an intrabrachial infusion of bradykinin before and after an intrabrachial infusion of Hoe-140 (a potent, selective, and long-acting bradykinin antagonist). Bradykinin caused profound vasodilatation after enalapril (peak, 357+/-67%) and less after losartan (peak, 230+/-46%). Despite this, Hoe-140 had no discernible effects after enalapril or losartan. Similarly, this was despite the finding that Hoe-140 significantly reduced vasodilatation to bradykinin after enalapril (peak, 192+/-35%) and losartan (peak, 66+/-13%). CONCLUSIONS: Inhibition of endogenous bradykinin breakdown does not appear to contribute to the effects of ACE inhibition or AT(1) antagonism in the forearm of patients with heart failure at rest, despite the very obvious effects of ACE inhibition compared with AT(1) antagonism on exogenous bradykinin.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Bradykinin_MeSH S_analogs_&_derivatives_MeSH Bradykinin_analogs_&_derivatives_MeSH S_antagonists_&_inhibitors_MeSH Bradykinin_antagonists_&_inhibitors_MeSH S_pharmacology_MeSH Bradykinin_pharmacology_MeSH S_therapeutic_use_MeSH Bradykinin_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Interactions_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10385769
----K E
----T Insights into the contemporary epidemiology and outpatient management of congestive heart failure.
----A OBJECTIVES: To evaluate the epidemiology, prognosis, and patterns of practice in patients with chronic congestive heart failure (CHF) treated and followed at a specialized clinic. METHODS: Prospective cohort study of consecutive patients referred to and followed up in a specialized heart failure clinic between September 1989 and March 1996. RESULTS: Of the 628 patients referred, 566 were confirmed to have CHF. Mean duration of follow-up was 518 +/- 490 days (range 1 to 2192 days). Vital status was available for 99.3% of patients. Mean age at enrollment was 66 years, 68% were men, 67% had an ischemic cause of heart disease, and 78% had systolic dysfunction. Patients with preserved systolic function were older, more often female, had higher mean systolic blood pressures, and a lower prevalence of ischemic heart disease, ventricular arrhythmias, or impaired renal function when compared with those with systolic dysfunction (all P </=.001). Although there was a significant negative trend in survival with decreasing ejection fraction (P =. 03), the survival experience of those with CHF and preserved systolic function did not significantly differ from those with systolic failure (P =.25). Multiple logistic regression analysis showed increased mortality risk was associated with increasing age, New York Heart Association class IV, ischemic cause of disease, elevated serum creatinine level, use of diuretics, and systolic dysfunction, whereas use of beta-blockers was associated with reduced risk. CONCLUSIONS: Our data suggest that a specialized outpatient clinic can improve practice patterns in patients with CHF. The high mortality risk in CHF with preserved systolic function suggests the need to find efficacious (and effective) therapies for this condition.
----P Journal_Article 
----M M_Aged_MeSH M_Ambulatory_Care_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Confounding_Factors_(Epidemiology)_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Prospective_Studies_MeSH M_Risk_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 10413638
----K E
----T Factors associated with failure of medical therapy in patients with unstable angina and non-Q wave myocardial infarction. A TIMI-IIIB database study.
----A CONTEXT: Current management of patients with unstable angina and non-Q wave myocardial infarction generally consists of intensive medical therapy, with angiography and revascularization sometimes limited to those who fail such therapy. AIM: To determine if certain baseline characteristics are predictive of patients who fail medical therapy, since such patients could then be expeditiously directed to a more invasive strategy in a cost-effective manner. METHODS: The study cohort consisted of the 733 patients in the Thrombolysis in Myocardial Ischemia (TIMI) IIIB study who were randomized to conservative strategy. Patients were to be treated with bedrest, anti-ischaemic medications, aspirin, and heparin, and were to undergo risk-stratifying tests, consisting of an exercise test with ECG and thallium scintigraphy, scheduled to be performed within 3 days prior to, or 5 days after, hospital discharge and 24 h Holter monitoring scheduled to begin 2-5 days after randomization. Baseline clinical and ECG characteristics were compared between patients who 'failed' medical therapy and those who did not 'fail'. Failure was defined using clinical end-points (death, myocardial infarction, or spontaneous ischaemia by 6 weeks after randomization) or a strongly positive risk-stratifying test. For each test an ordered failure profile of results was calculated and consisted of death, myocardial infarction, or rest ischaemia occurring prior to performance of the test, a markedly abnormal test result, and no abnormality. RESULTS: Clinical end-points occurred in 241 (33%) patients and were more likely to occur in patients who at presentation were older, had ST-segment depression on the qualifying ECG, or were being treated with heparin or aspirin. Characteristics independently predictive of developing a clinical event or an abnormal exercise treadmill test included: ST-segment depression on the qualifying ECG, history of prior angina, family history of premature coronary disease (i.e. onset <55 years of age), prior use of heparin or aspirin, and increasing age. By combining these baseline risk characteristics for each outcome the incidence of developing a clinical event ranged from 8% if none was present to 63% if all six were present, and of developing a markedly abnormal risk stratifying test from 8-21% if none were present to approximately 90% if all six were present. CONCLUSIONS: Baseline characteristics associated with developing a clinical event or a markedly abnormal risk stratifying test were similar: rest anginal episode accompanied by ST-segment depression and occurring despite treatment with aspirin and heparin, a history of angina, older age, and family history of coronary disease. Patients with these characteristics are appropriate candidates for expeditious cardiac catheterization and consideration for revascularization, while patients without them may be suitable for medical management alone.
----P Journal_Article 
----M M_Aged_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Cohort_Studies_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH P_Patient_Selection_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Thallium_Radioisotopes_MeSH S_diagnostic_use_MeSH Thallium_Radioisotopes_diagnostic_use_MeSH M_Treatment_Failure_MeSH 
****** 10419077
----K E
----T Ambulatory 24-h blood pressure assessment of the felodipine-metoprolol combination versus amlodipine in mild to moderate hypertension. Lorraine General Physician Investigators Group.
----A OBJECTIVE: To measure the time effect profiles of a once daily administered combination tablet felodipine-metoprolol 5/50 mg (Logimax, Astra) and amlodipine 5 mg (Norvasc, Pfizer) on blood pressure and heart rate using 24-h ambulatory blood pressure monitoring. DESIGN: Randomized multicentre parallel-group study with a single-blind placebo run-in period of 4 weeks duration and a 6-week double-blind active treatment period. PATIENTS AND METHODS: Out of 245 randomized outpatients (90 men, 155 women) with uncomplicated mild-to-moderate primary hypertension and mean sitting diastolic blood pressure (DBP) 95-115 mmHg inclusive, 212 (102 on felodipine-metoprolol, 110 on amlodipine) were eligible for analysis. 24-h ambulatory blood pressure monitoring was performed at the end of the placebo run-in (baseline) and after 6 weeks active treatment (posttreatment). RESULTS: Both felodipine-metoprolol and amlodipine induced smooth and consistent reduction in DBP and systolic blood pressure throughout the 24-h period, hence not altering the diurnal rhythm. However, felodipine-metoprolol reduced all average blood pressures (24-h, day- and night-time) more than amlodipine (for 24-h average blood pressure 14.4/9.5 mmHg and 8.9/5.5 mmHg, respectively). Medians of individual diastolic trough-to-peak (T/P) ratios were similar for felodipine-metoprolol and amlodipine (54 and 50%, respectively), while for the systolic T/P ratios, the corresponding values were 74 and 35%, repectively; no significant difference between treatments was seen. As distinguished from amlodipine, both heart rate and rate pressure product were markedly decreased on felodipine-metoprolol throughout the 24-h period and even during the early morning hours. In general, both treatments were well tolerated. CONCLUSIONS: Both felodipine-metoprolol and amlodipine achieved optimal control of blood pressure during the inter-dosing interval in line with their pharmokinetic profiles. The vasodilatory adverse events were slightly more reported with felodipine-metoprolol combination, but due to more pronounced lowering of the average blood pressures and the potent additional effect on heart rate and rate pressure product, the efficacy/tolerability balance seems to be equal to or better than that obtained with monotherapy such as amlodipine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Drug_Therapy__Combination_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10420860
----K E
----T Systematic review of antihypertensive therapies: does the evidence assist in choosing a first-line drug?
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10424315
----K E
----T No cardiovascular effects of single-dose pseudoephedrine in patients with essential hypertension treated with beta-blockers.
----A OBJECTIVE: The use of the decongestant pseudoephedrine has been cautioned in patients with arterial hypertension, due to the possible rise in blood pressure induced by the sympathostimulatory properties of the drug. This effect could be enhanced in hypertensives treated with beta-blockers, in whom the vasoconstrictor effect of alpha-adrenergic stimulation is unbalanced. The purpose of this study was to investigate the cardiovascular response to pseudoephedrine in hypertensive patients treated with different types of beta-blockers. METHODS: We recruited 29 (18 males) mild-to-moderate essential hypertensive patients [mean age 49(2) years] in a randomized, placebo-controlled, crossover trial. All participants received either placebo, or a nonselective (propranolol 160 mg once daily) or a selective (atenolol 100 mg once daily) beta-blocker for 1 week. At the end of each period, all patients received a single oral dose of pseudoephedrine (60 mg) and their blood pressure and heart rate were monitored at repeated intervals for 2 h. RESULTS: After 1 week of propranolol or atenolol, patients had significantly lower systolic blood pressure and heart rate than after placebo, whereas diastolic blood pressure was not significantly modified. The acute administration of pseudoephedrine did not change systolic and diastolic blood pressure and heart rate from baseline at the end of any of the treatment periods. CONCLUSIONS: A standard oral dose of pseudoephedrine does not significantly affect blood pressure values in hypertensive patients treated with beta-blockers, and therefore may be safely used in this subset of patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Ephedrine_MeSH S_adverse_effects_MeSH Ephedrine_adverse_effects_MeSH S_therapeutic_use_MeSH Ephedrine_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Vasoconstrictor_Agents_MeSH S_adverse_effects_MeSH Vasoconstrictor_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 10423656
----K E
----T Metabolic and antihypertensive effects of nebivolol and atenolol in normometabolic patients with mild-to-moderate hypertension.
----A This was a double-blind, randomized, two-center, active-controlled, prospective, parallel study designed to evaluate the effects of nebivolol at daily doses of 5 mg on lipid and carbohydrate metabolism and on blood pressure in comparison with atenolol at daily doses of 50 mg. Normometabolic subjects with mild-to-moderate essential hypertension were recruited for this study, which included a 4-week, single-blind placebo washout phase and a 12-week double-blind treatment phase. After 12 weeks of treatment, both drugs demonstrated a significant decrease from baseline in high-density lipoprotein (HDL) apolipoprotein A-I (HDL-apoA-I) (nebivolol, P <.02; atenolol, P <.05). A significant reduction in HDL cholesterol (HDL-C) from baseline was also observed with nebivolol (P <.05). There were no significant differences between the drugs for these parameters, and the ratio low-density lipoprotein cholesterol (LDL-C)-to-HDL-C did not change significantly after 12 weeks of active treatment with nebivolol or atenolol. There were no significant changes in total cholesterol, HDL (2) -C, HDL (3) -C, LDL-C, very-low-density lipoprotein cholesterol (VLDL-C), total triglycerides, HDL-triglycerides (TG), LDL-TG, VLDL-TG, total apoB, LDL-B, VLDL-B (including the ratio LDL-C-to-LDL-apoB), or Lp(a) during treatment with both drugs. No significant differences in plasma apoA-I and apoC-III as well as in apoA-I-, C-III-containing lipoprotein particles (including the apoC-III ratio) were observed between the drugs, neither before nor after each active treatment. There were no significant differences between the drugs or within each treatment group in plasma glucose, insulin, or C-peptide concentrations after a 2-hour oral glucose tolerance test. Mean clinic trough sitting systolic blood pressure (SBP)/diastolic blood pressure (DBP) significantly decreased from 150/98 mm Hg at baseline to 141/90 mm Hg at termination for nebivolol and from 160/99 mm Hg at baseline to 145/88 mm Hg at termination for atenolol. No significant between-treatment differences were observed for the mean clinic trough sitting SBP/DBP. Both drugs significantly increased the atrial natriuretic factor (ANF) N-terminal plasma levels, whereas no changes were observed in ANF C-terminal plasma concentrations. A significant decrease (P <. 05) in the plasma adrenocorticotropic hormone levels was observed after administration of both drugs. A significant decrease (P <.05) in plasma cortisol levels was observed only after atenolol treatment. The incidence of adverse events reported during nebivolol treatment was comparable to that observed during atenolol treatment. Heart rate was significantly reduced by both drugs. There were no significant changes in hematology, biochemistry, or urinalysis studies. Neither nebivolol nor atenolol adversely affected lipid or carbohydrate metabolism in normometabolic hypertensive patients. Both treatments demonstrated adequate and similar antihypertensive effects and were well tolerated.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Benzopyrans_MeSH S_administration_&_dosage_MeSH Benzopyrans_administration_&_dosage_MeSH S_adverse_effects_MeSH Benzopyrans_adverse_effects_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Corticotropin_MeSH S_blood_MeSH Corticotropin_blood_MeSH M_Double-Blind_Method_MeSH M_Ethanolamines_MeSH S_administration_&_dosage_MeSH Ethanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Ethanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrocortisone_MeSH S_blood_MeSH Hydrocortisone_blood_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Time_Factors_MeSH 
****** 10427351
----K E
----T Profiles of 5-HT 1B/1D agonists in acute migraine with special reference to second generation agents.
----A The efficacy of 5-hydroxytryptamine 1B/1D (5-HT 1B/1D) agonists is related to their inhibitory effects on neurogenic inflammation, mediated through serotoninergic control mechanisms. Recently, a series of oral second generation 5-HT 1B/1D agonists (eletriptan, naratriptan, rizatriptan and zolmitriptan) have been developed and are reviewed in this paper. Their in vitro and in vivo pharmacological properties, clinical efficacy, drug interactions, and adverse effects are evaluated and compared to the gold standard in the treatment of acute migraine, sumatriptan.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Animals_MeSH M_Clinical_Trials_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH M_Coronary_Vasospasm_MeSH S_chemically_induced_MeSH Coronary_Vasospasm_chemically_induced_MeSH M_Drug_Design_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Indoles_MeSH S_adverse_effects_MeSH Indoles_adverse_effects_MeSH S_chemistry_MeSH Indoles_chemistry_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Meninges_MeSH S_blood_supply_MeSH Meninges_blood_supply_MeSH M_Metabolic_Detoxication__Drug_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH M_Molecular_Structure_MeSH M_Nociceptors_MeSH S_physiology_MeSH Nociceptors_physiology_MeSH M_Oxazoles_MeSH S_adverse_effects_MeSH Oxazoles_adverse_effects_MeSH S_chemistry_MeSH Oxazoles_chemistry_MeSH S_therapeutic_use_MeSH Oxazoles_therapeutic_use_MeSH P_Oxazolidinones_MeSH M_Piperidines_MeSH S_adverse_effects_MeSH Piperidines_adverse_effects_MeSH S_chemistry_MeSH Piperidines_chemistry_MeSH S_therapeutic_use_MeSH Piperidines_therapeutic_use_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Pyrrolidines_MeSH S_adverse_effects_MeSH Pyrrolidines_adverse_effects_MeSH S_chemistry_MeSH Pyrrolidines_chemistry_MeSH S_therapeutic_use_MeSH Pyrrolidines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Rats_MeSH M_Receptor__Serotonin__5-HT1B_MeSH M_Receptor__Serotonin__5-HT1D_MeSH M_Receptors__Serotonin_MeSH S_drug_effects_MeSH Receptors__Serotonin_drug_effects_MeSH S_physiology_MeSH Receptors__Serotonin_physiology_MeSH M_Recurrence_MeSH M_Serotonin_Agonists_MeSH S_adverse_effects_MeSH Serotonin_Agonists_adverse_effects_MeSH S_classification_MeSH Serotonin_Agonists_classification_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Structure-Activity_Relationship_MeSH M_Sumatriptan_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_chemistry_MeSH Sumatriptan_chemistry_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Triazoles_MeSH S_adverse_effects_MeSH Triazoles_adverse_effects_MeSH S_chemistry_MeSH Triazoles_chemistry_MeSH S_therapeutic_use_MeSH Triazoles_therapeutic_use_MeSH M_Vasoconstrictor_Agents_MeSH S_adverse_effects_MeSH Vasoconstrictor_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 10429698
----K E
----T TIPS for prevention of recurrent bleeding in patients with cirrhosis: meta-analysis of randomized clinical trials.
----A PURPOSE: To compare the effects of transjugular intrahepatic portosystemic shunt (TIPS) creation with those of endoscopic treatment with or without propranolol administration (i.e, conventional treatment) on recurrent bleeding, encephalopathy, and mortality by using meta-analysis of 11 published randomized clinical trials. MATERIALS AND METHODS: Data from 11 relevant studies were retrieved by means of computerized and manual search. The combinability of the studies was assessed in terms of clinical and statistical criteria. Data were extracted on the basis of the intention-to-treat principle, and treatment effects were measured as risk differences between TIPS creation and conventional treatment. Pooled estimates were computed according to a random-effects model. RESULTS: A total of 750 patients were included in 11 trials. No significant heterogeneity was found for any of the outcomes. Pooled risk differences were recurrent bleeding, -31% (95% CI, -39%, -23%); encephalopathy, +16% (95% CI, +10%, +22%); death due to all causes, +2% (95% CI, -4%, +9%); and death due to bleeding, -5% (95% CI, -11%, +6%). Clinically important complications occurred in 22% of patients and were associated with both treatments. TIPS dysfunction occurred in 55% of patients. CONCLUSION: TIPS creation markedly reduces risk of rebleeding but increases risk of encephalopathy without affecting survival. Therefore, TIPS creation may not be the best first-choice therapy for prevention of recurrent variceal bleeding. Criteria for selection of candidates for TIPS creation should be assessed in future prospective studies.
----P Journal_Article Meta-Analysis 
----M M_Esophageal_and_Gastric_Varices_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hemostasis__Endoscopic_MeSH M_Hepatic_Encephalopathy_MeSH S_epidemiology_MeSH Hepatic_Encephalopathy_epidemiology_MeSH S_prevention_&_control_MeSH Hepatic_Encephalopathy_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Liver_Diseases_MeSH S_prevention_&_control_MeSH Liver_Diseases_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Recurrence_MeSH M_Risk_Factors_MeSH M_Sclerotherapy_MeSH 
****** 10439497
----K E
----T Treatment of hypertensive and hypercholesterolaemic patients in general practice. The effect of captopril, atenolol and pravastatin combined with life style intervention.
----A OBJECTIVE: To elucidate the effect on blood pressure and blood lipids of an angiotensin converting enzyme inhibitor (captopril), and a beta-receptor blocking agent (atenolol), given alone or in combination with a cholesterol reducing drug, the beta-hydroxy-methylglutaryl-coenzyme A reductase inhibitor pravastatin, in patients who were also encouraged to improve their lifestyle. DESIGN: A longitudinal study consisting of three phases. I: Lifestyle intervention alone. II: Continued lifestyle intervention combined with captopril or atenolol. III: Continued lifestyle intervention combined with the same drugs as in phase II and in addition pravastatin or placebo. SETTING: Fifty-four general practice surgeries in Norway. PARTICIPANTS: Hypertensive patients, 210 females and 160 males, treated or untreated with antihypertensive drugs with a sitting diastolic blood pressure between 95 and 115 mmHg and a serum total cholesterol between 6.5 mmol/l (7.0 for those age 60-67 years) and 9.0 mmol/l. RESULTS: The antihypertensive effect of captopril and atenolol was not influenced by concurrent administration of pravastatin. The effect of pravastatin was not limited by concurrent medication with captopril or atenolol. Improvement in lifestyle seemed to reduce the need for supplementary treatment with diuretics. CONCLUSION: Pravastatin can be used in combination with captopril or atenolol in the treatment of hypertensive and hypercholesterolaemic patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anticholesteremic_Agents_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Combined_Modality_Therapy_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norway_MeSH M_Pravastatin_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10441090
----K E
----T Meeting highlights. Highlights of the 48th scientific sessions of the American College of Cardiology.
----A 
----P News 
----M M_Alanine_MeSH S_analogs_&_derivatives_MeSH Alanine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Alanine_therapeutic_use_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_instrumentation_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_instrumentation_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antibodies__Monoclonal_MeSH S_therapeutic_use_MeSH Antibodies__Monoclonal_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Benzamidines_MeSH S_therapeutic_use_MeSH Benzamidines_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH P_Cardiology_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Defibrillators__Implantable_MeSH M_Double-Blind_Method_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Endothelial_Growth_Factors_MeSH S_therapeutic_use_MeSH Endothelial_Growth_Factors_therapeutic_use_MeSH M_Fatty_Acids__Omega-3_MeSH S_therapeutic_use_MeSH Fatty_Acids__Omega-3_therapeutic_use_MeSH M_Guanidines_MeSH S_therapeutic_use_MeSH Guanidines_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Immunoglobulins__Fab_MeSH S_therapeutic_use_MeSH Immunoglobulins__Fab_therapeutic_use_MeSH M_Lasers_MeSH S_therapeutic_use_MeSH Lasers_therapeutic_use_MeSH M_Lymphokines_MeSH S_therapeutic_use_MeSH Lymphokines_therapeutic_use_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Multicenter_Studies_MeSH M_Myocardial_Revascularization_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Pyrrolidines_MeSH S_therapeutic_use_MeSH Pyrrolidines_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Simvastatin_MeSH S_therapeutic_use_MeSH Simvastatin_therapeutic_use_MeSH M_Sodium-Hydrogen_Antiporter_MeSH S_antagonists_&_inhibitors_MeSH Sodium-Hydrogen_Antiporter_antagonists_&_inhibitors_MeSH M_Stents_MeSH M_Sulfones_MeSH S_therapeutic_use_MeSH Sulfones_therapeutic_use_MeSH M_Tedelparin_MeSH S_therapeutic_use_MeSH Tedelparin_therapeutic_use_MeSH M_Thrombolytic_Therapy_MeSH M_Ticlopidine_MeSH S_analogs_&_derivatives_MeSH Ticlopidine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Ticlopidine_therapeutic_use_MeSH M_Tissue_Plasminogen_Activator_MeSH S_genetics_MeSH Tissue_Plasminogen_Activator_genetics_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Vascular_Endothelial_Growth_Factor_A_MeSH M_Vascular_Endothelial_Growth_Factors_MeSH M_Vitamin_E_MeSH S_therapeutic_use_MeSH Vitamin_E_therapeutic_use_MeSH 
****** 10445794
----K E
----T Lack of effect of propranolol in the prevention of large oesophageal varices in patients with cirrhosis: a randomized trial. French-Speaking Club for the Study of Portal Hypertension.
----A OBJECTIVE: Beta-blockers have been shown to reduce portal pressure in patients with cirrhosis and limit the development of portosystemic shunts in portal hypertensive animals. Thus, a randomized double-blind trial was conducted to evaluate propranolol in the prevention of the development of large oesophageal varices in patients with cirrhosis without varices or with small varices. METHODS: One hundred and two patients received long-acting propranolol (160 mg/day) and 104 patients received a placebo. At inclusion, there was no significant difference between the two groups in terms of clinical characteristics or biochemical tests. At 2 years, the size of varices was estimated on video recordings. RESULTS: One-third of the patients were lost to follow-up, and 95%/97% of the remaining patients were compliant in the propranolol and placebo groups, respectively. At 2 years, the proportion of patients with large varices was 31% in the propranolol group and 14% in the placebo group (P< 0.05). Three and four patients bled in the propranolol and placebo groups, respectively, and nine and ten died, respectively. CONCLUSION: This trial suggests that propranolol administration cannot be recommended for the prevention of the development of large oesophageal varices in patients with cirrhosis; thus other studies are needed in selected subgroups of patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Failure_MeSH 
****** 10448805
----K E
----T Occurrence and progression of dementia in a community population aged 75 years and older: relationship of antihypertensive medication use.
----A OBJECTIVE: To examine whether antihypertensive medication use can affect the occurrence and progression of dementia. SUBJECTS AND METHODS: In a community cohort of 1810 persons aged 75 years and older, 225 prevalent cases of dementia were detected. Among the 1301 persons without dementia, 224 incident cases of dementia were identified during an average period of 3 years. Among the 225 prevalent cases of dementia, 79 were suitable for the analysis of cognitive decline. Information on drug use was collected for the 2 weeks preceding the baseline interview. RESULTS: Subjects taking antihypertensive medication (n = 651, 83.9% of whom took diuretics) had a lower prevalence of dementia than those not taking antihypertensive medication (P<.001). Subjects without dementia who were taking antihypertensive medication at baseline (n = 584) had a reduced incidence of dementia (adjusted relative risk, 0.7; 95% confidence interval, 0.6-1.0; P = .03). Furthermore, subjects taking diuretics (n = 484) had an adjusted relative risk of 0.7 (95% confidence interval, 0.5-1.0; P = .02) for all dementia, and subjects taking diuretic monotherapy (n = 345) had an adjusted relative risk of 0.6 (95% confidence interval, 0.4-0.9; P = .006). The use of other antihypertensive medication (calcium antagonists or beta-blockers), however, was related to a reduced risk of Alzheimer disease (adjusted relative risk, 0.6; 95% confidence interval, 0.3-1.2) only in the subpopulation with a higher baseline blood pressure (n = 458). Patients with dementia at baseline who were not taking diuretics had a 2-fold faster rate of decline in the score on the Mini-Mental State Examination than those taking diuretics. CONCLUSION: The use of diuretics may protect against dementia in elderly persons.
----P Journal_Article 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Alzheimer_Disease_MeSH S_complications_MeSH Alzheimer_Disease_complications_MeSH S_epidemiology_MeSH Alzheimer_Disease_epidemiology_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Catchment_Area_(Health)_MeSH M_Cognition_Disorders_MeSH S_diagnosis_MeSH Cognition_Disorders_diagnosis_MeSH M_Cohort_Studies_MeSH M_Community_Health_Services_MeSH M_Disease_Progression_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Incidence_MeSH M_Male_MeSH M_Neuropsychological_Tests_MeSH M_Prevalence_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10449213
----K I
----T Fixed-dose combination vs monotherapy in hypertension: a meta-analysis evaluation.
----A Fixed-dose combination antihypertensive therapy has received interest since the publication of the JNC-VI report. Relatively few head-to-head comparative studies between fixed-dose combinations and first-line monotherapies for hypertension have been published. The objective of this study was to conduct a meta-analysis of various first-line monotherapies and the fixed-dose combination of amlodipine/benazepril. The results of the meta-analysis were used to compare the efficacy and safety of the first-line monotherapies with amlodipine/benazepril. The meta-analysis included 82 studies that included 110 treatment groups (cohorts). The study compared nine different monotherapies and one combination therapy (amlodipine/benazepril). Of the 82 studies, 22 were placebo-controlled and 60 were active treatment controlled. The mean absolute decrease in supine diastolic blood pressure (BP) ranged from 9.7 to 13.3 mm Hg with verapamil showing the greatest effect and captopril the least (13.3 +/- 3.0 mm Hg; 9.7 +/- 2.9 mm Hg, respectively). When studies were weighted by sample size, atenolol, verapamil, lisinopril and amlodipine/benazepril showed the greatest BP effect. When studies were weighted by variance, amlodipine/benazepril and atenolol showed the greatest BP effect. The percentage of patients controlled on therapy ranged from 54% to 79%. Lisinopril and amlodipine/benazepril showed the greatest percent controlled. The overall incidence of adverse effects ranged from 12.1% to 41.8% with lisinopril having the lowest and nifedipine having the highest incidence. The overall incidence of adverse effects resulting in drug discontinuance ranged from 1.3% to 10.7%, with amlodipine/benazepril having the lowest and nifedipine having the highest incidence. The results of the meta-analysis indicate that amlodipine/benazepril produces above average reductions in BP with a lower than average incidence of overall side effects and the lowest incidence of adverse effects resulting in drug discontinuance. The fixed-dose combination of amlodipine/benazepril achieves its goal of effective BP lowering with a minimum of significant side effects.
----P Journal_Article Meta-Analysis 
----M M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzazepines_MeSH S_administration_&_dosage_MeSH Benzazepines_administration_&_dosage_MeSH S_adverse_effects_MeSH Benzazepines_adverse_effects_MeSH S_therapeutic_use_MeSH Benzazepines_therapeutic_use_MeSH M_Drug_Combinations_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_adverse_effects_MeSH Lisinopril_adverse_effects_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10449888
----K E
----T Angiotensin II antagonism and the heart: valsartan in left ventricular hypertrophy.
----A Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study the angiotensin II (AT(1) receptor) antagonist valsartan (Diovan((R)); 80 mg/160 mg q.d.) was compared with the beta-blocker atenolol (50 mg/100 mg q.d.) over 8 months in predominantly previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated with echocardiographic data. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001), and in the valsartan group (n = 9 with additional HCTZ) blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m(2) in the atenolol group and from 127 to 106 g/m(2) in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Valine_MeSH S_analogs_&_derivatives_MeSH Valine_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Valine_therapeutic_use_MeSH 
****** 10454307
----K E
----T The clinical impact of dynamic intraventricular obstruction during dobutamine stress echocardiography.
----A We selected 73 consecutive patients without myocardial-infarction, hypertrophic cardiomyopathy or hypertension complaining of effort chest discomfort/dyspnoea, and/or reporting exercise ischaemic ECG changes, and submitted them to simultaneous dobutamine stress echocardiography (DSE) and 99mTc tetrofosmin SPECT (T SPECT) and to coronary angiography to evaluate the clinical impact of intraventricular obstruction (IVO) during dobutamine infusion. Sixteen patients (22%, 7 males, mean age+/-SD 63+/-8 years, group 1) developed IVO (mean CW Doppler velocity+/-SD: 3.8+/-1.0 m/s) and 57 (41 males, mean age+/-SD 63+/-10 years, group 2) did not. The two groups had similar incidence of angina and ischaemic ECG changes at exercise tolerance test. DSE did not demonstrate wall motion abnormalities in any group 1 patient while T SPECT showed a perfusion defect in the only one with coronary artery disease (CAD). DSE reproduced symptoms in a higher percentage of patients with than without IVO, while there was no statistical difference in the reproduction of ischaemic ECG changes, despite CAD prevalence was much lower in group 1. Group 1 patients remained asymptomatic on beta-blockers at 12-month follow-up. Dobutamine-induced IVO, by reproducing symptoms, suggests that IVO plays a role in the clinical setting in patients without CAD complaining of unexplained reduced effort tolerance who should undergo DSE.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Flow_Velocity_MeSH M_Cardiotonic_Agents_MeSH S_adverse_effects_MeSH Cardiotonic_Agents_adverse_effects_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH M_Dobutamine_MeSH S_adverse_effects_MeSH Dobutamine_adverse_effects_MeSH P_Echocardiography__Doppler_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH S_adverse_effects_MeSH Exercise_Test_adverse_effects_MeSH M_Follow-Up_Studies_MeSH M_Heart_Ventricles_MeSH S_radionuclide_imaging_MeSH Heart_Ventricles_radionuclide_imaging_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Stroke_Volume_MeSH M_Tomography__Emission-Computed__Single-Photon_MeSH M_Ventricular_Outflow_Obstruction_MeSH S_chemically_induced_MeSH Ventricular_Outflow_Obstruction_chemically_induced_MeSH S_epidemiology_MeSH Ventricular_Outflow_Obstruction_epidemiology_MeSH S_physiopathology_MeSH Ventricular_Outflow_Obstruction_physiopathology_MeSH M_Video_Recording_MeSH 
****** 10457878
----K E
----T Comparison of intravenous metoprolol, verapamil and diltiazem on the attenuation of haemodynamic changes associated with tracheal extubation.
----A Changes in heart rate, systolic, diastolic and mean blood pressure were measured after extubation in 60 ASA Grade I and II patients to assess the effects of diltiazem (0.2 mg kg-1), verapamil (0.05 mg kg-1) and metoprolol (0.02 mg kg-1) given as a bolus 2 min before tracheal extubation. All the haemodynamic variables measured increased significantly after extubation in the control and diltiazem groups when compared with the base-line recordings (P < 0.05). Metoprolol effectively blocked the increases in heart rate after extubation and the increase in blood pressure in this group was less when compared with the control group (P < 0.05). Verapamil alleviated the increase in both heart rate and blood pressure. However, profound hypotension and bradycardia requiring therapy, occurred in the verapamil group. For this reason, careful observation is necessary when using verapamil and the routine use of this drug in patients with coronary artery disease requires further studies.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Bradycardia_MeSH S_chemically_induced_MeSH Bradycardia_chemically_induced_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH M_Diltiazem_MeSH S_therapeutic_use_MeSH Diltiazem_therapeutic_use_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Intervertebral_Disk_MeSH S_surgery_MeSH Intervertebral_Disk_surgery_MeSH P_Intubation__Intratracheal_MeSH M_Lumbar_Vertebrae_MeSH S_surgery_MeSH Lumbar_Vertebrae_surgery_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Systole_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_adverse_effects_MeSH Verapamil_adverse_effects_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 10455479
----K I
----T Impact of antihypertensive treatment on quality of life: comparison between bisoprolol and bendrofluazide.
----A OBJECTIVES: To compare quality of life with the selective beta1-blocker bisoprolol and the thiazide diuretic bendrofluazide in patients with mild to moderate hypertension. DESIGN AND SETTING: Multi centric, randomised, double-blind, two-way crossover study carried out at six general practice centres. SUBJECTS: Eighty-one patients with newly diagnosed or previously treated hypertension, who had a mean diastolic blood pressure (BP) of 95-120 mm Hg after receiving placebo for 4-6 weeks.Interventions: In random order, patients received bisoprolol (5 mg once daily) or bendrofluazide (2. 5 mg once daily) for 8 weeks. MAIN OUTCOME MEASURES: Quality of life and antihypertensive effect.Results: Decrease in systolic/diastolic BP did not differ between bisoprolol (10 +/- 2/13 +/- 1 mm Hg) and bendrofluazide (9 +/- 2/11 +/- 1 mm Hg). Between bisoprolol and bendrofluazide neither in the intention-to-treat nor in the efficacy analysis any difference was found in quality of life variables, such as Health Status Index, somatic symptoms, anxiety, depression, total psychiatric morbidity, cognitive symptoms and hostility score. Compared to baseline the Health Status Index improved (P < 0.05) during bisoprolol. None of the other investigated quality of life variables changed compared to baseline. No patients dropped out during bisoprolol or bendrofluazide treatment. Although, the total number of reported adverse events appeared lower during bendrofluazide than during bisoprolol treatment, it is unclear whether drug related adverse events also differ between the two drugs. CONCLUSIONS: At equipotent antihypertensive dosages, the effect of an 8-week treatment on quality of life does not differ between the selective beta1-blocker bisoprolol and the thiazide diuretic bendrofluazide.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Bendroflumethiazide_MeSH S_adverse_effects_MeSH Bendroflumethiazide_adverse_effects_MeSH S_therapeutic_use_MeSH Bendroflumethiazide_therapeutic_use_MeSH M_Bisoprolol_MeSH S_adverse_effects_MeSH Bisoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Quality_of_Life_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 10466460
----K 5
----T Pulse pressure as a risk factor for cardiovascular events in the MRC Mild Hypertension Trial.
----A OBJECTIVES: The aim of this study was to determine whether pulse pressure is a risk factor for coronary artery disease using data from the MRC trial of treatment of mild hypertension, and whether the effect of anti-hypertensive drug therapy on pulse pressure may be a determinant of outcome in treated patients. METHODS: Logistic regression and Cox regression analyses were used to compare systolic and diastolic blood pressure, pulse pressure and mean blood pressure as predictors of coronary events and stroke in the MRC Mild Hypertension Trial. The effects of anti-hypertensive drug treatment with bendrofluazide and propranolol on pulse pressure were assessed using 1-year follow-up data. Event rates in the placebo-treated group and responses to anti-hypertensive treatment were measured in quartiles of age-adjusted entry pulse pressure. A 'four-corners' analysis was performed, with subjects divided into the upper and lower halves of the distributions of systolic and diastolic blood pressure at entry. RESULTS: Pulse pressure was a stronger predictor of coronary events than systolic, diastolic or mean blood pressure in males by logistic regression. Pulse pressure was similar to systolic pressure as a coronary event predictor on Cox regression. Stroke was predicted most strongly by mean blood pressure. Fatal and non-fatal coronary event rates increased progressively in ascending quartiles of age-adjusted pulse pressure, but there was also a strong correlation with systolic blood pressure. The values of partial logistic regression coefficients in models containing both systolic and diastolic blood pressure also supported a role for pulse pressure in predicting coronary events and for mean blood pressure in predicting stroke. Coronary risk, but not stroke, was inversely related to diastolic blood pressure in the four-corners analysis. In a Cox model, regressions of coronary event probability on systolic blood pressure at entry were significantly and inversely related to diastolic blood pressure categorized in quartiles. Bendrofluazide but not propranolol decreased pulse pressure significantly and was associated with a reduction in cardiovascular events overall, but no definite relationship between the effect of drugs on pulse pressure and specific responses to treatment was seen. CONCLUSION: Pulse pressure is a strong risk factor for coronary events in untreated hypertensive male subjects in the MRC Mild Hypertension Trial, whereas stroke is best predicted by mean blood pressure. Bendrofluazide and propranolol have different effects on pulse pressure which may be related to their relative efficacy in the treatment of hypertension, but this possibility requires further study in more suitable populations.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Analysis_of_Variance_MeSH P_Blood_Pressure_MeSH M_Cardiovascular_Diseases_MeSH S_diagnosis_MeSH Cardiovascular_Diseases_diagnosis_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_physiopathology_MeSH Cardiovascular_Diseases_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Prognosis_MeSH M_Proportional_Hazards_Models_MeSH P_Pulse_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH 
****** 10466352
----K 1
----T [Multicenter prospective survey of prognosis of hypertensive elderly outpatient under antihypertensive treatment--morbidity and mortality of cardiovascular diseases and cancer]
----A Although calcium-channel blockers and angiotensin-I-converting enzyme inhibitors are often used for treatment of hypertension in the elderly in Japan compared to those in the United States and in European countries, there have been few investigations on the prognosis of the elderly receiving these antihypertensive treatments. The Research Group for "Guidelines on the Treatment of Hypertension in the Elderly" collaborated with the Comprehensive Research Projects on Aging and Health group of the Ministry of Health and Welfare of Japan in performing a 3-year survey on the outcome of 700 hypertensive elderly outpatients (> or = 60 years) receiving treatment of antihypertensive drugs. Antihypertensive drugs including dihydropyridine-type calcium channel blockers, beta blockers, angiotensin-I-converting enzyme inhibitors, diltiazem, diuretics and old-type antihypertensives (hydralazine, budralazine, and centrally acting drugs such as clonidine, methyldopa and guanabenz) were administered to 71.3%, 30.4%, 26.2%, 14.0%, 8.6%, and 6.4% of the 642 elderly patients surveyed for three years, at the time of registration, respectively. Morbidity and mortality rates of total cerebro-cardiovascular diseases, stroke, and heart diseases, were 27.6 and 7.81/1,000 patient-years, 15.1 and 3.6/1,000 patient-years, 10.4 and 4.2/1,000 patient-years, respectively. These results were similar or even better than those of megatrials of antihypertensive treatments for elderly patients in Europe and United States. After adjustment for potential confounding factors, multiple logistic analysis revealed that a past history of ischemic heart disease, use of the old-type antihypertensive drugs, male gender, and diastolic high blood pressure were independent risk factors for the morbidity of cerebro-cardiovascular diseases taking the group of non-cerebro-cardiovascular disease as the reference group. We also identified 22 cases of newly occurred malignancies including 7 fatal cases. However, none of the antihypertensives was significantly related to the occurrence of malignancies. These results lead support to the tendencies in the use of antihypertensive drugs in Japan.
----P Journal_Article Multicenter_Study 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_complications_MeSH Cardiovascular_Diseases_complications_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Japan_MeSH S_epidemiology_MeSH Japan_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neoplasms_MeSH S_complications_MeSH Neoplasms_complications_MeSH M_Prognosis_MeSH M_Prospective_Studies_MeSH 
****** 10467196
----K E
----T Pulmonary function, cardiac function, and exercise capacity in a follow-up of patients with congestive heart failure treated with carvedilol.
----A BACKGROUND: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure. METHODS: Twenty-one patients with New York Heart Association class II to III heart failure were randomly assigned (2 to 1) to carvedilol (25 mg twice daily, n = 14) or placebo (n = 7) for 6 months. Rest forced expiratory volume (FEV(1)), vital capacity, total lung capacity, carbon monoxide diffusing capacity, its alveolar-capillary membrane component, pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure), LV diastolic and systolic dimensions, stroke volume, ejection fraction, and fiber shortening velocity were measured at baseline and at 3 and 6 months. VO(2p), peak ratio of dead space to tidal volume (VD/VT(p)), ventilatory equivalent for carbon dioxide production (VE/VCO(2)), and VO(2) at anaerobic threshold (VO(2at)) were also determined. RESULTS: FEV(1), vital capacity, total lung capacity, carbon monoxide diffusing capacity, and the alveolar-capillary membrane component were impaired in chronic heart failure compared with 14 volunteers and did not vary with treatment. Carvedilol reduced end-diastolic pressure, end-diastolic diameter, and end-systolic diameter and increased ejection fraction, stroke volume, and fiber shortening velocity without affecting VO(2p), VO(2at), VD/VT(p), or VE/VCO(2) at 3 and 6 months. Placebo did not produce significant changes. CONCLUSIONS: In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH P_Exercise_Tolerance_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Lung_MeSH S_physiopathology_MeSH Lung_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxygen_Consumption_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Respiratory_Function_Tests_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 10485716
----K E
----T Aldosterone antagonism in heart failure.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_MeSH S_physiology_MeSH Aldosterone_physiology_MeSH M_Aldosterone_Antagonists_MeSH S_administration_&_dosage_MeSH Aldosterone_Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Algorithms_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Spironolactone_MeSH S_administration_&_dosage_MeSH Spironolactone_administration_&_dosage_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH 
****** 10486674
----K 1
----T [Hyperinsulinism, heart rate variability and circadian variation of arterial pressure in obese hypertensive patients]
----A AIMS: During insulin resistance, sympathetic nerve activity is increased. However insulin resistance is a common feature of obesity and essential hypertension, it is unclear if chronic hyperinsulinemia per se contributes to sympathetic overactivation. The purpose of our study was to explore++ the relationships between chronic hyperinsulinemia and heart rate variability (HRV), a non-intensive tool to assess autonomic function, in obese and hypertensive subjects. METHODS: 24 hours Holter ECG for HRV time and frequency domain analysis was performed in 77 patients, mean age 53 +/- 10 years, 52 men and 25 women, free of diabetes, without beta-blockers, divided in four groups according to three parameters, body mass index (BMI > 27 kg/m2 in man and > 25 kg/m2 in woman defined obesity), arterial pressure and insulinemia (fasting insulinemia > 25 mUI/L defined hyperinsulinemia): 27 patients obese, hypertensive, with hyperinsulinemia; 28 patients obese, hypertensive, without hyperinsulinemia; 12 patients non obese, hypertensive, without hyperinsulinemia; 10 patients obese, normotensive, without hyperinsulinemia. RESULTS: In comparison with the three other groups, patients with hyperinsulinemia showed a significant decrease (p < 0.05) of SDNN and the power of total spectrum (0.01-1 Hz) band, which are indexes of global HRV, and a significant decrease (p < 0.005) of SD and the normalized power of the low frequency (0.04-0.15 Hz) band, both indexes reflecting sympathetic modulation of HRV. In contrast, no significant difference was observed between the four groups for indexes of HRV reflecting parasympathetic tone. These relations were independent of mean RR. Fasting insulinemia was significantly (p < 0.0001) related with HRV in time domain (SDNN; r = -0.43; SD: r = -0.49) and spectral domain (total spectrum: r = -0.49; low frequency: r = -0.52). CONCLUSION: Chronic hyperinsulinemia appears to be an important determinant of HRV, particularly for the indexes reflecting sympathetic influence, independent of obesity and hypertension.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Chronic_Disease_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hyperinsulinism_MeSH S_physiopathology_MeSH Hyperinsulinism_physiopathology_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH 
****** 10557382
----K E
----T A standardized treatment protocol for blood pressure management in transport patients with a reported diagnosis of acute aortic dissection or symptomatic aortic aneurysm.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Air_Ambulances_MeSH S_standards_MeSH Air_Ambulances_standards_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Aortic_Aneurysm_MeSH S_complications_MeSH Aortic_Aneurysm_complications_MeSH S_drug_therapy_MeSH Aortic_Aneurysm_drug_therapy_MeSH M_Aortic_Rupture_MeSH S_complications_MeSH Aortic_Rupture_complications_MeSH S_drug_therapy_MeSH Aortic_Rupture_drug_therapy_MeSH M_Blood_Pressure_Determination_MeSH M_California_MeSH M_Comparative_Study_MeSH M_Emergency_Treatment_MeSH S_standards_MeSH Emergency_Treatment_standards_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Nitroprusside_MeSH S_administration_&_dosage_MeSH Nitroprusside_administration_&_dosage_MeSH M_Practice_Guidelines_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Quality_Assurance__Health_Care_MeSH M_Retrospective_Studies_MeSH M_Treatment_Outcome_MeSH 
****** 10490566
----K E
----T Lack of prevention of heart failure by serial electrical cardioversion in patients with persistent atrial fibrillation.
----A OBJECTIVE: To investigate the occurrence of heart failure complications, and to identify variables that predict heart failure in patients with (recurrent) persistent atrial fibrillation, treated aggressively with serial electrical cardioversion and antiarrhythmic drugs to maintain sinus rhythm. DESIGN: Non-randomised controlled trial; cohort; case series; mean (SD) follow up duration 3.4 (1.6) years. SETTING: Tertiary care centre. SUBJECTS: Consecutive sampling of 342 patients with persistent atrial fibrillation (defined as > 24 hours duration) considered eligible for electrical cardioversion. INTERVENTIONS: Serial electrical cardioversions and serial antiarrhythmic drug treatment, after identification and treatment of underlying cardiovascular disease. MAIN OUTCOME MEASURES: heart failure complications: development or progression of heart failure requiring the institution or addition of drug treatment, hospital admission, or death from heart failure. RESULTS: Development or progression of heart failure occurred in 38 patients (11%), and 22 patients (6%) died from heart failure. These complications were related to the presence of coronary artery disease (p < 0.001, risk ratio 3.2, 95% confidence interval (CI) 1.6 to 6.5), rheumatic heart disease (p < 0.001, risk ratio 5.0, 95% CI 2.4 to 10.2), cardiomyopathy (p < 0.001, risk ratio 5.0, 95% CI 2.0 to 12.4), atrial fibrillation for < 3 months (p = 0.04, risk ratio 2.0, 95% CI 1.0 to 3.7), and poor exercise tolerance (New York Heart Association class III at inclusion, p < 0.001, risk ratio 3.5, 95% CI 1.9 to 6. 7). No heart failure complications were observed in patients with lone atrial fibrillation. CONCLUSIONS: Aggressive serial electrical cardioversion does not prevent heart failure complications in patients with persistent atrial fibrillation. These complications are predominantly observed in patients with more severe underlying cardiovascular disease. Randomised comparison with rate control treatment is needed to define the optimal treatment for persistent atrial fibrillation in relation to heart failure.
----P Journal_Article 
----M M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_mortality_MeSH Atrial_Fibrillation_mortality_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH P_Electric_Countershock_MeSH M_Female_MeSH M_Flecainide_MeSH S_therapeutic_use_MeSH Flecainide_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Failure_MeSH M_Warfarin_MeSH S_therapeutic_use_MeSH Warfarin_therapeutic_use_MeSH 
****** 10496201
----K E
----T Candesartan in heart failure--assessment of reduction in mortality and morbidity (CHARM): rationale and design. Charm-Programme Investigators.
----A BACKGROUND: Chronic heart failure (CHF) is an increasing burden to health care. Pharmacological treatment with angiotensin-converting enzyme (ACE) inhibitors and beta blockers improve survival and reduce hospitalizations in patients with low left ventricular ejection fraction (LVEF). Despite these therapies, morbidity and mortality remains problematic. Furthermore, 30% to 50% of patients with CHF have a preserved LVEF. It is not known if treatments are of benefit in this group. DESIGN: Candesartan in Heart Failure-Assessment of Reduction in Mortality and Morbidity (CHARM) is a program designed to investigate the clinical usefulness of the long-acting angiotensin II type 1 receptor blocker, candesartan cilexetil, in a broad spectrum of patients with symptomatic heart failure. Patients with systolic dysfunction, tolerant or intolerant to an ACE-inhibitor, and patients with preserved systolic function are included. Specifically, the CHARM program consists of 3 independent, parallel, placebo-controlled studies in patients with (1) LVEF less than or equal to 40%, ACE-inhibitor treated (n = 2,300); (2) LVEF less than or equal to 40%, ACE-inhibitor intolerant (n = 1,700); (3) LVEF greater than 40%, not treated with ACE inhibitors (n = 2,500). The 3 studies will be combined to evaluate the effect of candesartan cilexetil on all-cause mortality in the broad spectrum of symptomatic heart failure. The primary objective in each trial is to evaluate the effects on the combined endpoint of cardiovascular mortality or CHF hospitalization. Other endpoints include the effects on myocardial infarction, all-cause hospitalization, and resource utilization. CHARM is intended to randomize 6,500 patients with symptomatic heart failure from 26 countries in Europe, the United States, Canada, South Africa, and Australia. The CHARM program started to enroll patients in March 1999. The follow-up period is a minimum of 2 years. The study is expected to end in the third quarter of 2002.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Drug_Evaluation_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Contraction_MeSH S_drug_effects_MeSH Myocardial_Contraction_drug_effects_MeSH M_Prodrugs_MeSH S_therapeutic_use_MeSH Prodrugs_therapeutic_use_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH P_Research_Design_MeSH M_Safety_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 10495686
----K 1
----T [Clinical study of the month. The MERIT-HF study]
----A MERIT-HF study was a multicenter, double-blind randomized placebo-controlled study which enrolled 3.991 class II-IV heart failure patients with a left ventricular ejection fraction < or = 40% who were already treated by optimal standard therapy (diuretic + ACE inhibitor or equivalent). Three thousand nine hundred ninety one patients were enrolled in the study: 2.001 received a placebo; 1.990 were assigned to metoprolol administration at the initial dose of 25 mg/day (12.5 mg for class III-IV patients) and progressively increased to a maximum daily dose of 200 mg. The study was prematurely stopped because, after an observation period of 3.980 patients x years, it demonstrated a significant mortality reduction in the treated group. All cause mortality was reduced by 34% (7.2% per patient x year vs 11%). Sudden death mortality and mortality due to progression of heart failure were reduced by 41% and 49%, respectively.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH 
****** 10498130
----K E
----T Trends in the post-hospitalization medical treatment of unstable angina pectoris: 1990 to 1995.
----A This study provides data on post-hospitalization medication treatment trends for unstable angina between 1990 and 1995. We conducted an observational cohort study at the Veterans Affairs Puget Sound Health Care System (VAPSHCS). Computerized records of hospital discharges and cardiac catheterizations were used to identify unstable angina diagnoses among veterans between 1990 and 1995. Discharge medications issued within 90 days after discharge were ascertained from computerized outpatient pharmacy records. Of the 1,100 veterans discharged with unstable angina, 885 (80%) filled a prescription through the VAPSHCS within 90 days after discharge. Neither use of aspirin nor use of beta blockers increased between 1990 and 1995: overall use averaged 76% for aspirin (78% of those without potential contraindications) and 32% for beta blockers (36% of those without potential contraindications). Use of non-dihydropyridine calcium antagonists--primarily diltiazem--decreased from 57% to 40% (p <0.01), whereas use of dihydropyridine calcium antagonists increased from 12% to 26% (p <0.01). Thus, pharmacy records indicated that aspirin use was high although it was lower than expected, possibly due to ready availability outside the VAPSHCS pharmacy. The low frequency of beta-blocker use and the increasing reliance on dihydropyridine calcium antagonists through 1995 to treat unstable angina may be an opportunity to improve veteran care according to Agency for Health Care Policy Research recommendations.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina__Unstable_MeSH S_drug_therapy_MeSH Angina__Unstable_drug_therapy_MeSH M_Aspirin_MeSH S_adverse_effects_MeSH Aspirin_adverse_effects_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Drug_Utilization_MeSH S_trends_MeSH Drug_Utilization_trends_MeSH M_Female_MeSH M_Forecasting_MeSH M_Human_MeSH M_Length_of_Stay_MeSH S_trends_MeSH Length_of_Stay_trends_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_drug_therapy_MeSH Myocardial_Ischemia_drug_therapy_MeSH M_Patient_Discharge_MeSH S_trends_MeSH Patient_Discharge_trends_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH P_Veterans_MeSH M_Washington_MeSH S_epidemiology_MeSH Washington_epidemiology_MeSH 
****** 10503802
----K I
----T Determination of power and sample size in the design of clinical trials with failure-time endpoints and interim analyses.
----A An important but difficult task in the design of a clinical trial to compare time to failure between two treatment groups is determination of the number of patients required to achieve a specified power of the test. Because patients typically enter the trial serially and are followed until they fail or withdraw from the study or until the study is terminated, the power of the test depends on the accrual pattern, the noncompliance rate, and the withdrawal rate in addition to the actual survival distributions of the two groups. Incorporating interim analyses and the possibility of early stopping into the trial increases its complexity, and although normal approximations have been developed for computing the significance level of the test when the log-rank or other rank statistics are used, there are no reliable analytic approximations for evaluating the power of the test. This article presents methods, based on Monte Carlo simulations and recent advances in group sequential testing with time-to-event responses, to choose appropriate test statistics, compute power and sample size at specified alternatives, check the adequacy of commonly used normal approximations of the type I error probability, and assess the performance of different interim analysis strategies. It also presents two computer programs implementing these methods.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Monte_Carlo_Method_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH P_Research_Design_MeSH P_Sample_Size_MeSH M_Software_MeSH P_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Treatment_Refusal_MeSH 
****** 10509550
----K E
----T Felodipine-metoprolol combination tablet: a valuable option to initiate antihypertensive therapy?
----A The aim of the present study was to assess the efficacy and tolerability of a calcium antagonist/beta-blocker fixed combination tablet used as first-line antihypertesnive therapy in comparison with an angiotensin converting enzyme inhibitor and placebo. Patients with uncomplicated essential hypertension (diastolic blood pressure between 95 and 110 mm Hg at the end of a 4-week run-in period) were randomly allocated to a double-blind, 12-week treatment with either a combination tablet of felodipine and metoprolol (Logimax), 5/50 mg daily (n = 321), enalapril, 10 mg daily (n = 321), or placebo (n = 304), with the possibility of doubling the dose after 4 or 8 weeks of treatment if needed (diastolic blood pressure remaining >90 mm Hg). The combined felodipine-metoprolol treatment controlled blood pressure (diastolic < or =90 mm Hg 24 h after dose) in 72% of patients after 12 weeks, as compared with 49% for enalapril and 30% for placebo. A dose adjustment was required in 38% of patients receiving the combination, in 63% of patients allocated to placebo, and 61% of enalapril-treated patients. The overall incidence of adverse events was 54.5% during felodipine-metoprolol treatment; the corresponding values for enalapril and placebo were 51.7% and 47.4%, respectively. Withdrawal of treatment due to adverse events occurred in 18 patients treated with the combination, in 10 patients on enalapril, and 12 patients on placebo. No significant change in patients' well-being was observed in either of the three study groups. These results show that a fixed combination tablet of felodipine and metoprolol allows to normalize blood pressure in a substantially larger fraction of patients than enalapril given alone. This improved efficacy is obtained without impairing the tolerability. The fixed-dose combination of felodipine and metoprolol, therefore, may become a valuable option to initiate antihypertensive treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Felodipine_MeSH S_therapeutic_use_MeSH Felodipine_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Tablets_MeSH M_Treatment_Outcome_MeSH 
****** 10508208
----K E
----T Association of the A-204C polymorphism in the cholesterol 7alpha-hydroxylase gene with variations in plasma low density lipoprotein cholesterol levels in the Framingham Offspring Study.
----A The first reaction of the catabolic pathway of cholesterol is catalyzed by CYP7 and serves as the rate-limiting step and major site of regulation of bile acid synthesis in the liver. A common A to C substitution at position -204 of the promoter of CYP7 gene has been associated with variations in plasma LDL-cholesterol concentrations but the effect of this polymorphism is unknown in the general population. The aim of the present study was therefore to investigate the association of this polymorphism to lipoprotein levels in a population-based sample of 1139 male and 1191 female Framingham Offspring participants. In men, the C variant was associated with higher plasma concentrations of LDL-cholesterol and this association remained significant after adjustment for familial relationship, age, BMI, smoking, alcohol intake, the use of beta-blockers, and apoE genotype. The C variant was also associated with an increased TC/HDL ratio in men. Variance components analysis indicated that allelic variability at nucleotide -204 of the CYP7 gene and polymorphism of the apoE gene accounted for 1 and 5% of the variation of plasma LDL-cholesterol concentrations, respectively. In women, however, there was no relationship between LDL-cholesterol and the A-204C polymorphism but subjects homozygous for the CC genotype had significantly lower triglyceride levels than heterozygotes. Moreover, no significant relationship was found between the A-204C variants and lipoprotein particle diameter or the prevalence of coronary heart disease in both genders. Thus, our results show that the A-204C polymorphism in the CYP7 gene is associated with statistically significant variations in LDL-C and triglyceride concentrations in men and women, respectively, but the cumulative effects of these variations on atherosclerotic risk remain uncertain.
----P Journal_Article 
----M M_Alleles_MeSH M_Apolipoproteins_E_MeSH S_blood_MeSH Apolipoproteins_E_blood_MeSH S_genetics_MeSH Apolipoproteins_E_genetics_MeSH M_Cholesterol_7-alpha-Hydroxylase_MeSH S_genetics_MeSH Cholesterol_7-alpha-Hydroxylase_genetics_MeSH M_Cohort_Studies_MeSH M_Coronary_Disease_MeSH S_epidemiology_MeSH Coronary_Disease_epidemiology_MeSH S_genetics_MeSH Coronary_Disease_genetics_MeSH M_DNA_MeSH S_blood_MeSH DNA_blood_MeSH M_Female_MeSH M_Genotype_MeSH M_Human_MeSH M_Leukocytes_MeSH S_metabolism_MeSH Leukocytes_metabolism_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Lipoproteins__VLDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__VLDL_Cholesterol_blood_MeSH M_Male_MeSH M_Massachusetts_MeSH M_Middle_Aged_MeSH M_Nuclear_Family_MeSH M_Pedigree_MeSH P_Polymorphism_(Genetics)_MeSH M_Promoter_Regions_(Genetics)_MeSH M_Risk_Factors_MeSH M_Sex_Characteristics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 10510985
----K E
----T The role of diastolic blood pressure when treating isolated systolic hypertension.
----A OBJECTIVE: To assess the role of treated diastolic blood pressure (DBP) level in stroke, coronary heart disease (CHD), and cardiovascular disease (CVD) in patients with isolated systolic hypertension (ISH). DESIGN: An analysis of the 4736 participants in the Systolic Hypertension in the Elderly Program (SHEP) was undertaken. The SHEP was a randomized multicenter double-blind outpatient clinical trial of the impact of treating ISH in men and women aged 60 years and older. MAIN OUTCOME MEASURES: Cox proportional hazards regression analysis, with DBP and systolic blood pressure (SBP) as time-dependent covariables. RESULTS: After adjustment for the baseline risk factors of race (black vs other), sex, use of antihypertensive medication before the study, a composite variable (diabetes, previous heart attack, or stroke), age, and smoking history (ever vs never) and adjustment for the SBP as a time-dependent variable, we found, for the active treatment group only, that a decrease of 5 mm Hg in DBP increased the risk for stroke (relative risk, [RR], 1.14; 95% confidence interval [CI], 1.05-1.22), for CHD (RR, 1.08; 95% CI, 1.00-1.16), and for CVD (RR, 1.11; 95% CI, 1.05-1.16). CONCLUSIONS: Some patients with ISH may be treated to a level that uncovers subclinical disease, and some may be overtreated. Further studies need to determine whether excessively low DBP can be prevented by more careful titration of antihypertensive therapy while maintaining SBP control. It is reassuring that patients receiving treatment for ISH never perform worse than patients receiving placebo in terms of CVD events.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Ambulatory_Care_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cerebrovascular_Disorders_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH S_physiopathology_MeSH Cerebrovascular_Disorders_physiopathology_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Diastole_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multicenter_Studies_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_MeSH M_Systole_MeSH 
****** 10511135
----K E
----T Effects of doxazosin and atenolol on circulating endothelin-1 and von Willebrand factor in hypertensive middle-aged men.
----A Elevated levels of endothelin-1 (ET-1) and von Willebrand factor (vWF), both markers indicative of endothelial function, are associated with hypertension. In a randomized open study we investigated the effect of antihypertensive treatment with the alpha-blocker doxazosin (n = 23) or the beta-blocker atenolol (n = 22) for 22 weeks on circulating levels of ET-1 and vWF in middle-aged men with essential hypertension. Blood pressure reduction was satisfactorily achieved with both drugs, although the decrease in the atenolol group was larger than that in the doxazosin group. A reduction in the levels of vWF occurred in both groups, being more pronounced in the alpha-blocker group compared with the decrease on beta blockers, p = 0.004 and p = 0.056, respectively. In the alpha-blocker group, there was a significant correlation (r = 0.50, p = 0.022) between the reduction in diastolic blood pressure and the decline in vWF. A highly significant decrease in plasma ET-1 was obtained during beta blockade (p = 0.007), whereas no significant change occurred within the alpha-blocker group. There was, however, no correlation between the decrease in blood pressure and the reduction in ET-1. The different favorable effects of alpha and beta blockers on endothelial function expressed as vWF and ET-1, could indicate that the effects are probably related not only to the blood pressure per se, but also to the different pharmacologic mechanisms of the drugs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Biological_Markers_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Doxazosin_MeSH S_pharmacology_MeSH Doxazosin_pharmacology_MeSH M_Endothelin-1_MeSH S_blood_MeSH Endothelin-1_blood_MeSH M_Endothelium_MeSH S_drug_effects_MeSH Endothelium_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_von_Willebrand_Factor_MeSH S_metabolism_MeSH von_Willebrand_Factor_metabolism_MeSH 
****** 10513787
----K E
----T Atenolol versus amlodipine versus isosorbide-5-mononitrate on anginal symptoms in syndrome X.
----A The effects of a beta blocker (atenolol), a calcium antagonist (amlodipine), and a nitrate (isosorbide-5-mononitrate) on anginal symptoms in 10 patients with syndrome X were assessed in a crossover, double-blind, randomized trial. Only atenolol was found to significantly improve chest pain episodes, suggesting that it should be the preferred drug when starting pharmacologic treatment of patients with syndrome X.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Analysis_of_Variance_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Statistics__Nonparametric_MeSH M_Syndrome_X_MeSH S_drug_therapy_MeSH Syndrome_X_drug_therapy_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10517737
----K E
----T Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo.
----A BACKGROUND: We evaluated whether angiotensin II (Ang II) influenced intercellular adhesion molecule (ICAM)-1 expression by human vascular endothelial cells derived from umbilical cord veins (HUVECs) and plasma soluble ICAM-1 levels in vivo. METHODS: AND RESULTS: Cultured HUVECs were incubated with Ang II (from 10(-9) to 10(-6) mol/L) with or without candesartan and PD12319 (inhibitors of Ang II AT(1) and AT(2) receptors, respectively) for various times up to 4 hours. Total RNA was then extracted from HUVECs, and Northern blots were probed with a 1.9-kb ICAM-1 cDNA fragment. HUVEC supernatants were used to assess soluble ICAM-1 release by ELISA. Northern blot analysis detected a strong increase of ICAM-1 mRNA after 2-hour incubation with Ang II. The response was inhibited by candesartan. Soluble ICAM-1 release by HUVECs also increased (P<0. 002) after 2-hour Ang II stimulation. In vivo, Ang II (at an initial rate of 1.0 ng. kg(-1). min(-1), to be increased each 30 minutes by 2.0 ng. kg(-1). min(-1) to the final rate of 7.0 ng. kg(-1). min(-1)) was infused in 8 normotensive and 12 essential hypertensive individuals. In the latter, Ang II was reinfused after 4 weeks on either placebo (n=3), losartan (50 mg UID, n=5), or atenolol (50 mg UID, n=4) treatment. Plasma soluble ICAM-1 levels increased after Ang II infusion in hypertensives and normotensives (P<0.0001 after 90 minutes). Losartan reduced baseline soluble ICAM-1 levels (P<0.05) and Ang II-related ICAM-1 increments. CONCLUSIONS: Ang II upregulates ICAM-1 expression by HUVECs and stimulates in vitro and in vivo soluble ICAM-1 release. AT(1) receptor blockade inhibits such endothelial effects of Ang II.
----P Journal_Article 
----M M_Adult_MeSH M_Angiotensin_II_MeSH S_pharmacology_MeSH Angiotensin_II_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Cells__Cultured_MeSH M_Endothelium__Vascular_MeSH S_cytology_MeSH Endothelium__Vascular_cytology_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH M_Female_MeSH M_Gene_Expression_Regulation_MeSH S_drug_effects_MeSH Gene_Expression_Regulation_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Intercellular_Adhesion_Molecule-1_MeSH S_biosynthesis_MeSH Intercellular_Adhesion_Molecule-1_biosynthesis_MeSH S_genetics_MeSH Intercellular_Adhesion_Molecule-1_genetics_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_RNA__Messenger_MeSH S_biosynthesis_MeSH RNA__Messenger_biosynthesis_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptor__Angiotensin__Type_2_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_drug_effects_MeSH Receptors__Angiotensin_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Umbilical_Veins_MeSH 
****** 10524661
----K E
----T Migraine polypharmacy and the tolerability of sumatriptan: a large-scale, prospective study.
----A Polypharmacy (the prescription of more than one therapy for a single patient) and subcutaneous (s.c.) sumatriptan tolerability were prospectively studied in 12,339 migraineurs, each followed for up to 1 year. Inclusion/exclusion criteria were minimal and mirrored United States Imitrex labeling. Drug usage and compliance monitoring were automatically interfaced with prescription refill. Concomitant drugs were used by 79% of patients, with analgesics, antidepressants, and sedatives used most commonly. No adverse interactions between sumatriptan and neurological drugs were found, possibly reflecting relative inability of the former to cross the blood-brain barrier. No difference in cardiovascular adverse events was associated with oral contraceptive use, which was more common than expected. No other drug class influenced adverse event probability, although sample sizes for these comparisons was sometimes <400 patients. This study confirms the prevalence of polypharmacy in migraine, identifies the drugs used, and concludes that, on a population basis, the tolerability of s.c. sumatriptan, when used according to labeled instructions, is unaffected by these concomitant drugs.
----P Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Analgesics__Opioid_MeSH S_administration_&_dosage_MeSH Analgesics__Opioid_administration_&_dosage_MeSH S_therapeutic_use_MeSH Analgesics__Opioid_therapeutic_use_MeSH M_Anti-Asthmatic_Agents_MeSH S_therapeutic_use_MeSH Anti-Asthmatic_Agents_therapeutic_use_MeSH M_Anti-Infective_Agents_MeSH S_therapeutic_use_MeSH Anti-Infective_Agents_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_administration_&_dosage_MeSH Anti-Inflammatory_Agents__Non-Steroidal_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Anticonvulsants_MeSH S_administration_&_dosage_MeSH Anticonvulsants_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Antidepressive_Agents_MeSH S_adverse_effects_MeSH Antidepressive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Comorbidity_MeSH M_Contraceptives__Oral__Hormonal_MeSH S_adverse_effects_MeSH Contraceptives__Oral__Hormonal_adverse_effects_MeSH S_therapeutic_use_MeSH Contraceptives__Oral__Hormonal_therapeutic_use_MeSH M_Depression_MeSH S_drug_therapy_MeSH Depression_drug_therapy_MeSH S_epidemiology_MeSH Depression_epidemiology_MeSH M_Drug_Evaluation_MeSH P_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Epilepsy_MeSH S_drug_therapy_MeSH Epilepsy_drug_therapy_MeSH S_epidemiology_MeSH Epilepsy_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypnotics_and_Sedatives_MeSH S_administration_&_dosage_MeSH Hypnotics_and_Sedatives_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hypnotics_and_Sedatives_therapeutic_use_MeSH M_Injections__Subcutaneous_MeSH M_Male_MeSH M_Methysergide_MeSH S_administration_&_dosage_MeSH Methysergide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Methysergide_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_epidemiology_MeSH Migraine_epidemiology_MeSH M_Patient_Acceptance_of_Health_Care_MeSH M_Prospective_Studies_MeSH M_Serotonin_Agonists_MeSH S_adverse_effects_MeSH Serotonin_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Smoking_MeSH S_epidemiology_MeSH Smoking_epidemiology_MeSH M_Sumatriptan_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Valproic_Acid_MeSH S_administration_&_dosage_MeSH Valproic_Acid_administration_&_dosage_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH M_Vasoconstrictor_Agents_MeSH S_adverse_effects_MeSH Vasoconstrictor_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 10524662
----K E
----T Open-labeled long-term study of the efficacy, safety, and tolerability of subcutaneous sumatriptan in acute migraine treatment.
----A In a multicenter study, a long-term analysis was made of the efficacy, safety, and tolerability of subcutaneous (s.c.) sumatriptan in the acute treatment of migraine attacks over a period of up to 18 months. A total of 2263 patients took part in the study, all able to perform their own acute treatment of migraine attacks at home by s.c. administration of 6 mg of sumatriptan. A headache diary was used by each patient to record the various migraine parameters before the injection and 1 h and 2 h after it. A total of 43,691 attacks were treated and analyzed during the study period from October 1991 to June 1993. Therapy was successful in 89.5% of attacks. Freedom from headache was achieved in 71.0% of cases. In 22.7% of the attacks a second injection was administered on recurrence of the headache; 82.9% of the patients achieved an intraindividual therapy success rate ranging from over 80% to 100%. In the course of treatment there was no change in either the therapy success rate or in the frequency of attacks. Some 4.9% of the patients withdrew from the study because of insufficient efficacy or adverse events. A total of 44.5% of patients reported adverse events, and these were rated serious in the case of 1.7%. S.c. administration of sumatriptan for acute migraine therapy is an effective treatment method, with reliable action, that can be used with good tolerability provided the contraindications are taken into account.
----P Journal_Article Multicenter_Study 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Analgesics_MeSH S_administration_&_dosage_MeSH Analgesics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Antiemetics_MeSH S_administration_&_dosage_MeSH Antiemetics_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antiemetics_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cohort_Studies_MeSH M_Drug_Evaluation_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Headache_MeSH S_chemically_induced_MeSH Headache_chemically_induced_MeSH M_Human_MeSH M_Injections__Subcutaneous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Patient_Dropouts_MeSH M_Prospective_Studies_MeSH M_Recurrence_MeSH M_Safety_MeSH M_Serotonin_Agonists_MeSH S_administration_&_dosage_MeSH Serotonin_Agonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_administration_&_dosage_MeSH Sumatriptan_administration_&_dosage_MeSH S_adverse_effects_MeSH Sumatriptan_adverse_effects_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Time_Factors_MeSH M_Vasoconstrictor_Agents_MeSH S_administration_&_dosage_MeSH Vasoconstrictor_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Vasoconstrictor_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH 
****** 10523477
----K E
----T Effectiveness of nifedipine GITS in combination with atenolol in chronic stable angina.
----A Nifedipine gastrointestinal therapeutic system (GITS) is a once-daily formulation of nifedipine that provides stable plasma concentrations over the entire 24 h dosing interval. Two-hundred and one patients with Canadian Cardiovascular Society class II to III angina who were on 50 mg of atenolol yet still experiencing angina symptoms were randomized to receive either placebo or nifedipine GITS 30, 60 or 90 mg/day. After four weeks of treatment, the changes in time from baseline to onset of 1 mm ST segment depression in the 183 eligible patients were 26.7+/-10.2 s, 40.9+/-11.3 s, 63.2+/-12.9 s and 70.3+/-12.6 for the placebo, and 30, 60 and 90 mg/day groups, respectively. These differences were significant (P<0.05) for the 60 and 90 mg/day groups compared with placebo and for the 60 mg/day group compared with the 30 mg/day group. The times to onset of pain and termination of exercise showed similar prolongation but did not achieve statistical significance. During the one-year open label phase of the study, patients exhibited statistically significant improvements in the time to onset of ST segment depression, time to anginal pain and time to termination of exercise at a mean dose of 52.3 mg/day of nifedipine GITS. Adverse events were primarily vasodilatory in nature. This study supports the use of nifedipine GITS in patients with chronic stable angina inadequately controlled on beta-blocker alone.
----P Clinical_Trial Clinical_Trial__Phase_II Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 10523946
----K E
----T [Beta-blockade--a new therapeutic modality in chronic heart insufficiency]
----A Heart failure due to decreased left ventricular function is a condition with a considerable morbidity and mortality. Until recently beta-blocker treatment has been considered contraindicated in this condition. During the last 20 years a number of investigations have pointed to a possible positive effect of beta-blocker treatment in chronic heart failure and recently several major randomized trials have shown a significantly increased survival during beta-blocker treatment. This review summarizes the background for the use of beta-blocker treatment in chronic heart failure patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_English_Abstract_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 10525926
----K 1
----T [Efficacy of metoprolol in prevention of supraventricular arrhythmias after coronary artery bypass grafting]
----A Atrial fibrillation is in 20-50% the most frequent dysrhythmia after coronary artery bypass grafting (CABG) and a possible cause for hemodynamical complications and prolongation off the medical treatment in patients. Therefore, the effect of beta-blocking with metoprolol for prevention of supraventricular arrhythmias (SVA) was investigated in a prospective and randomized trial. 200 patients after CABG were randomized in a drug and control group (average age 63.2 years, 154 male, 46 female). Patients of the drug group (n=100) were treated with metoprolol (1mg/kg/BW) beginning on day one after operation, whereas patients of the control group (n=100) received therapy only in case of occurrence of atrial fibrillation. ECG, blood pressure, and electrolyte concentrations were measured regularly until the tenth day after surgery. Reasons for exclusion were an ejection fraction (< 30%, SA- and AV-block or simultaneous application of epinephrine and metoprolol. There were no significant differences between the patients of drug and control group with respect to age, sex ejection fraction, previous medication, number and type of bypass grafts, cardiopulmonary bypass time, and perioperative ischemic events. However, a statistically significant difference was seen in the occurrence of supraventricular arrhythmias in both groups, 4 patients of the therapy group (4%) in contrast to 37 patients of the control (37%) developed supraventricular arrhythmias during the postoperative observation period (p<0.0001). Both groups differed in total time of hospital stay by 1.5 days (control group: 9.83+/-2.88 days; drug group: 8.42+/-2.81 days), which was statistically significant (p<0.05). All patients of the drug group could be discharged with a stable sinus rhythm, whereas 7 patients of the control group were discharged with persistent atrial fibrillation. The difference was statistically significant as well (p<0.01). Neither typical side effects of metoprolol, nor AV-blocks, bradycardia (f<60/min) or symptoms of low blood pressure could be observed. The conclusion of this trial is a recommendation for a preventive application of 50mg metoprolol/day after coronary artery bypass surgery, which can reduce the incidence of SVA as well as the hospital stay statistically significant.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH P_Coronary_Artery_Bypass_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Length_of_Stay_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH M_Middle_Aged_MeSH M_Postoperative_Care_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Prospective_Studies_MeSH M_Tachycardia__Supraventricular_MeSH S_prevention_&_control_MeSH Tachycardia__Supraventricular_prevention_&_control_MeSH 
****** 10525515
----K E
----T Impact of concurrent amiodarone treatment on the tolerability and efficacy of carvedilol in patients with chronic heart failure.
----A OBJECTIVE: To assess the safety and efficacy of carvedilol when administered to heart failure patients already receiving amiodarone. DESIGN: Retrospective analysis of the clinical outcome of 230 patients treated with carvedilol for chronic heart failure, stratified according to whether they were already receiving amiodarone (amiodarone group, 80 patients) or not (non-amiodarone group, 130 patients) at baseline. SETTING: Heart failure clinic at a university affiliated public teaching hospital. MAIN OUTCOME MEASURES: Incidence of adverse events; changes in functional status and echocardiographic dimensions at three months. RESULTS: Adverse reactions to carvedilol occurred in 33 (41%) of the amiodarone group and 43 (29%) of the non-amiodarone group (p = 0.049). Carvedilol was discontinued in 21 (26%) of the amiodarone group and 37 (25%) of the non-amiodarone group (NS). The clinical outcome at three months did not differ significantly between the two groups; 31 (39%) of the amiodarone group improved their New York Heart Association status, 28 (35%) were unchanged, and 21 (26%) deteriorated compared with 67 (45%), 51 (34%), and 32 (21%), respectively, for the non-amiodarone group (NS). Both groups had highly significant decreases in heart rate and left ventricular end systolic dimension, and a significant increase in left ventricular ejection fraction after three months of carvedilol treatment, with no significant differences between the groups. CONCLUSIONS: The beneficial effects of carvedilol on left ventricular remodelling, systolic function, and symptomatic status are not affected by concurrent treatment with amiodarone. Adverse reactions necessitating cessation of carvedilol are no more frequent in patients receiving amiodarone.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_adverse_effects_MeSH Amiodarone_adverse_effects_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Survival_Rate_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 10529932
----K 3
----T The dorzolamide/timolol combination versus timolol plus pilocarpine: patient preference and impact on daily life. United States Patient Preference Study Group. International Patient Preference Study Group.
----A PURPOSE: To compare the 2.0% dorzolamide/0.5% timolol fixed combination (COSOPT; Merck & Co., Whitehouse Station, NJ) to 0.5% timolol plus 2.0% pilocarpine given concomitantly, and to determine patient preference, tolerability, and impact on daily life in patients with elevated intraocular pressure (IOP). METHODS: Two multi-center, randomized, cross-over, observer masked studies were conducted, one in the United States (97 patients) and one in Europe (93 patients). The Comparison of Ophthalmic Medications for Tolerability questionnaire was used to assess patient preference and perception of side effects and activity limitations resulting from study medications. Intraocular pressure was measured before and 2 hours after the morning dose of study medication (hour 0 and hour 2). RESULTS: In both studies, among patients with a preference, the combination was preterred to timolol plus pilocarpine by a ratio of 4 to 1. The most commonly cited reason for this preference was side effects. Patients in both studies also reported that the combination interfered significantly less with daily life in terms of side effects and activity limitations. They also reported missing significantly fewer doses of study medication while taking the combination and being significantly more satisfied with it. The efficacy of these two treatments was not significantly different, based on IOP measurements at hour 0 and 2 hours after administration. Patients reported significantly more adverse events while receiving timolol plus pilocarpine in both studies, and in the U.S. study, significantly more patients discontinued therapy while receiving timolol plus pilocarpine than while receiving the combination. CONCLUSION: Compared with timolol plus pilocarpine, patients preferred the combination of 2% dorzolamide/0.5% timolol, and reported less interference in daily activities, better tolerability, and better compliance with therapy.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M P_Activities_of_Daily_Living_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_adverse_effects_MeSH Carbonic_Anhydrase_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Miotics_MeSH S_adverse_effects_MeSH Miotics_adverse_effects_MeSH S_therapeutic_use_MeSH Miotics_therapeutic_use_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH M_Patient_Satisfaction_MeSH M_Pilocarpine_MeSH S_adverse_effects_MeSH Pilocarpine_adverse_effects_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH M_Questionnaires_MeSH M_Sulfonamides_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 10558453
----K E
----T Antihypertensive drugs: diuretics and betablockers are the best assessed.
----A (1) In trials involving hypertensive non diabetic patients under 65, some diuretics and betablockers have prevented strokes, without conferring protection from coronary events or death.  In one trial captopril had an effect comparable to that of diuretics or betablockers in terms of overall cardiovascular prevention, but was a little less effective in preventing strokes.  (2) In trials involving hypertensive subjects over 65, some diuretics and betablockers have reduced the risk of stroke, coronary events, heart failure, and death.  In one trial a diuretic was superior to a betablocker in terms of preventive efficacy and adverse effects.  Nitrendipine, in combination with other antihypertensive drugs, prevented strokes in one trial.  (3) In a trial involving hypertensive diabetic patients, captopril and atenolol reduced the risk of stroke, heart failure and worsening of retinal disease, without preventing coronary events or death.  In two trials coronary events were more frequent on dihydropyridine than on an angiotensin-coverting-enzyme (ACE) inhibitor.  (4) In one trial a diuretic reduced the risk of relapse after stroke, even in patients without severe hypertension.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH P_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cerebrovascular_Disorders_MeSH S_etiology_MeSH Cerebrovascular_Disorders_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Disorders_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH 
****** 12959269
----K E
----T Influence of CYP2D6-dependent metabolism on the steady-state pharmacokinetics and pharmacodynamics of metoprolol and nicardipine, alone and in combination.
----A 1 The metabolism of metoprolol depends in part on the genetically determined activity of the CYP2D6 isoenzyme. In vitro studies have shown that nicardipine is a potent inhibitor of CYP2D6 activity. Since the combination of metoprolol and nicardipine is likely to be used for the treatment of hypertension, we examined the interaction between these two drugs at steady-state. 2 Fourteen healthy volunteers, seven extensive and seven poor metabolisers of dextromethorphan were studied in a double-blind, randomised cross-over four-period protocol. Subjects received nicardipine 50 mg every 12 h, metoprolol 100 mg every 12 h, a combination of both drugs and placebo during 5.5 days. Steady-state pharmacokinetics of nicardipine and metoprolol were analyzed. Beta-adrenoceptor blockade was assessed as the reduction of exercise-induced tachycardia. 3 During treatment with metoprolol, alone or in combination with nicardipine, its steady-state plasma concentrations were higher in subjects of the poor metaboliser phenotype than in extensive metabolisers. Beta-adrenoceptor blockade was also more pronounced in poor metabolisers than in extensive metabolisers of dextromethorphan during treatment with metoprolol alone or in combination with nicardipine (24.0 +/- 2.4% vs 17.1 +/- 3.5% and 24.1 +/- 2.5% vs 15.4 +/- 2.7% reduction in exercise trachycardia, respectively, P < 0.01 in each case). 4 Nicardipine produced a small increase in plasma metoprolol concentration in extensive metabolisers from 35.9 +/- 16.6 to 45.8 +/- 15.4 ng ml(-1) (P < 0.02), but had no significant effect in poor metabolisers. However, nicardipine did not alter the R/S metoprolol ratio in plasma 3 h after dosing, the plasma concentration of S-(-)-metoprolol 3 h after dosing or the beta-adrenoceptor blockade produced by metoprolol in subjects of both phenotypes. The partial metabolic clearance of metoprolol to alpha-hydroxy-metoprolol was not altered significantly in extensive metabolisers. Plasma nicardipine concentration and beta-adrenoceptor blocking effects did not differ between the phenotypes and were not influenced by metoprolol. We conclude that beta-adrenoceptor blockade during repeated dosing with metoprolol is more pronounced in poor than in extensive metaboliser subjects, that nicardipine decreases a CYP2D6-independent route of metoprolol elimination but does not increase beta-adrenoceptor blockade during repeated dosing with metoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH M_Adult_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Cross-Over_Studies_MeSH M_Cytochrome_P-450_CYP2D6_MeSH S_metabolism_MeSH Cytochrome_P-450_CYP2D6_metabolism_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Drug_Interactions_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Isomerism_MeSH M_Male_MeSH M_Metoprolol_MeSH S_antagonists_&_inhibitors_MeSH Metoprolol_antagonists_&_inhibitors_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH M_Nicardipine_MeSH S_pharmacology_MeSH Nicardipine_pharmacology_MeSH M_Phenotype_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12959272
----K E
----T Haemodynamic comparison of amlodipine and atenolol in essential hypertension using the quantascope.
----A 1 We have utilised a non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensation volume flow (ACVF), to assess the cardiovascular effects of amlodipine and atenolol over 3 months in 24 patients with essential hypertension. 2 Both amlodipine and atenolol, at 4 and 12 weeks, similarly reduced mean arterial pressure (12 weeks amlodipine -12.6 mmHg, atenolol -14.9 mmHg; P < 0.01 for each vs baseline). 3 The heart rate fell on atenolol, both at 4 weeks (amlodipine -3 vs atenolol -12 beats min(-1); P < 0.05) and 12 weeks (-1 vs -11 beats min(-1); P < 0.05), without change on amlodipine. 4 Stroke volume initially rose on atenolol without change on amlodipine (4 weeks amlodipine -1.3 ml vs atenolol +10.1 ml; P = 0.05) but between drug effects were not different at 12 weeks. 5 The systemic vascular resistance was reduced on amlodipine (12 weeks: amlodipine -176 dyn s cm(-5): P < 0.05) without change on atenolol (atenolol -48 dyn s cm(-5): NS). 6 The cardiac stroke work was lowered on amlodipine both at 4 weeks (P < 0.01) and 12 weeks (P < 0.05) and statistically different from the unaltered atenolol values at both time points. 7 Skin nutrient flow or fingertip temperature was not altered by either treatment. 8 These results are consistent with contrasting mechanisms of action--vasodilator for amlodipine and decreased cardiac pumping for atenolol. The greater reduction in cardiac stroke work on amlodipine compared with atenolol warrants further investigation during longer-term studies.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Middle_Aged_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultrasonography__Doppler_MeSH M_Vascular_Resistance_MeSH S_drug_effects_MeSH Vascular_Resistance_drug_effects_MeSH 
****** 11822540
----K 5
----T Beta-adrenergic blocking drugs in the treatment of hypertension.
----A The reduction in blood pressure seen with the use of beta-blocking drugs was an unexpected finding. Initially there was resistance to their use as the reduction of cardiac output and increase in peripheral resistance from beta-blockade was considered an undesirable pharmacological action for a drug in the treatment of hypertension. However, beta-blockers have now become established in the treatment of hypertension and have been recommended as a first line choice in various guidelines, although their exact mode of action remains a matter for debate. In broad terms beta-blocking drugs are at least of similar efficacy to the other major classes of antihypertensive drugs. They may be usefully combined with other anti-hypertensives, as is often required. There is some evidence that the beta-1 selective agents are more efficacious than the non-selective beta-blockers. Notwithstanding some observations to the contrary beta-blockers are often effective antihypertensive agents in the elderly and in black patients; the combination of being elderly and black, however, appears to result in a reduced fall in blood pressure. If they are given early in pregnancy they lead to a low birth weight. Co-existant disease may influence the choice of a beta-blocker to treat hypertension. Beta-blockers are valuable agents in ischaemic heart disease, notably the control of chronic angina pectoris and to improve prognosis post-myocardial infarction. While initial dose titration has to be extremely careful, heart failure is now a strong indication for the use of a beta-blocker, as prognosis is much improved. Diabetes should no longer be regarded as a contra-indication to the use of a beta-1 selective agent. Recent work confirms that beta-blockers should be given to patients undergoing surgery who have a high cardiac risk. Outcome studies suggest overall that in younger patients beta-blockers reduce the incidence of strokes and myocardial infarction. There is no convincing evidence of a difference between the ACE inhibitor captopril and the combination of diuretic and a beta-blocker. In high risk patients, i.e. those with diabetes, no difference was seen between captopril and atenolol. Diuretics may result in better outcome measurements in the elderly compared to beta-blockade but in combination, "conventional treatment" is as effective in terms of total mortality, strokes and myocardial infarction as ACE inhibitors or calcium antagonists. Co-existant asthma remains an important contraindication to beta-blockade, but not chronic obstructive airways disease where a beta-blocker should be used with caution if it is indicated, e.g. post-infarction. Quality of life measurements, at least with beta-1 selective agents compare favourably with other anti-hypertensive drugs. Beta-blockers, without partial agonist activity, should not be stopped abruptly, particularly in patients with, or at high risk of, co-existant ischaemic disease because of the danger of post-beta-blockade cardiac sympathetic hypersensitivity; alternatively bed rest should be instituted to reduce the risk of sympathetic stimulation.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Controlled_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Risk_Factors_MeSH 
****** 12053057
----K 4
----T Nonselective Beta-adrenergic blockade augments fasting hyperkalemia in hemodialysis patients.
----A BACKGROUND/AIM: Fasting hyperkalemia in patients with end-stage renal failure is a well-documented phenomenon. Both a decreased secretion of insulin and decreased beta-adrenergic receptor sensitivity may take part in this effect. METHODS: Twelve anuric, long-term (6.4 +/- 2.7 years; mean +/- SD) hemodialysis patients underwent three periods of 18-hour fasting (from 6 p.m. to 12 a.m.). At the beginning of each fasting period a single dose of the nonselective beta-blocker, nadolol (80 mg), or the beta(1)-selective blocker, betaxolol (20 mg), or placebo were given in a random order and in blinded fashion. The wash-out period was 7 days. RESULTS: The mean decrease in blood pressure was similar after nadolol and betaxolol (18 +/- 10 vs. 19 +/- 11 mm Hg) as was a decrease in heart rate (20 +/- 3 and 19 +/- 6, respectively). Serum potassium was not different before each of the fasting periods. The increase in serum potassium during fasting was highly significant in each case. The mean increase in serum potassium was 1.2 +/- 0.4 mmol/l after nadolol, 0.9 +/- 0.6 after betaxolol and 0.6 +/- 0.6 after placebo. This effect was significantly larger after nadolol than after placebo (p = 0.01), but this relation was not significant with respect to betaxolol (p = 0.30). Serum insulin as well as glucose decreased significantly and to a similar extent during each fasting period. Plasma aldosterone was unchanged. CONCLUSION: Nonselective beta-adrenergic blockade increases the hyperkalemic effect of fasting in hemodialysis patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Blood_Glucose_MeSH M_Blood_Pressure_MeSH M_Fasting_MeSH M_Female_MeSH M_Human_MeSH M_Hyperkalemia_MeSH S_chemically_induced_MeSH Hyperkalemia_chemically_induced_MeSH S_etiology_MeSH Hyperkalemia_etiology_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_blood_MeSH Kidney_Failure__Chronic_blood_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_therapy_MeSH Kidney_Failure__Chronic_therapy_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH P_Renal_Dialysis_MeSH M_Sodium_MeSH S_blood_MeSH Sodium_blood_MeSH 
****** 12074350
----K E
----T Serum hepatocyte growth factor concentration is correlated with the forearm vasodilator response in hypertensive patients.
----A To evaluate the clinical importance of serum hepatocyte growth factor (HGF) concentration, we designed two clinical investigations. The first study analyzed the correlation between serum HGF concentration and clinical arterial stiffness or the vasodilator response to reactive hyperemia in hypertensive patients. The second study investigated the correlation between changes in serum HGF concentration and clinical arterial stiffness or reactive hyperemia during treatment with cilazapril or atenolol. A total of 210 hypertensive patients were analyzed in the first study, and 25 patients with essential hypertension were evaluated in the second study. Pulse wave velocity (PWV), strain gauge plethysmography, and serum HGF concentration were measured in the first study. We also evaluated these factors before and after treatment with either cilazapril (2.0 mg/day) or atenolol (25 mg/day) for 6 months in the second study. Serum HGF concentration was negatively correlated to reactive hyperemia in overall (r = 0.434, P < .0001) and nontreatment (r = 0.452, P < .0001) hypertensive patients. Arterial stiffness was weakly related to serum HGF concentration (P < .05) after adjusting for age and mean blood pressure (BP). By multiple regression analysis, only serum HGF concentration showed a strong independent correlation with reactive hyperemia, age and mean BP with PWV. Moreover, a relationship between endothelium-dependent vasodilation and serum HGF concentration was observed during treatment with cilazapril or atenolol (r = 0.406, P < .005). These results suggest that in evaluation of serum HGF concentration, the forearm vasodilator response to reactive hyperemia and PWV might be useful for managing hypertension in patients who are receiving antihypertensive therapy.
----P Evaluation_Studies Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Arteriosclerosis_MeSH S_physiopathology_MeSH Arteriosclerosis_physiopathology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cilazapril_MeSH S_pharmacology_MeSH Cilazapril_pharmacology_MeSH M_Endothelium__Vascular_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Hepatocyte_Growth_Factor_MeSH S_blood_MeSH Hepatocyte_Growth_Factor_blood_MeSH M_Human_MeSH M_Hyperemia_MeSH S_physiopathology_MeSH Hyperemia_physiopathology_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH P_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 12126264
----K E
----T Long-term exposure to telmisartan as monotherapy or combination therapy: efficacy and safety.
----A This multicentre, open-label extension study to four controlled trials involved 888 patients with mild-to-moderate primary hypertension. Patients received telmisartan 40-80 mg once daily with add-on hydrochlorothiazide (HCTZ; 12.5-25 mg) if necessary and/or other antihypertensives to achieve diastolic blood pressure (DBP) control (<90 mmHg). Treatment continued for up to 4 years. At treatment end, 578 (65.1%) patients were on telmisartan monotherapy, 106 (11.9%) were on telmisartan + HCTZ 12.5 mg, 101 (11.4%) were on telmisartan + HCTZ 25 mg, and 103 (11.6%) were on telmisartan + another antihypertensive + HCTZ. Overall, 84.4% (746/884) patients achieved DBP control. The highest proportion of responders was in the telmisartan monotherapy (40 or 80 mg) treatment category (89.0% 1,511/574 patients]). The mean change in systolic blood pressure (SBP)/DBP from the previous trial baseline to last available trough was -21.2/-17.3 mmHg with telmisartan alone, -24.6/-16.7 mmHg with telmisartan + HCTZ, and - 18.7/-14.9 mmHg with telmisartan + another antihypertensive +/- HCTZ. Most adverse events were of mild-to-moderate intensity and unrelated to treatment. The proportions of patients discontinuing the study due to adverse events, by treatment at onset, were 7.3% (65/888) with telmisartan monotherapy, 6.6% (20/304) with telmisartan + HCTZ and 2.9% (3/103) with telmisartan + another antihypertensive +/- HCTZ. There were 15 deaths during the study, but none was considered drug related. Thus, telmisartan alone or in combination with other antihypertensives achieved and maintained clinically relevant reductions in DBP and SBP. This long-term analysis supports the favourable efficacy and safety profile of telmisartan both as monotherapy and in combination with other antihypertensive drugs.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_toxicity_MeSH Antihypertensive_Agents_toxicity_MeSH M_Benzimidazoles_MeSH S_administration_&_dosage_MeSH Benzimidazoles_administration_&_dosage_MeSH S_toxicity_MeSH Benzimidazoles_toxicity_MeSH M_Benzoates_MeSH S_administration_&_dosage_MeSH Benzoates_administration_&_dosage_MeSH S_toxicity_MeSH Benzoates_toxicity_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Consumer_Product_Safety_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Therapeutic_Equivalency_MeSH 
****** 12126265
----K E
----T Nebivolol vs amlodipine as first-line treatment of essential arterial hypertension in the elderly.
----A The antihypertensive efficacy of nebivolol and amlodipine and their tolerability were compared in a multicentre, randomized, active-controlled, double-blind parallel-group trial in elderly patients with mild to moderate essential arterial hypertension. One hundred and eighty-four subjects aged > or = 65 years were screened. After a run-in phase of 4 weeks, only 168 of these were randomized with either nebivolol 2.5-5 mg daily (n = 81) or amlodipine 5-10 mg daily (n = 87) over a period of 12 weeks. The response rate to treatment and the changes of sitting diastolic blood pressure (BP) at week 12 were similar between the two groups. A lower sitting systolic BP (SBP) was detected with amlodipine at week 4 (p < 0.05) and at week 8 (p < 0.05). Standing BP showed no changes between the two groups; only SBP was lower with amlodipine at week 8 (p < 0.05). Heart rate was lower at all treatment visits with nebivolol (p < 0.001). The incidence of adverse events was no different between the two groups; however the incidence of headache and ankle oedema was significantly higher with amlodipine (p < 0.05). In elderly subjects with essential hypertension, the antihypertensive efficacy of nebivolol and amlodipine was similar. Both drugs were well tolerated, although amlodipine was accompanied by higher incidence of drug-related adverse events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Amlodipine_MeSH S_administration_&_dosage_MeSH Amlodipine_administration_&_dosage_MeSH S_toxicity_MeSH Amlodipine_toxicity_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_toxicity_MeSH Antihypertensive_Agents_toxicity_MeSH M_Benzopyrans_MeSH S_administration_&_dosage_MeSH Benzopyrans_administration_&_dosage_MeSH S_toxicity_MeSH Benzopyrans_toxicity_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Edema_MeSH S_chemically_induced_MeSH Edema_chemically_induced_MeSH M_Ethanolamines_MeSH S_administration_&_dosage_MeSH Ethanolamines_administration_&_dosage_MeSH S_toxicity_MeSH Ethanolamines_toxicity_MeSH M_Headache_MeSH S_chemically_induced_MeSH Headache_chemically_induced_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 12131543
----K E
----T Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study.
----A OBJECTIVE : To examine the time course of left ventricular (LV) geometric response to blood pressure (BP) control during 2 years of systematic antihypertensive treatment. DESIGN : A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens. SETTING : The LIFE trial, in which hypertensive patients with electrocardiographic LVH (Cornell voltage-duration product > 2440 mm x ms and/or Sokolow-Lyon voltage criteria SV1 + RV5-6 > 38 mm) were randomized to >or= 4 years double-blinded treatment with losartan or atenolol. PARTICIPANTS : A total of 754 LIFE participants with serial echocardiographic measurements of LV geometry. INTERVENTIONS : None. MAIN OUTCOME MEASURES : LV wall thicknesses, diameter and mass, and its indices. RESULTS : Mean systolic/diastolic BP fell from 173/95 to 150/84 mmHg after 1 year (P < 0.001) and to 148/83 mmHg at year 2 (P = not significant). Mean echocardiographic LV mass fell from 233 g at baseline to 206 g after 1 year (P < 0.001, adjusted for change in systolic BP) and to 195 g at year 2 (P < 0.001 versus year 1), with a parallel decrease in indexed LV mass [from 56.1 to 49.7 g/m2.7 (P < 0.001), to 47.1 g/m2.7 (P < 0.001 versus year 1)]. Relative wall thickness decreased from 0.41 at baseline to 0.37 at year 1 (P < 0.001), to 0.36 at year 2 (P < 0.001 versus year 1). As a result, there were serial decreases in prevalences of eccentric LVH [44 to 38%, and to 30% (P < 0.001 versus year 1)] and concentric LVH [24 to 7% (P < 0.001), to 2% (P < 0.05 versus year 1)], and increases in the proportion with normal LV geometry [22 to 50% (P < 0.001), and to 64% (P < 0.01 versus year 1)]. CONCLUSIONS : Sustained BP reduction in hypertensive patients with target organ damage causes continued decrease in echocardiographic LV mass and prevalence of anatomic LVH for at least 2 years despite only small BP decreases after the first year of blinded therapy. These data document cardiac benefit of sustained BP control and suggest that maximum LVH regression with effective antihypertensive treatment requires at least 2 years.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comparative_Study_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Endpoint_Determination_MeSH M_Europe_MeSH S_epidemiology_MeSH Europe_epidemiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Ventricles_MeSH S_ultrasonography_MeSH Heart_Ventricles_ultrasonography_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_epidemiology_MeSH Hypertrophy__Left_Ventricular_epidemiology_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prevalence_MeSH M_Regression_Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_Ventricular_Remodeling_MeSH S_physiology_MeSH Ventricular_Remodeling_physiology_MeSH 
****** 12172314
----K E
----T Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study.
----A OBJECTIVE : To compare the relationships of treatment-induced reductions of left ventricular hypertrophy to the changes in clinic and ambulatory blood pressure (BP). DESIGN : Double-blind and randomized treatment with irbesartan or atenolol for 48 weeks. PATIENTS : Patients with hypertension and left ventricular hypertrophy (n = 66) with a seated diastolic BP 90-115 mmHg (average of three measurements one minute apart by nurses). MAIN OUTCOME MEASURES : Registrations of echocardiographic left ventricular (LV) mass. Clinic and ambulatory BP. RESULTS : In the total material, nurse-measured BP was reduced by 23 +/- 15/16 +/- 7.7 mmHg and 24-h ambulatory BP fell 20 +/- 15/14 +/- 8.5 mmHg by treatment. The correlation between the change in nurse-measured BP and LV mass index (LVMI) induced by treatment was r = 0.35, P = 0.004 for systolic BP and r = 0.26, P = 0.03 for diastolic BP. Corresponding values for 24-h ambulatory BP were r = 0.29, P = 0.02 and r = 0.35, P = 0.004, respectively, with similar correlations for day- and night-time ambulatory BP. The nurse-recorded BP was slightly higher than ambulatory BP (systolic clinic - systolic 24-h ambulatory BP = 5 mmHg). Using 130/80 mmHg as a cut-off value for normal 24-h ambulatory BP, eight subjects had normal diastolic or systolic ambulatory BP, or both. Interestingly, these patients also experienced LVMI regression following treatment (low/normal ABP, -13 +/- 21 g/m2; remaining patients, -18 +/- 22 g/m2, P > 0.5). CONCLUSIONS : In patients with hypertension and left ventricular hypertrophy, ambulatory BP is not superior to carefully standardized nurse-recorded seated BP in terms of associations with treatment-induced changes in LV mass.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Determination_MeSH S_nursing_MeSH Blood_Pressure_Determination_nursing_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 12172327
----K E
----T Effects of six anti-hypertensive medications on cognitive performance.
----A OBJECTIVE: To describe and compare the effects of six different antihypertensive medications on cognitive performance. DESIGN : Prospective, randomized, and double-blind with treatment cross-over. SETTING : University hypertension clinic and neuropsychology laboratory. PARTICIPANTS: Ninety-eight Caucasian men between 25 and 55 years of age with mild-to-moderate essential hypertension (88 of whom completed the study), and 32 normotensive men with similar socio-demographic characteristics. INTERVENTIONS : Six-week treatment periods with atenolol, metoprolol, hydrochlorothiazide, methyldopa, enalapril and verapamil, and 2-week placebo baseline and wash-out periods. MAIN OUTCOME MEASURES : In-depth neuropsychological assessments and several mood questionnaires were completed during placebo (baseline) periods and active treatment periods. Practice effects due to repeated neuropsychological testing were estimated from data collected concurrently in the normotensive participants. RESULTS : The antihypertensive treatments lowered blood pressure comparably and did not affect mood or anxiety. Small treatment effects were noted in four of seven domains of cognitive performance. Irrespective of medication type, treatment reduced the simple motor speed (P < 0.001), and slowed completion of two tests measuring perceptuo-motor speed and mental flexibility (P </= 0.05). Manual dexterity declined somewhat with metoprolol and methyldopa (P = 0.01). In contrast, all antihypertensive agents favorably affected performance on several tests that require working memory (P < 0.01). Performance on other tests assessing grip strength, learning and memory, attention and executive function was not affected. CONCLUSION : Short-term treatment with standard antihypertensive medications was associated with some small decrements in psychomotor performance and small improvements in working memory, without notable drug-class differences. Long-term effects await further study.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cognition_MeSH S_drug_effects_MeSH Cognition_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH M_Male_MeSH M_Memory_MeSH S_drug_effects_MeSH Memory_drug_effects_MeSH M_Middle_Aged_MeSH M_Neuropsychological_Tests_MeSH M_Prospective_Studies_MeSH M_Psychomotor_Performance_MeSH S_drug_effects_MeSH Psychomotor_Performance_drug_effects_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12172328
----K E
----T Gender influence on the dose-ranging of a low-dose perindopril-indapamide combination in hypertension: effect on systolic and pulse pressure.
----A BACKGROUND : Dose-ranging of antihypertensive agents have been done to optimize diastolic blood pressure (DBP) reduction, but with little information on systolic (SBP), mean (MBP), or pulse (PP) pressures. A low-dose combination of perindopril (Per) and indapamide (Ind) has been shown to reduce more SBP than atenolol for the same DBP reduction. However, the possible influence of gender on this finding has never been tested. PURPOSE : A database of five randomized, double-blind, dose-ranging studies was established to determine the optimal dose of the Per/Ind combination in hypertensive men and women. A total of 2907 patients were treated by either placebo or various combinations associating Per (2, 4, 8 mg) and Ind (0.625, 1.25, 2.5 mg). RESULTS : In the overall population, there was a significant dose-response relationship (P < 0.001) for doubling the dose of Per 2/Ind 0.625 mg up to Per 8/Ind 2.5 mg with a progressive fall in SBP, DBP, MBP. When men and women were analyzed by dose, SBP, DBP and MBP (but not PP) decreased significantly more in women than in men until the Per 4/Ind 1.25 dosage was reached. Thereafter, with higher dosages, generating a slight but significant hypokalemia, the finding was reversed, resulting in a gender interaction in the overall population. CONCLUSION : In hypertensive subjects, the low-dose combinations Per 2/Ind 0.625 and Per 4/Ind 1.25 are the most effective in reducing blood pressure and avoiding hypokalemia. This effect is more pronounced in women, in which increased SBP and PP are predominant hemodynamic features.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Databases__Factual_MeSH M_Diuretics__Sulfamyl_MeSH S_administration_&_dosage_MeSH Diuretics__Sulfamyl_administration_&_dosage_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Indapamide_MeSH S_administration_&_dosage_MeSH Indapamide_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH M_Sex_Characteristics_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12175626
----K 4
----T Nadolol is superior to isosorbide mononitrate for the prevention of the first variceal bleeding in cirrhotic patients with ascites.
----A BACKGROUND/AIMS: beta-blockers effectively prevent first variceal bleeding (FVB) in cirrhotic patients. In patients with ascites, however, their use might be precluded by a high rate of contraindications and side effects. We compared the efficacy and applicability of nadolol and isosorbide-mononitrate (IsMn) in preventing FVB in a population of cirrhotic patients at high risk of variceal bleeding with ascites, who can be frequently intolerant to beta-blockers. METHODS: A total of 80 consecutive cirrhotic patients with ascites and esophageal varices (25% average risk of bleeding at 1 year) were considered, 28 were excluded due to contraindications and 52 were randomly assigned to receive nadolol (n=25) or IsMn (n=27). RESULTS: Frequency of contraindications was greater for beta-blockers than IsMn (35 versus 0%, P=0.001). During 21.3+/-11.6 months of follow-up, side effects forced six patients taking nadolol and four taking IsMn to stop treatment. Bleeding occurred in two patients taking nadolol and ten taking IsMn. The probability of bleeding was significantly lower in the nadolol group (P<0.05), whereas overall survival was similar (seven patients on IsMn and eight on nadolol died, P=0.3). CONCLUSIONS: In patients with ascites IsMn is tolerated but ineffective while nadolol is effective but less tolerated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Ascites_MeSH S_complications_MeSH Ascites_complications_MeSH S_mortality_MeSH Ascites_mortality_MeSH M_Blood_Pressure_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_drug_therapy_MeSH Gastrointestinal_Hemorrhage_drug_therapy_MeSH S_mortality_MeSH Gastrointestinal_Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH M_Kidney_MeSH S_physiology_MeSH Kidney_physiology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_mortality_MeSH Liver_Cirrhosis_mortality_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_administration_&_dosage_MeSH Nadolol_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 12182261
----K E
----T Comparison of the effects of losartan and atenolol on common carotid artery intima-media thickness in patients with hypertension: results of a 2-year, double-blind, randomized, controlled study.
----A BACKGROUND: Hypertension induces progressive pathologic changes in the arterial wall. Experimental findings suggest that these changes, which include intima-media thickening, may be mediated, at least in part, by angiotensin II (AII). OBJECTIVE: The Losartan Vascular Regression Study (LAARS) was a double-blind, parallel-group, randomized, controlled, multicenter study designed to compare the effects of the AII antagonist losartan and the beta-blocker atenolol on ultrasonographically determined intimamedia thickness (IMT) of the common carotid artery (CCA) in patients with mild to moderate essential hypertension. METHODS: The primary end point of the study was the yearly rate of change (YRC) from baseline of the mean IMT of the CCA (CCA-IMT(mean)) averaged over 2 years of treatment. Secondary end points included IMT of the common femoral artery and sitting systolic and diastolic blood pressures (SiSBP/SiDBP). Safety assessments of losartan and atenolol were made by statistical and clinical review of the incidence of adverse experiences as well as review of vital signs and laboratory values. A total of 414 patients with essential hypertension were screened for study inclusion at 36 study centers in Germany and Brazil. Patients received losartan (50 mg once daily) or atenolol (50 mg once daily) for 24 months. Target blood pressure (SiSBP/SiDBP <140/<90 mm Hg) was achieved by adding hydrochlorothiazide 12.5 mg once daily, doubling the dose of study drug, or adding an open-label calcium channel blocker sequentially, as needed. RESULTS: Of the original 414 patients screened, 280 hypertension patients (SiDBP 95-115 mm Hg), aged 35 to 65 years, with an IMT of 0.8 to 1.5 mm of the right or left CCA, were randomized to treatment with either losartan (n = 142) or atenolol (n = 138). Both losartan and atenolol therapy produced comparable reductions in CCA-IMTmean over 24 months compared with baseline; the average YRC was -0.038 +/- 0.004 mm/y (P < or = 0.001) for losartan and -0.037 +/- 0.004 mm/y (P < or = 0.001) for atenolol. There were no significant differences between groups. Losartan showed a greater reduction of femoral artery IMT than did atenolol; the average YRC was -0.024 mm/y (P < or = 0.05) for losartan and -0.017 mm/y for atenolol (P = NS), with no significant difference between groups. Both agents produced similar significant reductions in SiSBP and SiDBP and were generally well tolerated. Approximately 7% of losartan patients had drug-related clinical adverse events, compared with 12% of atenolol patients. Conclusions: The findings of LAARS, the first large study with an AII antagonist that examined IMT, suggest that AII antagonism reverses the early stages of vascular hypertrophy in patients with hypertension. Further studies are needed to delineate the relative importance of AII antagonism versus blood pressure reduction per se in mediating the beneficial vascular effects of losartan.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Carotid_Artery__Common_MeSH S_drug_effects_MeSH Carotid_Artery__Common_drug_effects_MeSH S_pathology_MeSH Carotid_Artery__Common_pathology_MeSH S_physiopathology_MeSH Carotid_Artery__Common_physiopathology_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_pathology_MeSH Hypertension_pathology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH M_Tunica_Intima_MeSH S_drug_effects_MeSH Tunica_Intima_drug_effects_MeSH S_pathology_MeSH Tunica_Intima_pathology_MeSH S_physiopathology_MeSH Tunica_Intima_physiopathology_MeSH M_Tunica_Media_MeSH S_drug_effects_MeSH Tunica_Media_drug_effects_MeSH S_pathology_MeSH Tunica_Media_pathology_MeSH S_physiopathology_MeSH Tunica_Media_physiopathology_MeSH 
****** 12195121
----K E
----T Effects of nebivolol and atenolol on small arteries and microcirculatory endothelium-dependent dilation in hypertensive patients undergoing isometric stress.
----A OBJECTIVE: To examine the effects on small arteries and on the cutaneous microcirculatory system of nebivolol and atenolol in hypertensive patients. DESIGN: Twenty hypertensive patients were randomly assigned to receive nebivolol or atenolol in a single-blind, placebo-controlled cross-over study. Piezoelectric plethysmography on the third finger, laser Doppler on the third finger at rest and after iontophoretic administration of acetylcholine, and pressure-heart rate monitoring, were carried out both at rest and during handgrip. The tests were performed 45 min after 5 mg nebivolol or 100 mg atenolol administration, then repeated 2 days later with a placebo and, after a further 2 days, with atenolol or nebivolol again. RESULTS: Both atenolol and nebivolol reduced diastolic blood pressure values and heart rate, as well the increase of blood pressure and heart rate during handgrip. No change was recorded after placebo. Piezoelectric plethysmography showed a significant increase in the ratio between time to peak and total time (PT/TT), calculated on the sphygmic wave, during handgrip (0.295 0.005 versus 0.231 0.015, P<0.005). After nebivolol, a decrease was recorded in rest conditions (0.185 0.008 versus 0.231 0.015, P<0.005) with no statistically significant increase during handgrip, whereas atenolol showed an increase in the PT/TT ratio at rest, with a sustained response during handgrip. Laser Doppler showed an increased response to acetylcholine only after nebivolol. CONCLUSIONS: Nebivolol and atenolol significantly reduced diastolic blood pressure and heart rate, favourably modulating response to handgrip. Nebivolol improved small artery distensibility index. Endothelium-dependent cutaneous vasodilation after acetylcholine demonstrated a lack of response with atenolol whereas nebivolol favourably acts on endothelial function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Acetylcholine_MeSH S_pharmacology_MeSH Acetylcholine_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Arteries_MeSH S_drug_effects_MeSH Arteries_drug_effects_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Diastole_MeSH M_Endothelium__Vascular_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Ethanolamines_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Hand_Strength_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Isometric_Contraction_MeSH M_Male_MeSH M_Microcirculation_MeSH S_drug_effects_MeSH Microcirculation_drug_effects_MeSH M_Middle_Aged_MeSH M_Single-Blind_Method_MeSH M_Stress_MeSH S_physiopathology_MeSH Stress_physiopathology_MeSH M_Time_Factors_MeSH P_Vasodilation_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH 
****** 12195129
----K 3
----T Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy.
----A OBJECTIVE: To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH. DESIGN: A multinational, randomized, double-blind trial. SETTING: Hospital. PATIENTS: Hypertensive patients with an echocardiographically documented left ventricular mass index (LVMI) 120 g/m(2) (men) or 105 g/m(2) (women). INTERVENTIONS: Patients allocated randomly to groups received either losartan or atenolol 50 mg/day for 36 weeks, with possible titration to 100 mg/day, and addition of hydrochlorothiazide 12.5 or 25 mg/day. MAIN OUTCOME MEASURES: Changes in LVMI and sitting systolic (SBP) and diastolic (DBP) blood pressures after 36 weeks of treatment (study powered for non-inferiority hypothesis). All echocardiographic data were read in a central laboratory by staff blinded to the treatments and sequence of echocardiographic tapes. RESULTS: The estimated treatment difference between the losartan and atenolol regimens (mean change from baseline at week 36) in LVMI was -2.5 g/m(2) [95% confidence interval (CI) -7.36 to 2.37 g/m(2) ] in favor of losartan, indicating that losartan was significantly non-inferior ( 0.001, non-inferiority limit 8 g/m(2) ) and numerically superior to atenolol in reducing LVMI. The losartan-based regimen significantly reduced LVMI after 36 weeks compared with baseline (-6.56 g/m(2) , 95% CI -10.24 to -2.88 g/m(2) , P<0.001), whereas the atenolol-based regimen had no significant effect (-3.71 g/m, 95% CI -7.75 to 0.32 g/m(2) , P= NS). In a subset of 82 patients, significant changes in serum concentrations of atrial natriuretic peptide, brain natriuretic peptide and immunoreactive amino-terminal pro-brain natriuretic peptide were recorded in losartan-treated ( 0.01) but not atenolol-treated patients. Losartan and atenolol significantly decreased SBP and DBP from baseline after 6, 12, 24 and 36 weeks. The changes from baseline in DBP were greater in the atenolol group at weeks 6 and 36 [difference -2.6 mmHg ( P= 0.016) at week 36]. However, both treatment regimens achieved similar SBP/DBP values at week 36 (141.1 +/- 12.8/86.8 +/- 8.2 mmHg for losartan and 141.4 +/- 17.2/85.0 +/- 10.1 mmHg for atenolol, respectively). Overall, losartan treatment was associated with significantly fewer drug-related clinical adverse events, compared with atenolol (10 and 22%, respectively, P= 0.028). CONCLUSIONS: Both losartan- and atenolol-based regimens effectively decreased blood pressure. Losartan was non-inferior and numerically superior to atenolol in regression of LVH. The reduction in hypertrophy with losartan treatment was accompanied by reductions in circulating concentrations of cardiac natriuretic peptides. Losartan, by specifically blocking angiotensin II, may therefore have effects on the heart beyond those expected from the decrease in blood pressure alone. Losartan was better tolerated than atenolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH P_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Neurotransmitters_MeSH S_blood_MeSH Neurotransmitters_blood_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12195132
----K E
----T Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study.
----A BACKGROUND: There has been uncertainty about the risk of new-onset diabetes in hypertensive individuals treated with different blood pressure-decreasing drugs. OBJECTIVES: To study this risk in hypertensive individuals who were at risk of developing diabetes mellitus in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. METHODS: In the LIFE study, with a double-masked, randomized, parallel-group design, 9193 patients (46% men) with hypertension (mean age 67 years, average pressure 174/98 mmHg after placebo run-in) and electrocardiogram-documented left ventricular hypertrophy were randomly assigned to once-daily losartan- or atenolol-based antihypertensive treatment and followed for at least 4 years (mean 4.8 years). At baseline, 7998 patients did not have diabetes mellitus and were thus at risk of developing this condition during the study. To demonstrate ability to predict new-onset diabetes, we developed a prediction score using the significant variables from multivariate analyses (serum glucose, body mass index, serum high-density lipoprotein cholesterol, systolic blood pressure and history of prior use of antihypertensive drugs). RESULTS: There was a steadily increasing risk of diabetes with increasing level-of-risk score; patients in the highest quartile were at considerably greater risk than those in the three lower ones. Treatment with losartan was associated with lower risk of development of diabetes within each of the four quartiles of the risk score. As previously reported, new-onset diabetes mellitus occurred in 242 patients receiving losartan (13.0 per 1000 person-years) and 320 receiving atenolol (17.5 per 1000 person-years); relative risk 0.75 (95% confidence interval 0.63 to 0.88; P<0.001). CONCLUSIONS: New-onset diabetes could be strongly predicted by a newly developed risk score using baseline serum glucose concentration (non-fasting), body mass index, serum high-density lipoprotein cholesterol concentration, systolic blood pressure and history of prior use of antihypertensive drugs. Independently of these risk factors, fewer hypertensive patients with left ventricular hypertrophy developed diabetes mellitus if they were treated with losartan than if they were treated with atenolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_etiology_MeSH Hypertrophy__Left_Ventricular_etiology_MeSH M_Incidence_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12227681
----K E
----T Oxidative stress and TGFbeta in kidney-transplanted patients with cyclosporin-induced hypertension. Effect of carvedilol and nifedipine.
----A Cyclosporin is a powerful stimulator of oxidative stress signaling, leading to TGFbeta production, NO degradation, endothelial dysfunction, hypertension and post-transplant nephropathy. Carvedilol, alpha1-beta-blocker with strong antioxidant activity, may interfere with this chain of events. Therefore, we measured monocyte ecNOS, TGFbeta and heme oxygenase-1 (HO-1) mRNA level and plasma nitrite/nitrate, 3-nitrotyrosine, an estimate of peroxynitrite, and total plasma antioxidant power in kidney-transplanted patients with post-transplant hypertension, before and after treatment with carvedilol, 25 - 50 mg o.d. orally for 4 months (n = 15). The dihydropyridine calcium channel blocker nifedipine (n = 10) was used as comparator antihypertensive drug. Blood pressure fell to a similar extent with both drugs. Carvedilol increased plasma antioxidant power and HO-1 mRNA and reduced 3-nitrotyrosine and TGFbeta mRNA levels, while the same was not observed with nifedipine. Monocyte ec NOS mRNA levels and plasma nitrite/nitrate were higher in the patients than in a normotensive healthy control group and were unaffected by either treatment. In conclusion, carvedilol reduces the oxidative stress and corrects the altered cellular signaling mediated by oxidative stress in CsA-induced post-transplant hypertension. Therefore, it may prevent long-term complications, such as endothelial dysfunction, fibrogenesis and post-transplant nephropathy by decreasing NO degradation and production of TGFbeta, a key fibrogenic cytokine, and by activating HO-1 production.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cyclosporine_MeSH S_adverse_effects_MeSH Cyclosporine_adverse_effects_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Heme_Oxygenase_(Decyclizing)_MeSH S_biosynthesis_MeSH Heme_Oxygenase_(Decyclizing)_biosynthesis_MeSH S_blood_MeSH Heme_Oxygenase_(Decyclizing)_blood_MeSH S_drug_effects_MeSH Heme_Oxygenase_(Decyclizing)_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_chemically_induced_MeSH Hypertension_chemically_induced_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Immunosuppressive_Agents_MeSH S_adverse_effects_MeSH Immunosuppressive_Agents_adverse_effects_MeSH P_Kidney_Transplantation_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Nitric_Oxide_MeSH S_blood_MeSH Nitric_Oxide_blood_MeSH M_Nitric-Oxide_Synthase_MeSH S_blood_MeSH Nitric-Oxide_Synthase_blood_MeSH S_drug_effects_MeSH Nitric-Oxide_Synthase_drug_effects_MeSH M_Oxidative_Stress_MeSH S_drug_effects_MeSH Oxidative_Stress_drug_effects_MeSH M_Postoperative_Complications_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH S_metabolism_MeSH Postoperative_Complications_metabolism_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_RNA__Messenger_MeSH S_biosynthesis_MeSH RNA__Messenger_biosynthesis_MeSH S_drug_effects_MeSH RNA__Messenger_drug_effects_MeSH M_Signal_Transduction_MeSH S_drug_effects_MeSH Signal_Transduction_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Transforming_Growth_Factor_beta_MeSH S_biosynthesis_MeSH Transforming_Growth_Factor_beta_biosynthesis_MeSH S_blood_MeSH Transforming_Growth_Factor_beta_blood_MeSH S_drug_effects_MeSH Transforming_Growth_Factor_beta_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Tyrosine_MeSH S_analogs_&_derivatives_MeSH Tyrosine_analogs_&_derivatives_MeSH S_biosynthesis_MeSH Tyrosine_biosynthesis_MeSH S_blood_MeSH Tyrosine_blood_MeSH S_drug_effects_MeSH Tyrosine_drug_effects_MeSH 
****** 12228852
----K E
----T Comparison of the effects of antihypertensive treatment with angiotensin II blockade and beta-blockade on carotid wall structure and haemodynamics: protocol and baseline demographics.
----A Several systemic factors have been shown to contribute to the acceleration of large vessel atheroma. Correction of these factors leads to a reduction in the progression of plaque formation and associated arterial wall thickness. Atheroma remains, however, a focal disease, developing at characteristic sites within the arterial tree. These sites are typically at areas of vessel branching or marked curvature, and correspond to regions of high tensile stress and low sheer stress, leading to the hypothesis that local haemodynamic factors and vessel wall mechanics potentiate the focal development of atheroma. Current assessment of vascular haemodynamics suffers from an inability to handle complex flow, and does not allow accurate determination of locally varying flow, and shear stress patterns. The application of computational fluid dynamic (CFD) flow simulation techniques to ultrasound and local pressure data, however, allows a comprehensive, non-invasive appraisal of haemodynamic flow parameters to be performed. The Candesartan cilexetil and Atenolol Carotid Haemodynamic Endpoint Trial (CACHET) study compares the effects of two antihypertensive regimens, one b-blocker-based, the other angiotensin receptor blocker based, on carotid intima-media thickness. The collection of ultrasound and pressure data on each subject provides a unique opportunity to apply these data to the CFD model to study the effects of these antihypertensive regimens on local fluid dynamics. This will lead to a greater understanding of the relationship of these factors to atheroma formation and regression.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Arteriosclerosis_MeSH S_drug_therapy_MeSH Arteriosclerosis_drug_therapy_MeSH S_pathology_MeSH Arteriosclerosis_pathology_MeSH S_ultrasonography_MeSH Arteriosclerosis_ultrasonography_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Benzimidazoles_MeSH S_administration_&_dosage_MeSH Benzimidazoles_administration_&_dosage_MeSH M_Biphenyl_Compounds_MeSH S_administration_&_dosage_MeSH Biphenyl_Compounds_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Carotid_Artery__Common_MeSH S_pathology_MeSH Carotid_Artery__Common_pathology_MeSH S_physiology_MeSH Carotid_Artery__Common_physiology_MeSH S_ultrasonography_MeSH Carotid_Artery__Common_ultrasonography_MeSH M_Cerebrovascular_Circulation_MeSH S_drug_effects_MeSH Cerebrovascular_Circulation_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Image_Processing__Computer-Assisted_MeSH M_Laser-Doppler_Flowmetry_MeSH M_Male_MeSH M_Manometry_MeSH M_Middle_Aged_MeSH M_Models__Cardiovascular_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12230591
----K 5
----T Migraine: preventive treatment.
----A Migraine is a common episodic headache disorder. A comprehensive headache treatment plan includes acute attack treatment to relieve pain and impairment and long-term preventive therapy to reduce attack frequency, severity, and duration. Circumstances that might warrant preventive treatment include: (i) migraine that significantly interferes with the patient's daily routine despite acute treatment; (ii) failure, contraindication to, or troublesome side-effects from acute medications; (iii) overuse of acute medications; (iv) special circumstances, such as hemiplegic migraine; (v) very frequent headaches (more than two a week); or (vi) patient preference. Start the drug at a low dose. Give each treatment an adequate trial. Avoid interfering, overused, and contraindicated drugs. Re-evaluate therapy. Be sure that a woman of childbearing potential is aware of any potential risks. Involve patients in their care to maximize compliance. Consider co-morbidity. Choose a drug based on its proven efficacy, the patient's preferences and headache profile, the drug's side-effects, and the presence or absence of coexisting or co-morbid disease. Drugs that have documented high efficacy and mild to moderate adverse events (AEs) include beta-blockers, amitriptyline, and divalproex. Drugs that have lower documented efficacy and mild to moderate AEs include selective serotonin reuptake inhibitors (SSRIs), calcium channel antagonists, gabapentin, topiramate, riboflavin, and non-steroidal anti-inflammatory drugs.
----P Journal_Article Review Review__Tutorial 
----M M_Analgesics_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Clinical_Trials_MeSH S_methods_MeSH Clinical_Trials_methods_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH 
****** 12239942
----K E
----T Effects of 5-isosorbide mononitrate and propranolol on subclinical hepatic encephalopathy and renal function in patients with liver cirrhosis.
----A BACKGROUND/AIMS: In patients with cirrhosis pharmacological treatment of portal hypertension using beta-blockers and vasodilators has raised concerns for its potential deleterious effects on renal function and encephalopathy. To clarify this issue we evaluated the effects of propranolol and 5-isosorbide mononitrate or both on subclinical hepatic encephalopathy and renal function in a prospective randomized double-blinded study. METHODOLOGY: Thirty patients Child-Pugh A or B, with esophageal varices, normal renal function and non-previous pharmacological treatment were studied. After a basal period, patients received during 4 weeks 5-isosorbide mononitrate (80 mg/day) or placebo. In the next 4 weeks, propranolol was added to both groups. At baseline and at the end of each study period we assessed: renal function tests; plasma renin activity and aldosterone; subclinical hepatic encephalopathy (electroencephalograms, visual evoked potentials and psychometric studies). Mean arterial pressure, cardiac output (echo-Doppler) and indocyanine green retention were also measured. RESULTS: The most common alterations at baseline were increased arterial ammonia levels (85%), abnormal indocyanine green retention (75%), abnormal trail making B (44%), decreased inulin clearance (30%) and high plasma renin activity (27%). After 4 weeks of 5-isosorbide mononitrate or placebo no significant changes were observed in any variable. Five out of 14 patients receiving 5-isosorbide mononitrate were withdrawn due to side effects. The addition of propranolol decreased significantly plasma renin activity in both groups and cardiac output in those receiving 5-isosorbide mononitrate but did not change other variables. CONCLUSIONS: In patients with compensated or slightly decompensated liver cirrhosis 5-isosorbide mononitrate, propranolol or the association of both did not produce detectable worsening of subclinical hepatic encephalopathy or renal function.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_pharmacology_MeSH Isosorbide_Dinitrate_pharmacology_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Liver_MeSH S_drug_effects_MeSH Liver_drug_effects_MeSH S_physiopathology_MeSH Liver_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Liver_Function_Tests_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12243374
----K E
----T Do ancillary properties of antihypertensive drugs explain the outcome results of recent trials?
----A BACKGROUND: In a quantitative overview of published trials, we investigated whether some pharmacological properties of antihypertensive drugs, besides reduction in blood pressure, explain cardiovascular outcomes in hypertensive or high-risk patients. METHODS: Across trials, using meta-regression, we correlated odds ratios with differences in systolic blood pressure between study groups. We then compared odds ratios of benefit observed in recent trials with those predicted by metaregression on the basis of the differences in systolic pressure between randomised groups. RESULTS: Significant differences in systolic pressure between randomised groups (experimental minus reference) were observed in the ALLHAT (-2/+1), CAPPP(-3/-1) and NORDIL (-3.1/+0.2) trials. Furthermore, the differences in achieved systolic and/or diastolic pressure between study groups were also significant in the hypertension trials which involved untreated control patients, as well as in MIDAS (-3.5/ approximately 0 mm Hg), HOPE (-3.3/-1.0 mm Hg), PART2 (-5/-4 mm Hg), and SCAT (4/-2 mm Hg) (1). The differences between the observed odds ratios and those predicted by the meta-regression between outcome and difference in systolic pressure did not reach statistical significance except for the NORDIL trial, in which the risk of stroke was lower on diltiazem than on the older drugs despite a 3.1 mm Hg higher systolic pressure on the calcium-channel blocker. CONCLUSIONS: The finding that in the reviewed trials blood pressure reduction largely accounted for outcome emphasizes the desirability of blood pressure control. The hypothesis that converting-enzyme inhibitors or alpha-blockers might influence cardiovascular prognosis over and beyond their antihypertensive effect remains unproved.
----P Journal_Article Meta-Analysis 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_Determination_MeSH M_Cardiovascular_Diseases_MeSH S_complications_MeSH Cardiovascular_Diseases_complications_MeSH S_diagnosis_MeSH Cardiovascular_Diseases_diagnosis_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Linear_Models_MeSH M_Male_MeSH M_Odds_Ratio_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Sensitivity_and_Specificity_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12359989
----K E
----T The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial.
----A BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan. Single nucleotide polymorphisms in the CYP2C9 gene result in the expression of three important variants, CYP2C9*1(wild-type), CYP2C9*2 and CYP2C9*3, the last two exhibiting reduced catalytic activity compared with the wild-type. The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan. However, its influence on clinical response to treatment with the AT(1) receptor antagonist, irbesartan, has not been investigated. OBJECTIVE: To determine whether the CYP2C9genotype influences the blood pressure-decreasing response to antihypertensive treatment with irbesartan. DESIGN AND METHODS: One hundred and two patients with essential hypertension and left ventricular hypertrophy were allocated randomly to groups to receive double-blind treatment with either irbesartan (n = 49) or the beta(1)-adrenergic receptor blocker, atenolol ( n= 53). Blood pressure was measured before and after 12 weeks of treatment. genotyping was performed using solid-phase minisequencing. RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036). A similar trend was seen for systolic blood pressure. In contrast, no relation was seen between the CYP2C9 genotype and blood pressure response to atenolol, a drug not metabolized via CYP2C9. CONCLUSIONS: The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Aryl_Hydrocarbon_Hydroxylases_MeSH S_drug_effects_MeSH Aryl_Hydrocarbon_Hydroxylases_drug_effects_MeSH S_genetics_MeSH Aryl_Hydrocarbon_Hydroxylases_genetics_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_administration_&_dosage_MeSH Biphenyl_Compounds_administration_&_dosage_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_genetics_MeSH Blood_Pressure_genetics_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH S_genetics_MeSH Diastole_genetics_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Female_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Predictive_Value_of_Tests_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH S_genetics_MeSH Systole_genetics_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12374234
----K 4
----T Hemodynamic effects of propranolol and nitrates in cirrhotics with transjugular intrahepatic portosystemic stent-shunt.
----A BACKGROUND: The combination of tailored TIPS with vasoactive drugs might allow reduction of the rate of subsequent shunt-related sequelae. METHODS: We studied cirrhotic patients 8 weeks (median) after TIPS insertion (8-10 mm) for variceal bleeding. Nitrate (0.1 mg/kg) and propranolol (0.15 mg/kg) alone or combined (same dosages) were infused (I h) sequentially at 1-h intervals (n = 17). Similarly, propranolol was randomly compared to placebo (NaCl, n = 14). We measured mean arterial pressure (MAP, mmHg), heart rate (HR) and portal pressure gradient (PPG: portal minus central venous pressure) prior to and after drugs. RESULTS: Propranolol reduced PPG (mean +/- s, mmHg) significantly (14.8 +/- 3.7 versus 12.1 +/- 3.7; -21% +/- 10%; P < 0.001), while nitrates alone (14.3 +/- 3.4 versus 13.7 +/- 3.4; -11% +/- 3%; P=0.06) or nitrates plus propranolol (12.9 +/- 4 versus 12.4 +/- 4; -7% +/- 8%; P=0.2) induced only minor additive effects on portal pressure. However, nitrate reduced MAP (P < 0.001) and increased HR (P < 0.01), whereas propranolol reduced only HR (P < 0.001) with unchanged MAP, and the combination decreased MAP (P < 0.001). Compared to placebo (no effect), propranolol decreased PPG (14.4 +/- 5.6 versus 11.1 +/- 5.5; -23% +/- 11%; P < 0.001) and HR (P < 0.001). Overall, most patients (92%) responded to propranolol and 54% showed a marked PPG decrease (>20%). CONCLUSIONS: Propranolol significantly reduced portal pressure in cirrhotic patients after TIPS, whereas nitrates induced only minor benefit. TIPS-treated patients might therefore profit from additive propranolol therapy allowing limited shunts to be applied initially and/or to reduce the need for TIPS revisions in the case of shunt-dysfunction during follow-up.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_prevention_&_control_MeSH Hypertension__Portal_prevention_&_control_MeSH M_Liver_Cirrhosis_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Portal_Pressure_MeSH S_drug_effects_MeSH Portal_Pressure_drug_effects_MeSH P_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12389882
----K E
----T Cyclooxygenase-2 inhibitor-associated acute renal failure: case report with rofecoxib and review of the literature.
----A Cyclooxygenase (COX)-2 inhibitors are widely prescribed for their antiinflammatory and analgesic effects. The potential for COX-2 inhibitors to exert deleterious effects on renal function similar to those of traditional nonsteroidal antiinflammatory drugs is not well defined. Until recently, COX-1 was considered responsible for the synthesis of renal prostaglandins. However, COX-2 is also constitutively expressed in the human kidney Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. We describe the case of a 71-year-old woman who developed acute renal failure after receiving a 50-mg dose of the selective COX-2 inhibitor rofecoxib.
----P Case_Reports Journal_Article Review Review_Literature 
----M M_Aged_MeSH M_Clinical_Trials_MeSH M_Cyclooxygenase_Inhibitors_MeSH S_adverse_effects_MeSH Cyclooxygenase_Inhibitors_adverse_effects_MeSH M_Female_MeSH M_Human_MeSH M_Isoenzymes_MeSH S_antagonists_&_inhibitors_MeSH Isoenzymes_antagonists_&_inhibitors_MeSH M_Kidney_Failure__Acute_MeSH S_chemically_induced_MeSH Kidney_Failure__Acute_chemically_induced_MeSH M_Lactones_MeSH S_adverse_effects_MeSH Lactones_adverse_effects_MeSH M_Prostaglandin-Endoperoxide_Synthase_MeSH 
****** 12397571
----K E
----T Asthma, beta-agonists, and development of congestive heart failure: results of the ABCHF study.
----A BACKGROUND: Previous studies demonstrated an association between asthma and idiopathic dilated cardiomyopathy (IDCM), raising concerns regarding chronic beta-agonist inhaler use. The purpose of this investigation was to replicate that association. METHODS AND RESULTS: We identified 67 patients with IDCM and 130 controls with predominately ischemic cardiomyopathy. Patients were administered a structured, detailed phone survey by blinded interviewers, and had chart abstractions performed. We had 80% power to detect an odds ratio (OR) > or = 2.6 for the relation of asthma and IDCM. A history of asthma was present in 19.4% v 12.3% for cases and controls respectively, OR, 1.72, (95% confidence interval [CI], 0.72, 4.09), P = .18. The duration of asthma was higher in cases: 32.3 (19.7) years v 13.8 (15.0) years (P = 0.007). With adjustment for confounders, multivariate analyses revealed no significant relations between asthma or beta-agonist use and the later development of IDCM. CONCLUSIONS: It is unlikely that previously occurring asthma or beta-agonist use has a strong relationship to the development of IDCM; however, IDCM and atopic diseases may cluster in families, warranting further work into the genetic relations between atopy and IDCM.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Arteriosclerosis_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH S_etiology_MeSH Coronary_Arteriosclerosis_etiology_MeSH M_Dyspnea__Paroxysmal_MeSH S_drug_therapy_MeSH Dyspnea__Paroxysmal_drug_therapy_MeSH S_epidemiology_MeSH Dyspnea__Paroxysmal_epidemiology_MeSH S_etiology_MeSH Dyspnea__Paroxysmal_etiology_MeSH M_Echocardiography_MeSH M_Family_Health_MeSH M_Female_MeSH M_Heart_Catheterization_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Interviews_MeSH M_Male_MeSH M_Michigan_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Pulmonary_Wedge_Pressure_MeSH S_physiology_MeSH Pulmonary_Wedge_Pressure_physiology_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Treatment_Outcome_MeSH 
****** 12421112
----K E
----T Fixed combination trandolapril/verapamil sustained-release: a review of its use in essential hypertension.
----A In well designed studies in patients with mild to moderate hypertension, combinations of the sustained-release (SR) formulation of the nondihydropyridine calcium channel antagonist verapamil 120 to 240 mg/day and the ACE inhibitor trandolapril 0.5 to 8 mg/day were significantly more effective in reducing sitting systolic blood pressure (SBP) and diastolic blood pressure (DBP) from baseline than placebo. In most randomised studies, combinations of verapamil SR 120 to 240 mg/day and trandolapril 0.5 to 8 mg/day were significantly more effective in lowering sitting DBP and SBP than the corresponding monotherapies administered at the same dosage. Trandolapril/verapamil SR 2/180 mg/day provided significantly more effective 24-hour ambulatory blood pressure (BP) control than of the corresponding monotherapies. Moreover, trandolapril/verapamil SR reduced BP in patients inadequately controlled with either of the corresponding monotherapies. The antihypertensive efficacy of trandolapril/verapamil SR 2/180 mg/day was generally similar to that of other combinations of antihypertensive agents (metoprolol/hydrochlorothiazide, atenolol/chlorthalidone, lisinopril/hydrochlorothiazide, enalapril/hydrochlorothiazide) in patients with hypertension, including those with type 2 diabetes mellitus. Trandolapril/verapamil SR reduced BP in patients with hypertension and type 2 diabetes or primary renal disease, Black patients and elderly patients. Trandolapril/verapamil SR was more effective than the individual components administered as monotherapy in reducing proteinuria in patients with type 2 diabetes or primary renal disease. Trandolapril/verapamil SR had a neutral or beneficial effect on metabolic parameters (glucose, insulin, lipids) in patients with hypertension, including those with type 2 diabetes. Trandolapril/verapamil SR preserved left ventricular function in patients with heart failure. Fewer cardiac events occurred after therapy with trandolapril/verapamil SR than after trandolapril alone in post-myocardial infarction patients with congestive heart failure. The incidence of adverse events in recipients of trandolapril/verapamil SR was similar to that of the individual components, and that of other combination therapies. In placebo-controlled trials conducted in the US, headache, upper respiratory tract infections, cough, constipation, atrioventricular block (first degree) and dizziness were the most commonly reported adverse events in recipients of combinations of verapamil SR (120 to 240 mg/day) and trandolapril (0.5 to 8 mg/day). In conclusion, the fixed-dose combination of trandolapril/verapamil SR is an effective treatment for patients with hypertension, including those with type 2 diabetes. Trandolapril/verapamil SR tended to be more effective than monotherapy with either verapamil SR or trandolapril, and generally showed antihypertensive efficacy similar to that of other combination antihypertensive therapies. Current data support the use of trandolapril/verapamil SR as an alternative treatment when monotherapy with either agent is not effective. Data from large clinical trials currently being conducted will assist in fully defining the role of trandolapril/verapamil SR as a cardio- and renoprotective agent.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacokinetics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Area_Under_Curve_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Calcium_Channel_Blockers_pharmacokinetics_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Drug_Combinations_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Indoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_MEDLINE_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Verapamil_pharmacokinetics_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12428993
----K E
----T Atrial fibrillation in the elderly: facts and management.
----A Although atrial fibrillation is not widely known by the general public, in developed countries it is the most common arrhythmia. The incidence increases markedly with advancing age. Thus, with the growing proportion of elderly individuals, atrial fibrillation will come to represent a significant medical and socioeconomic problem. The consequences of atrial fibrillation have the greatest impact. The risk of thromboembolism is well known; other outcomes of atrial fibrillation are less well recognised, such as its relationship with dementia, depression and death. Such consequences are responsible for diminished quality of life and considerable economic cost. Atrial fibrillation is characterised by rapid and disorganised atrial activity, with a frequency between 300 and 600 beats/minute. The ventricles react irregularly, and may contract rapidly or slowly depending on the health of the conduction system. Clinical symptoms are varied, including palpitations, syncope, dizziness or embolic events. Atrial fibrillation may be paroxysmal, persistent or chronic, and a number of attacks are asymptomatic. Suspicion or confirmation of atrial fibrillation necessitates investigation and, as far as possible, appropriate treatment of underlying causes such as hypertension, diabetes mellitus, hypoxia, hyperthyroidism and congestive heart failure. In the evaluation of atrial fibrillation, cardiac exploration is invaluable, including electrocardiogram (ECG) and echocardiography, with the aim of detecting cardiac abnormalities and directing management. In elderly patients (arbitrarily defined as aged >75 years), the management of atrial fibrillation varies; it requires an individual approach, which largely depends on comorbid conditions, underlying cardiac disease, and patient and physician preferences. This management is essentially based on pharmacological treatment, but there are also nonpharmacological options. Two alternatives are possible: restoration and maintenance of sinus rhythm, or control of ventricular rate, leaving the atria in arrhythmia. Pharmacological options include antiarrhythmic drugs, such as class III agents, beta-blockers and class IC agents. These drugs have some adverse effects, and careful monitoring is necessary. The nonpharmacological approach to atrial fibrillation includes external or internal direct-current cardioversion and new methods, such as catheter ablation of specific foci, an evolving science that has been shown to be successful in a very select group of atrial fibrillation patients. Another serious challenge in the management of chronic atrial fibrillation in older individuals is the prevention of stroke, its primary outcome, by choosing an appropriate antithrombotic treatment (aspirin or warfarin). Several risk-stratification schemes have been validated and may be helpful to determine the best antithrombotic choice in individual patients.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH P_Atrial_Fibrillation_MeSH S_diagnosis_MeSH Atrial_Fibrillation_diagnosis_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH P_Electric_Countershock_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Heart_Valve_Diseases_MeSH S_complications_MeSH Heart_Valve_Diseases_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Rheumatic_Heart_Disease_MeSH S_complications_MeSH Rheumatic_Heart_Disease_complications_MeSH 
****** 12441210
----K 3
----T Improvement of insulin sensitivity by a long-acting nifedipine preparation (nifedipine-CR) in patients with essential hypertension.
----A BACKGROUND: Nifedipine has been reported to cause impairment of insulin sensitivity. But recently a controlled-released formulation of nifedipine (nifedipine-GITS) has been reported that it could improve insulin sensitivity. METHODS: We evaluated insulin sensitivity in two groups of essential hypertensive subjects before and after treatment with either long-acting nifedipine (nifedipine-CR, Adalat CR tablets; Bayer Yakuhin, Osaka, Japan) (n = 10) or metoprolol (n = 9). Insulin sensitivity was evaluated from the steady-state plasma glucose (SSPG) level measured at the steady-state insulin level (20 to 30 microU/mL) using a modification of the SSPG method previously reported. RESULTS: The SSPG was initially high, but was significantly reduced by nifedipine-CR treatment (from 133 +/- 14 mg/dL to 95 +/- 8 mg/dL). However, SSPG was not significantly altered by treatment in the metoprolol group (from 103 +/- 15 mg/dL to 119 +/- 12 mg/dL). CONCLUSIONS: Our results indicate that the long-acting nifedipine (nifedipine-CR) is associated with improved insulin sensitivity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Area_Under_Curve_MeSH P_Blood_Glucose_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Fatty_Acids__Nonesterified_MeSH S_blood_MeSH Fatty_Acids__Nonesterified_blood_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Insulin_MeSH S_blood_MeSH Insulin_blood_MeSH P_Insulin_Resistance_MeSH M_Ketones_MeSH S_blood_MeSH Ketones_blood_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12441211
----K 3
----T Tolerability of long-term treatment with lercanidipine versus amlodipine and lacidipine in elderly hypertensives.
----A BACKGROUND: Irrespective of their clinical relevance, side effects cannot be considered a negligible problem in antihypertensive therapy. The aim of this trial was to evaluate the tolerability profile of lercanidipine with that of two other calcium antagonists (amlodipine and lacidipine) in elderly hypertensives. METHODS: In a multicenter, double-blind, parallel study 828 elderly (aged > or =60 years) hypertensives were randomized to lercanidipine 10 mg/day (n = 420), amlodipine 5 mg/day (n = 200), or lacidipine 2 mg/day (n = 208) (ratio 2:1:1). If blood pressure (BP) control was unsatisfactory (systolic BP/diastolic BP > or =140/90 mm Hg), the dose of the double-blind medication was doubled and, as a further step, enalapril or atenolol (plus diuretic, if needed) was added. Patients were treated for an average of 12 months. RESULTS: Amlodipine patients had significantly (P <.001) higher rates of edema (19%) and of early study discontinuations due to edema (8.5%) compared with lercanidipine (9% and 2.1%) and lacidipine patients (4% and 1.4%). Similarly, edema-related symptoms (lower limb swelling and heaviness) occurred significantly (P <.01) more often with amlodipine (50% and 45%, respectively) than with lercanidipine (35% and 33%) and lacidipine (34% and 31%). Most edema cases occurred in the first 6 months, a between-treatment difference being evident since beginning of treatment. Other drug-related adverse events did not differ between treatments. Blood pressure was equally and effectively reduced in the three groups. CONCLUSIONS: The two lipophilic dihydropyridine calcium antagonists, lercanidipine and lacidipine, have an antihypertensive effect comparable to that of amlodipine, but a better tolerability profile.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_adverse_effects_MeSH Amlodipine_adverse_effects_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_adverse_effects_MeSH Calcium_Channel_Blockers_adverse_effects_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dihydropyridines_MeSH S_adverse_effects_MeSH Dihydropyridines_adverse_effects_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Edema_MeSH S_chemically_induced_MeSH Edema_chemically_induced_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Peripheral_Vascular_Diseases_MeSH S_chemically_induced_MeSH Peripheral_Vascular_Diseases_chemically_induced_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12448067
----K 1
----T [Effects of terazosine and atenolol on serum lipids in essential hypertension]
----A BACKGROUND: Only a few studies have evaluated the efficacy of alpha-blocking agents in combination with other classes of antihypertensive agents, especially in patients not adequately controlled by monotherapy. As alpha-blockers have an additional beneficial effect on serum lipids, it seems reasonable to use them instead of beta-blockers or diuretics in insufficiently treated hypertensive patients with hyperlipidemia. MATERIALS AND METHODS: All patients with insufficient blood pressure control with either a calcium channel blocker or an ACE inhibitor and evidence of hyperlipidemia (total serum cholesterol > 5.69 mmol/L) were included into an open, randomized and prospective study to evaluate the effects of terazosin and atenolol on lipid profile in hypertensive patients. The patients received either terazosin (n = 26; dose 1 to 10 mg) or atenolol (n = 28; dose 25 to 100 mg). Blood pressure was assessed by 24-hour ambulatory blood pressure measurement and serum lipids were evaluated at the time of inclusion and 12 weeks later. RESULTS: Blood pressure was similar after 12 weeks of treatment (atenolol: 129 (9)/75 (7) mm Hg; terazosin: 128 (11)/75 (9) mm Hg) and total cholesterol was significantly reduced after 12 weeks of treatment (atenolol: Diff 0-12 weeks: 7.29 (1.32) versus 6.62 (1.14 mmol/L, p = 0.006; terazosin: 7.34 (0.93) versus 6.67 (0.85) mmol/L, p = 0.002). In the terazosin group, HDL-cholesterol increased and triglycerides decreased significantly (Diff 0-12 weeks: HDL-chol: 1.55 (0.31) versus 1.63 (0.44) mmol/L, p = 0.04; TG: 1.93 (1.17) versus 1.34 (0.64) mmol/L, p = 0.03). Comparing both groups a significant difference was found with regard to HDL-cholesterol and triglycerides (atenolol versus terazosin: HDL-chol: -0.05 (0.12) versus +0.08 (0.1) mmol/L, p = 0.04; TG: -0.18 (0.61) versus--0.59 (0.6), p = 0.03). CONCLUSIONS: The alpha-blocker terazosin is as effective as atenolol when combined with either an ACE inhibitor or a calcium-channel blocker as a part of a multidrug regimen to achieve sufficient blood pressure control. In addition, terazosin is superior to atenolol with regard to the effect on the lipid profile of hypertensive and hyperlipidemic patients and seems therefore a reasonable alternative to beta-blockers in hypertensive patients with hyperlipidemia.
----P Clinical_Trial Evaluation_Studies Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_alpha-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Antagonists_adverse_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_blood_MeSH Hypercholesterolemia_blood_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prazosin_MeSH S_administration_&_dosage_MeSH Prazosin_administration_&_dosage_MeSH S_adverse_effects_MeSH Prazosin_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Prazosin_analogs_&_derivatives_MeSH M_Prospective_Studies_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 12447861
----K E
----T Randomized comparison of long-term carvedilol and propranolol administration in the treatment of portal hypertension in cirrhosis.
----A Short-term carvedilol administration is more powerful than propranolol in decreasing hepatic venous pressure gradient (HVPG) in cirrhotic patients, but induces arterial hypotension that may prevent its long-term use in portal hypertensive patients. This study compared the HVPG reduction and safety of long-term carvedilol and propranolol. Fifty-one cirrhotic patients were randomly assigned to receive carvedilol (n = 26) and propranolol (n = 25). Hemodynamic measurements and renal function were assessed at baseline and after 11.1 +/- 4.1 weeks. Carvedilol caused a greater decrease in HVPG than popranolol (-19 +/- 2% vs. -12 +/- 2%; P <.001). The proportion of patients achieving an HVPG reduction >/=20% or </=12 mm Hg was greater after carvedilol (54% vs. 23%; P <.05). Carvedilol, but not propranolol caused a significant decrease in mean arterial pressure (MAP) (-11 +/- 1% vs. -5 +/- 3%; P =.05) and a significant increase in plasma volume (PV) and body weight (11 +/- 5% and 2 +/- 1%, respectively; P <.05). Glomerular filtration rate (GFR) was unchanged with either drug, but the dose of diuretics was increased more frequently after carvedilol (27% vs. 8%; P =.07). Adverse events requiring discontinuation of treatment occurred in 2 patients receiving carvedilol and in 3 receiving propranolol. In conclusion, carvedilol has a greater portal hypotensive effect than propranolol in patients with cirrhosis. However, its clinical applicability may be limited by its systemic hypotensive effects. Further trials are needed to confirm the therapeutic potential of carvedilol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Kidney_MeSH S_physiology_MeSH Kidney_physiology_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12451325
----K E
----T Metabolic effects of combined antihypertensive treatment in patients with essential hypertension.
----A Single-drug treatment of essential hypertension (HT) is often insufficient to normalize blood pressure (BP), and high doses of antihypertensive agents can have adverse effects on glucose tolerance (GT) and insulin sensitivity. This study tested whether aggressive BP lowering with combination treatment had any influence on GT or insulin action. In all, 29 nonobese (body mass index [BMI], <30 kg/m ), normolipidemic patients with established HT (159 +/- 3/99 +/- 1 mm Hg) but normal GT were recruited. Eleven normotensive (125 +/- 3/85 +/- 1 mm Hg) subjects were matched to the patients for both anthropometric and metabolic variables. Following baseline studies (serum lipid profile, oral GT, insulin release, and insulin sensitivity assessed by the insulin clamp technique), patients were randomized in a double-blind fashion to two combination regimens (verapamil 180 mg/day + trandolapril 2 mg/day or atenolol 50 mg/day + nifedipine 20 mg/day) and restudied 3 months later. Blood pressure was normalized in both groups (with decrements of 25 +/- 5/17 +/- 2 and 29 +/- 3/15 +/- 2 mm Hg, respectively). Lipid profile, GT, insulin release, and insulin sensitivity of both glucose uptake and lipolysis were unchanged following both treatments. The authors conclude that in nonobese, normolipidemic, glucose-tolerant hypertensive patients, BP normalization with combination therapy is feasible at no cost in terms of undesired effects on glucose and lipid metabolism and insulin sensitivity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glucose_Tolerance_Test_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_pharmacology_MeSH Indoles_pharmacology_MeSH M_Insulin_MeSH S_metabolism_MeSH Insulin_metabolism_MeSH S_secretion_MeSH Insulin_secretion_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nifedipine_MeSH S_administration_&_dosage_MeSH Nifedipine_administration_&_dosage_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH 
****** 12455715
----K E
----T The reproducibility of the circadian BP rhythm in treated hypertensive patients with polycystic kidney disease and mild chronic renal impairment--a prospective ABPM study.
----A BACKGROUND: Diurnal BP rhythm is known to be abnormal (reduced BP fall with sleep) in chronic renal failure, dialysis and renal transplantation patients. In subjects with primary hypertension and with reduced diurnal BP fall with sleep there is consistent evidence of increased target-organ damage. However, the few studies that have addressed the reproducibility of diurnal rhythm in normal or hypertensive subjects have concluded that the BP fall with sleep is poorly reproducible. It is not known whether the same is true for patients with renal disease. METHODS: In 30 subjects with autosomal polycystic kidney disease (ADPKD), mild chronic renal failure and normal office BP levels on standardised anti-hypertensive treatment, ambulatory blood pressure monitoring (ABPM) was done three times over a twelve month period to assess the reproducibility of blood pressure fall with sleep. RESULTS: When comparing ABPM 2 with the ABPM 1 recording (3 months difference between measurements) only 43.3% of the patients maintained the initial dipping category (defined by quartiles of the ABPM 1 diurnal BP distribution). The same proportion of subjects had a similar dipping category, when ABPM 3 was compared to ABPM 1 (9 months difference between measurements), but a large (24%) subset of patients had dramatic shifts in their amplitude in nocturnal BP fall, significantly greater than those recorded after a shorter inter-measurement interval. Equally important, our study reveals the fact that, with time, there is no tendency to decrease circadian variation: a similar proportion (a quarter to one third) of patients increased or decreased their amplitude in nocturnal BP fall, at 3 and 9 months. When several ABPM measurements are repeated for the same patients, the repeatability is even worse, since only 36.6% of our study population maintained the initial dipping category across all three ABPM determinations (ABPM 1 and ABPM 2 and ABPM 3). CONCLUSIONS: There is a widespread abnormality in diurnal BP rhythm in ADPKD patients with renal impairment, but the extent of this abnormality varies considerably over time. It is too simplistic to assume that, having arbitrarily categorised subjects into "dippers" or "non-dippers", these labels will always be valid. Thus, it would be unwise to extrapolate the impact of a single baseline circadian BP profile on organ target end points.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Blood_Pressure_Determination_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_diagnosis_MeSH Kidney_Failure__Chronic_diagnosis_MeSH S_drug_therapy_MeSH Kidney_Failure__Chronic_drug_therapy_MeSH M_Male_MeSH M_Polycystic_Kidney_Diseases_MeSH S_complications_MeSH Polycystic_Kidney_Diseases_complications_MeSH S_diagnosis_MeSH Polycystic_Kidney_Diseases_diagnosis_MeSH S_drug_therapy_MeSH Polycystic_Kidney_Diseases_drug_therapy_MeSH M_Prospective_Studies_MeSH M_Reproducibility_of_Results_MeSH M_Risk_Assessment_MeSH M_Sensitivity_and_Specificity_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH 
****** 12461301
----K E
----T Success and predictors of blood pressure control in diverse North American settings: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT).
----A CONTEXT: Blood pressure control (<140/90 mm Hg) rates for hypertension fall far short of the US national goal of 50% or more. Achievable control rates in varied practice settings and geographic regions and factors that predict improved blood pressure control are not well identified. OBJECTIVE: To determine the success and predictors of blood pressure control in a large hypertension trial involving a multiethnic population in diverse practice settings. DESIGN: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial is a randomized, double-blind, active-controlled clinical trial with a mean follow-up of 4.9 years. Participant enrollment began in February 1994 and follow-up was completed in March 2002. SETTING: A total of 623 centers in the United States, Canada, and the Caribbean. PARTICIPANTS: A total of 33,357 participants (aged > or =55 years) with hypertension and at least one other coronary heart disease risk factor. INTERVENTIONS: Participants were randomly assigned to receive (double-blind) chlorthalidone, 12.5-25 mg/d (n=15,255), amlodipine 2.5-10 mg/d (n=9048), or lisinopril 10-40 mg/d (n=9054) after other medication was discontinued. Doses were increased within these ranges and additional drugs from other classes were added as needed to achieve blood pressure control (<140/90 mm Hg). MAIN OUTCOME MEASURES: The outcome measures for this report are systolic and diastolic blood pressure, the proportion of participants achieving blood pressure control (<140/90 mm Hg), and the number of drugs required to achieve control in all three groups combined. RESULTS: Mean age was 67 years, 47% were women, 35% black, 36% diabetic; 90% were on antihypertensive drug treatment at entry. At the first of two pre-randomization visits, blood pressure was <140/90 mm Hg in only 27.4% of participants. After 5 years of follow-up, the percent controlled improved to 66%. Systolic blood pressure was <140 mm Hg in 67% of participants, diastolic blood pressure was <90 mm Hg in 92%, the mean number of drugs prescribed was 2.0+/-1.0, and the percent on > or =2 drugs was 63%. Blood pressure control varied by geographic regions, practice settings, and demographic and clinical characteristics of participants. CONCLUSIONS: These data demonstrate that blood pressure may be controlled in two thirds of a multiethnic hypertensive population in diverse practice settings. Systolic blood pressure is more difficult to control than diastolic blood pressure, and at least two antihypertensive medications are required for most patients to achieve blood pressure control. It is likely that the majority of people with hypertension could achieve a blood pressure <140/90 mm Hg with the antihypertensive medications available today.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Canada_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_ethnology_MeSH Myocardial_Infarction_ethnology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH M_West_Indies_MeSH 
****** 12461307
----K 5
----T Sexual dysfunction in patients with hypertension: implications for therapy.
----A Sexual dysfunction associated with hypertension or antihypertensive therapies may impact the ability of patients to stay on therapy and lead to deterioration in patients' quality of life. Therefore, it is important for practitioners to become familiar with the wide variation in sexual side effects produced by antihypertensive agents and to discuss the potential occurrence of these side effects with their patients. In many cases, a change in the patient's drug regimen may help patients overcome specific sexual side effects experienced with certain treatments. Practitioners should consider selecting an antihypertensive therapy that is highly effective in lowering blood pressure but preserves patients quality of life. The effect of medications on sexual function remains controversial. Some blinded trials report little difference between placebo and specific medications, whereas other studies indicate that antihypertensive medications increase sexual dysfunction, which has an impact on quality of life. Recent evidence suggests that losartan, an angiotensin II antagonist, is not typically associated with development of sexual dysfunction and may actually positively impact several indices of sexual function (erectile function, sexual satisfaction, and frequency of sexual activity) as well as perceived quality of life. Thus, angiotensin II antagonists may offer a therapeutic option to prevent or correct erectile dysfunction in patients with hypertension. The favorable effects of these agents on sexual function may be related, in part, to their ability to block angiotensin II, which has recently become recognized as an important mediator of detumescence and possibly erectile dysfunction.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Impotence_MeSH S_chemically_induced_MeSH Impotence_chemically_induced_MeSH S_physiopathology_MeSH Impotence_physiopathology_MeSH S_prevention_&_control_MeSH Impotence_prevention_&_control_MeSH M_Male_MeSH M_Sexual_Behavior_MeSH S_drug_effects_MeSH Sexual_Behavior_drug_effects_MeSH M_Sexual_Dysfunctions__Psychological_MeSH S_chemically_induced_MeSH Sexual_Dysfunctions__Psychological_chemically_induced_MeSH S_physiopathology_MeSH Sexual_Dysfunctions__Psychological_physiopathology_MeSH S_prevention_&_control_MeSH Sexual_Dysfunctions__Psychological_prevention_&_control_MeSH 
****** 12468190
----K E
----T Chronic hypertension in pregnancy.
----A 
----P Clinical_Trial Comment Letter Randomized_Controlled_Trial 
----M M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Fetal_Growth_Retardation_MeSH S_chemically_induced_MeSH Fetal_Growth_Retardation_chemically_induced_MeSH S_epidemiology_MeSH Fetal_Growth_Retardation_epidemiology_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Infant__Low_Birth_Weight_MeSH M_Infant__Newborn_MeSH M_Pregnancy_MeSH P_Pregnancy_Outcome_MeSH M_Pregnancy_Toxemias_MeSH S_diagnosis_MeSH Pregnancy_Toxemias_diagnosis_MeSH S_drug_therapy_MeSH Pregnancy_Toxemias_drug_therapy_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH 
****** 12471656
----K 1
----T [Baseline characteristics and management of patients less than 45 years of age hospitalized for acute coronary syndromes: results from the nationwide French PREVENIR 1 and PREVENIR 2 studies]
----A Of 2,626 patients admitted for acute coronary syndromes and participating in the PREVENIR 1 and 2 registries, 202 (8%) were aged less than 45 years. Younger patients were more often smokers (79% versus 37%), but systemic hypertension and diabetes were less frequent. Reperfusion therapy was more frequently used in the younger patients (63% versus 46%). At hospital discharge, aspirin and angiotensin converting enzyme inhibitors were prescribed as often in younger and older patients. In contrast, beta-blocking agents and statins were used more often in the younger patients. More younger patients participated in a cardiac rehabilitation programme. Left ventricular ejection fraction was less altered in the younger age group and none of the younger patients died between hospital discharge and six months follow-up.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Age_Factors_MeSH M_Angina__Unstable_MeSH S_mortality_MeSH Angina__Unstable_mortality_MeSH S_prevention_&_control_MeSH Angina__Unstable_prevention_&_control_MeSH S_therapy_MeSH Angina__Unstable_therapy_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Chi-Square_Distribution_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Follow-Up_Studies_MeSH M_France_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Stroke_Volume_MeSH M_Time_Factors_MeSH 
****** 12471688
----K 1
----T [Assessment of the effects of antihypertensive drugs on stress-induced cardiovascular changes]
----A The authors reviewed some of the most relevant studies dedicated to the assessment of the effects of the antihypertensive drugs on the stress-induced cardiovascular changes. The rises in both blood pressure and heart rate turned out not to be significantly altered by calcium channel blockers, ACE inhibitors, moxonidine, nor beta-blockers, whereas they seemed to be slightly blunted by alpha-blocking drugs. However, since baseline blood pressure was significantly lower in treated hypertensives than in placebo-given patients, all antihypertensive drugs eventually resulted in a lower blood pressure level during stress, as compared with untreated patients. Regarding white coat effect, which has to be considered as a very particular stress, it appeared to be lowered to the same extent by placebo and antihypertensive drugs; moreover, its changes were not associated with any clinical beneficial effect.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_alpha-Antagonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Pressure_Determination_MeSH S_psychology_MeSH Blood_Pressure_Determination_psychology_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH M_Comparative_Study_MeSH M_English_Abstract_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Placebos_MeSH M_Randomized_Controlled_Trials_MeSH P_Stress__Psychological_MeSH S_physiopathology_MeSH Stress__Psychological_physiopathology_MeSH 
****** 12476475
----K 2
----T Effects of four antihypertensive monotherapies on cardiac mass and function in hypertensive patients with left ventricular hypertrophy: randomized prospective study.
----A AIM: To compare the effects of four antihypertensive drugs, which have reportedly different effectiveness in reducing myocardial mass. METHODS: A randomized, double-blind, prospective study included 80 hypertensive patients with left ventricular (LV) hypertrophy confirmed both electrocardiographically and echocardiographically. We investigated the effects of indapamide, nicardipine, propranolol, and chlorthalidone on arterial blood pressure and LV mass and function. RESULTS: Sixty-four patients (34 men and 30 women) completed the 6-month study. No significant differences in antihypertensive effects of the four medications were found. The average decrease in systolic and diastolic blood pressure was 12.8% and 10.4%, respectively. All four antihypertensive medications caused pronounced reduction in LV mass, between 7.9% in the propranolol group and 10.1% in the nicardipine group, with no significant difference between the groups. In patients receiving diuretics, predominant decrease was observed in LV mass and LV mass index. In patients treated with propranolol, the thickness of both the LV wall and interventricular septum was reduced, whereas the reduction in LV mass, LV wall and interventricular septum thickness was found in patients treated with nicardipine. There was no significant correlation between the changes in LV mass and other variables (blood pressure, and systolic and diastolic function). Systolic function did not improve with the reversion of LV hypertrophy in any group of patients, but improvement was observed in some indices of diastolic function. The early and late LV filling velocity and their ratio did not improve significantly, either. Clinically relevant side effects were not observed. CONCLUSION: All four antihypertensive monotherapies achieved a comparable control of hypertension and reduction in LV hypertrophy.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_pharmacology_MeSH Chlorthalidone_pharmacology_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Croatia_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_physiopathology_MeSH Heart_Ventricles_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Indapamide_MeSH S_pharmacology_MeSH Indapamide_pharmacology_MeSH S_therapeutic_use_MeSH Indapamide_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nicardipine_MeSH S_pharmacology_MeSH Nicardipine_pharmacology_MeSH S_therapeutic_use_MeSH Nicardipine_therapeutic_use_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH 
****** 12475466
----K E
----T Delisting of infants and children from the heart transplantation waiting list after carvedilol treatment.
----A OBJECTIVES: We performed a prospective, randomized, double-blind, placebo-controlled study of carvedilol effects in children with severe, chronic heart failure (HF), despite the use of conventional therapy. BACKGROUND: Little is known about the effects of carvedilol in youngsters with chronic HF and severe left ventricular (LV) dysfunction. METHODS: We conducted a double-blind, placebo-controlled study of 22 consecutive children with severe LV dysfunction. The children had chronic HF and left ventricular ejection fraction (LVEF) <30%. Patients were randomly assigned to receive either placebo (8 patients) or the beta-blocker carvedilol (14 patients) at 0.01 mg/kg/day titrated up to 0.2 mg/kg/day, followed-up for six months. RESULTS: During the follow-up and the up-titration period in the carvedilol group, four patients died and one underwent heart transplantation. In patients receiving carvedilol evaluated after six months, a significant increase occurred in LVEF, from 17.8% (95% confidence interval [CI], 14.1 to 21.4%) to 34.6% (95% CI, 25.2 to 44.0%); p = 0.001. Modified New York Heart Association (NYHA) functional class improved in nine patients taken off the transplant waiting list. All nine patients were alive at follow-up. In the placebo group, during the six-month follow-up, two patients died, and two underwent heart transplantation. Four patients persisted with HF symptoms (NYHA functional class IV). No significant change occurred in LVEF or fractional shortening. CONCLUSIONS: Carvedilol added to standard therapy may reduce HF progression and improve cardiac function, allowing some youngsters to be removed from the heart transplantation waiting list.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antioxidants_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Brazil_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Child_MeSH M_Child_Welfare_MeSH M_Child__Preschool_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH P_Heart_Transplantation_MeSH M_Human_MeSH M_Infant_MeSH M_Infant_Welfare_MeSH M_Male_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Radionuclide_Ventriculography_MeSH M_Severity_of_Illness_Index_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_therapy_MeSH Ventricular_Dysfunction__Left_therapy_MeSH P_Waiting_Lists_MeSH 
****** 12478497
----K 5
----T Treatment of hypertension from volume to vasoconstriction: The ACE up your sleeve.
----A Control of hypertension in the vascular patient is clearly a priority. However, these patients often will have significant co-morbidities that may influence the choice of medication, a decision that also may be affected by cost or Health Plan directives. Wherever possible, monotherapy should be attempted first, although in select circumstances combination therapy may be more appropriate. The 5 main categories of drugs used in the initial treatment of hypertensive vascular diseases are (1). diuretics, (2). beta-adrenergic blockers, (3). calcium channel blockers, (4). angiotensin-converting enzyme (ACE) inhibitors, and (5). angiotensin receptor blockers (ARBs). There are also other less commonly used drugs. Each of the antihypertensive agents is roughly equally effective, producing a good antihypertensive response in 40% to 60% of cases. Some antihypertensives, especially ACE and ARBs, also may have beneficial effects on the vascular and metabolic systems separate from their blood pressure lowering effects, which suggests they may be beneficial even if blood pressure is well maintained with other agents. This report covers the basic information required for the vascular surgeon to become familiar with the various medications and their indications, dosage, and side effects. It also provides some guidelines in selecting relevant antihypertensive treatment regimens for the elderly patient with arterial vascular disease.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_pharmacology_MeSH Diuretics_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 12482211
----K 5
----T Central cholinergic challenging of migraine by testing second-generation anticholinesterase drugs.
----A The antinociceptive activity of donepezil, a novel cholinesterase inhibitor, was investigated in the mouse hot plate test. Donepezil (5 to 10 mg kg(-1) i.p.) induced a dose-dependent antinociception that reached its maximum effect 15 minutes after injection. Donepezil antinociception was prevented by the antimuscarinic drug scopolamine. At analgesic doses, donepezil did not alter gross animal behavior. These results indicate that donepezil is endowed by muscarinic antinociceptive properties, suggesting this compound as a potential therapeutic approach for the treatment of painful pathologies. Therefore, we investigated donepezil's effect in migraine. Donepezil (5 mg per os, evening assumption) was effective as a prophylatic agent in patients suffering from migraine with or without aura by reducing the number of hours with pain, the number of attacks, and the severity of the pain attack. The efficacy of donepezil was compared with that of the beta-blocker propranolol (40 mg bid per os), showing higher activity. Response rates of a large-sized open study devoid of entry criteria regarding migraine subtypes suggest the drug as an excellent prophylactic compound for migraine in general practice. Clinical results also indicate that the activation of the cholinergic system can represent a novel prophylactic approach to migraine.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Analgesics_MeSH S_pharmacology_MeSH Analgesics_pharmacology_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Animals_MeSH M_Anxiety_MeSH S_chemically_induced_MeSH Anxiety_chemically_induced_MeSH M_Central_Nervous_System_MeSH S_drug_effects_MeSH Central_Nervous_System_drug_effects_MeSH M_Cholinesterase_Inhibitors_MeSH S_adverse_effects_MeSH Cholinesterase_Inhibitors_adverse_effects_MeSH S_pharmacology_MeSH Cholinesterase_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Cholinesterase_Inhibitors_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Indans_MeSH S_adverse_effects_MeSH Indans_adverse_effects_MeSH S_pharmacology_MeSH Indans_pharmacology_MeSH S_therapeutic_use_MeSH Indans_therapeutic_use_MeSH M_Male_MeSH M_Mice_MeSH M_Migraine_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Nausea_MeSH S_chemically_induced_MeSH Nausea_chemically_induced_MeSH M_Piperidines_MeSH S_adverse_effects_MeSH Piperidines_adverse_effects_MeSH S_pharmacology_MeSH Piperidines_pharmacology_MeSH S_therapeutic_use_MeSH Piperidines_therapeutic_use_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Sleep__REM_MeSH S_drug_effects_MeSH Sleep__REM_drug_effects_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH M_Vomiting_MeSH S_chemically_induced_MeSH Vomiting_chemically_induced_MeSH 
****** 12486510
----K 3
----T A comparison of the fixed combination of latanoprost and timolol with its individual components.
----A PURPOSE: To evaluate the intraocular pressure (IOP)-reducing effect of the fixed combination of 0.005% latanoprost and 0.5% timolol compared with the individual monotherapies. METHODS: A 6-month, randomised, double-masked, controlled multicentre study followed by 6 months of open-label treatment was carried out in patients with glaucoma or ocular hypertension with pre-enrolment IOP >/=25 mmHg on glaucoma medication or >/=30 mmHg if untreated. Following a 2- to 4-week run-in period on timolol twice daily, 436 patients were randomised: 140 to fixed combination therapy once daily in the morning, 147 to latanoprost once daily in the morning and 149 to timolol twice daily. During the open-label extension, patients received fixed combination drug once daily in the morning. RESULTS: The difference in mean change from baseline in diurnal IOP from week 2 to week 26 was -1.2 mmHg between fixed combination and latanoprost (95% confidence interval. CI: -1.8 to -0.5; P<0.001; repeated-measures analysis of covariance). The corresponding difference between fixed combination and timolol was -1.9 mmHg (95% CI -2.5 to -1.2; P<0.001). No long-term drift in IOP was detected in patients treated for 12 months with fixed combination. All treatments were well tolerated with no major differences among groups in the incidence of clinically relevant adverse events. CONCLUSION: The fixed combination of 0.005% latanoprost and 0.5% timolol administered once daily in the morning for 6 months was more effective in reducing IOP than the individual components alone and was effective over 12 months.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 12488264
----K 4
----T A randomised, double masked, multicentre clinical trial comparing bimatoprost and timolol for the treatment of glaucoma and ocular hypertension.
----A Aim: To evaluate the safety and efficacy of bimatoprost 0.03% once daily or twice daily compared with timolol 0.5% twice daily in patients with glaucoma or ocular hypertension. METHODS: Multicentre, double masked, randomised, parallel group, 3 month trial comparing bimatoprost once daily (n=240), bimatoprost twice daily (n=240), and timolol twice daily (n=122). The primary efficacy end point was diurnal intraocular pressure (IOP) (8 am, 10 am, 4 pm). Safety measures included adverse events, ocular parameters, and systemic variables. RESULTS: Bimatoprost once daily provided significantly lower mean IOP than timolol twice daily at all times and follow up visits (p<0.001). At month 3, mean IOP reductions from baseline at 10 am (peak timolol effect) were bimatoprost once daily, 8.0 mm Hg (32.4%); bimatoprost twice daily, 6.3 mm Hg (25.2%); timolol, 5.5 mm Hg (22.7%). Bimatoprost twice daily was also more effective than timolol, but was not as effective as bimatoprost once daily. A higher percentage of patients achieved low target pressures with bimatoprost once daily than with timolol. The most frequent side effects with bimatoprost were eyelash growth and mild conjunctival hyperaemia. Systemic safety parameters were not affected by bimatoprost. CONCLUSIONS: Bimatoprost 0.03% once daily demonstrated superior efficacy compared with timolol 0.5% twice daily in patients with elevated IOP. Bimatoprost once daily was more effective than twice daily dosing.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lipids_MeSH S_administration_&_dosage_MeSH Lipids_administration_&_dosage_MeSH S_adverse_effects_MeSH Lipids_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH M_Treatment_Outcome_MeSH 
****** 12495391
----K E
----T Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial.
----A CONTEXT: Implantable cardioverter defibrillator (ICD) therapy with backup ventricular pacing increases survival in patients with life-threatening ventricular arrhythmias. Most currently implanted ICD devices provide dual-chamber pacing therapy. The most common comorbid cause for mortality in this population is congestive heart failure. OBJECTIVE: To determine the efficacy of dual-chamber pacing compared with backup ventricular pacing in patients with standard indications for ICD implantation but without indications for antibradycardia pacing. DESIGN: The Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial, a single-blind, parallel-group, randomized clinical trial. SETTING AND PARTICIPANTS: A total of 506 patients with indications for ICD therapy were enrolled between October 2000 and September 2002 at 37 US centers. All patients had a left ventricular ejection fraction (LVEF) of 40% or less, no indication for antibradycardia pacemaker therapy, and no persistent atrial arrhythmias. INTERVENTIONS: All patients had an ICD with dual-chamber, rate-responsive pacing capability implanted. Patients were randomly assigned to have the ICDs programmed to ventricular backup pacing at 40/min (VVI-40; n = 256) or dual-chamber rate-responsive pacing at 70/min (DDDR-70; n = 250). Maximal tolerated medical therapy for left ventricular dysfunction, including angiotensin-converting enzyme inhibitors and beta-blockers, was prescribed to all patients. MAIN OUTCOME MEASURE: Composite end point of time to death or first hospitalization for congestive heart failure. RESULTS: One-year survival free of the composite end point was 83.9% for patients treated with VVI-40 compared with 73.3% for patients treated with DDDR-70 (relative hazard, 1.61; 95% confidence interval [CI], 1.06-2.44). The components of the composite end point, mortality of 6.5% for VVI-40 vs 10.1% for DDDR-70 (relative hazard, 1.61; 95% CI, 0.84-3.09) and hospitalization for congestive heart failure of 13.3% for VVI-40 vs 22.6% for DDDR-70 (relative hazard, 1.54; 95% CI, 0.97-2.46), also trended in favor of VVI-40 programming. CONCLUSION: For patients with standard indications for ICD therapy, no indication for cardiac pacing, and an LVEF of 40% or less, dual-chamber pacing offers no clinical advantage over ventricular backup pacing and may be detrimental by increasing the combined end point of death or hospitalization for heart failure.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH P_Cardiac_Pacing__Artificial_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Catheter_Ablation_MeSH M_Comparative_Study_MeSH P_Defibrillators__Implantable_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Pacemaker__Artificial_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Tachycardia__Ventricular_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_therapy_MeSH Ventricular_Dysfunction__Left_therapy_MeSH M_Warfarin_MeSH S_therapeutic_use_MeSH Warfarin_therapeutic_use_MeSH 
****** 12500181
----K 5
----T Vascular mediators in the injured liver.
----A 
----P Journal_Article Review Review_Literature 
----M M_Angiotensin_II_MeSH S_metabolism_MeSH Angiotensin_II_metabolism_MeSH M_Carbon_Monoxide_MeSH S_metabolism_MeSH Carbon_Monoxide_metabolism_MeSH M_Catecholamines_MeSH S_metabolism_MeSH Catecholamines_metabolism_MeSH M_Endothelins_MeSH S_metabolism_MeSH Endothelins_metabolism_MeSH M_Human_MeSH M_Liver_Circulation_MeSH S_physiology_MeSH Liver_Circulation_physiology_MeSH M_Liver_Diseases_MeSH S_metabolism_MeSH Liver_Diseases_metabolism_MeSH M_Nitric_Oxide_MeSH S_metabolism_MeSH Nitric_Oxide_metabolism_MeSH M_Prostaglandins_MeSH S_metabolism_MeSH Prostaglandins_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12505115
----K I
----T The effects of beta-blockers on morbidity and mortality in a population-based cohort of 11,942 elderly patients with heart failure.
----A PURPOSE: Randomized trials have shown that beta-blockers prevent morbidity and mortality in heart failure. However, whether beta-blockers are effective in older patients or those with conditions that would have led to their exclusion from these trials remains unclear. SUBJECTS AND METHODS: The associations between beta-blocker use and outcomes were examined in a population-based cohort of 11,942 older (age >/=65 years) patients with incident heart failure between 1994 and 1999. Cox proportional hazards models were used to adjust for propensity scores, age, sex, comorbid conditions, and other medications. RESULTS: The mean (+/- SD) age of the patients was 79 +/- 8 years, 5819 (49%) were men, and 2569 (22%) had Charlson comorbidity scores of at least 2. During follow-up (median, 21 months), 3539 patients were hospitalized for heart failure and 6757 died. Overall, 1162 patients received beta-blockers. After adjustment, beta-blocker use was associated with substantial reductions in all-cause mortality (hazard ratio [HR] = 0.72; 95% confidence interval [CI]: 0.65 to 0.80), mortality due to heart failure (HR = 0.65; 95% CI: 0.47 to 0.90), and hospitalizations for heart failure (HR = 0.82; 95% CI: 0.74 to 0.92). These endpoints were less frequent in patients treated with beta-blockers than in untreated patients in all examined subgroups. All doses of beta-blockers were associated with benefit, but there was a trend towards greater benefit in patients prescribed higher doses. CONCLUSIONS: The benefits of beta-blockers seen in randomized trials extend to older patients and to those with conditions that would have led to their exclusion from the trials. There is a need for a randomized trial comparing different doses of beta-blockers in heart failure.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Alberta_MeSH S_epidemiology_MeSH Alberta_epidemiology_MeSH M_Cohort_Studies_MeSH M_Confidence_Intervals_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Proportional_Hazards_Models_MeSH M_Risk_Assessment_MeSH M_Survival_Analysis_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 12509760
----K 5
----T A guide to drug discovery: Target selection in drug discovery.
----A Target selection in drug discovery--defined here as the decision to focus on finding an agent with a particular biological action that is anticipated to have therapeutic utility--is influenced by a complex balance of scientific, medical and strategic considerations. In this article, we provide an introduction to the key issues in target selection and discuss the rationale for decision making.
----P Journal_Article Review Review__Tutorial 
----M M_Biotechnology_MeSH S_economics_MeSH Biotechnology_economics_MeSH S_methods_MeSH Biotechnology_methods_MeSH M_Drug_Industry_MeSH S_economics_MeSH Drug_Industry_economics_MeSH S_methods_MeSH Drug_Industry_methods_MeSH S_trends_MeSH Drug_Industry_trends_MeSH M_Health_Care_Sector_MeSH M_Human_MeSH M_Legislation__Drug_MeSH S_trends_MeSH Legislation__Drug_trends_MeSH M_Pharmacology_MeSH S_economics_MeSH Pharmacology_economics_MeSH S_methods_MeSH Pharmacology_methods_MeSH M_Receptors__Drug_MeSH S_drug_effects_MeSH Receptors__Drug_drug_effects_MeSH 
****** 12512397
----K 5
----T Strategies for pharmacologic treatment of high functioning autism and Asperger syndrome.
----A The treatment of complex, polymorphous disorders like HFA/AS always brings a particular challenge to pharmacotherapy. Additionally, the specific characteristics presented by HFA/AS introduce unique complications to patient care and place unusual demands on a clinician's skill and experience. To provide safe and effective treatment, the clinician must understand the core features of the disorder and the manifestations of the condition in his or her patient. Furthermore, a thorough understanding of the family, school, and community resources and limitations is necessary. Once an assessment has been made, focusing on target symptoms provides a crucial framework for care. Knowing manifestations of symptoms and characterizing their distribution and behavior in that patient is most important. For patients with HFA/AS it is particularly essential to coordinate behavioral and pharmacologic objectives. The target symptoms should be tracked carefully and placed into a priority system that is based on the risks and disability they create for the patient. The skill of pharmacotherapy also means setting out realistic expectations, keeping track of the larger systems of care at school and home, and collaboration with parents and care providers. There is an expanding range and pace of biologic and intervention research into HFA/AS. The genetic work has produced exciting leads that are likely to be helpful to future generations [82-84], but the task of clinicians is to tend to today's patients. As we discover more about the complex neural circuitry subserving repetitive behaviors, reward systems, and social cognition, there are good reasons to believe our treatments will become more sophisticated and specific. Psychopharmacology is also moving to design medications that target more specific populations of receptor and brain functions. This is likely to produce medicines that have fewer side effects, are more effective, and are more symptom-specific. Pharmacotherapy is not the ultimate treatment for HFA/AS but it has a definite place. Medication can be a critical element in a comprehensive treatment plan. There is a wider range of medications with more specific biologic effects than ever before. For patients with HFA/AS these newer agents are safer and less disruptive. When paired with clinicians who are becoming more skilled at recognizing and managing symptoms, patients have a greater opportunity to reach their potential and lead pleasurable lives.
----P Journal_Article 
----M M_Adolescent_MeSH M_Asperger_Syndrome_MeSH S_diagnosis_MeSH Asperger_Syndrome_diagnosis_MeSH S_drug_therapy_MeSH Asperger_Syndrome_drug_therapy_MeSH S_psychology_MeSH Asperger_Syndrome_psychology_MeSH M_Autistic_Disorder_MeSH S_diagnosis_MeSH Autistic_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Autistic_Disorder_drug_therapy_MeSH S_psychology_MeSH Autistic_Disorder_psychology_MeSH M_Child_MeSH M_Combined_Modality_Therapy_MeSH M_Female_MeSH M_Human_MeSH P_Intelligence_MeSH S_drug_effects_MeSH Intelligence_drug_effects_MeSH M_Male_MeSH M_Patient_Care_Team_MeSH M_Psychotropic_Drugs_MeSH S_adverse_effects_MeSH Psychotropic_Drugs_adverse_effects_MeSH S_therapeutic_use_MeSH Psychotropic_Drugs_therapeutic_use_MeSH 
****** 12513113
----K 5
----T Beta-blockers after acute myocardial infarction in elderly patients with diabetes mellitus: time to reassess.
----A Beta-blockers effectively reduce mortality and recurrent cardiovascular events in patients surviving myocardial infarction. However, these agents are underused in clinical practice, especially in older patients with diabetes mellitus. The current literature shows that beta-blockers are at least as effective in older diabetic patients as in other patients, without major safety concerns for their possible adverse effects. The use of these agents in clinical practice should therefore be encouraged, in order to reduce the burden of cardiovascular mortality and morbidity in older diabetic patients post-infarction.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_metabolism_MeSH Diabetes_Mellitus_metabolism_MeSH M_Heart_Failure__Congestive_MeSH S_chemically_induced_MeSH Heart_Failure__Congestive_chemically_induced_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Factors_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12515103
----K 1
----T [Coronary artery disease observed in general hospitals: ETTIC study.Comparison between trimetazidine and mononitrate isosorbide for patients receiving betablockers]
----A The extended use of interventional surgery of revascularisation has modified the prognosis and the evolution of ischaemic heart diseases. However, both coronary artery bypass graft and percutaneous transluminal coronary angioplasty failed to make the symptomatic or subclinical ischaemic manifestations of chronic coronary insufficiency disappear. The interest of using betablockers as a first-line therapy was widely demonstrated. However, their combination with another efficient molecule is often necessary. The aim of this trial has been to appreciate the efficiency of the association of a betablocker with either trimetazidine or with isosorbide monoitrate. Hundred and eighty five patients retaining a positive effort test despite 100 mg of atenolol, received in addition, either 60 mg of trimetazidine (93 cases) of 60 mg of isosorbide mononitrate (92 cases) for a two-month period and are then re-evaluated at the end of this period. The ischaemic threshold is delayed in a significant way in both groups (p < 0.0001; trimetazidine +7%, isosorbide mononitrate +10.7%). Twenty-three percent of the exercise tests under trimetzidine and 19% under isosorbide mononitrate become negative after two months of the therapeutic combination. The clinical improvement is even clearer with the disappearance of the angina crisis during the week before the second exercise test in 63% of the cases under trimetazidine and 54% of the cases under isosorbide mononitrate, among the patients who had kept it under atenolol at the inclusion. In conclusion, the combination of a second efficient molecule, trimetazidine or isosorbide mononitrate, brings a functional and objective improvement to patients with insufficient chronic coronary disease not totally controlled using a betablocker, even with high dosage. One should notice two important advantages in favour of the trimetazidine: one is practical due to a better tolerance (lack of cephalalgia), the other is conceptual (use of the complementary metabolic approach of cellular oxygenation rather than the haemodynamic approach of nitrate compounds which are already in concurrency with all other anti-ischaemic molecules).
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Coronary_Arteriosclerosis_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH M_Drug_Therapy__Combination_MeSH M_English_Abstract_MeSH M_Exercise_Test_MeSH M_Hospitals__General_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Treatment_Outcome_MeSH M_Trimetazidine_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12516008
----K 5
----T Overview: depression in the elderly.
----A Depression in the elderly population is a major public health problem. It has a high prevalence, is frequently co-morbid with medical illnesses, impacts negatively on quality of life, increases the number of visits to different medical services, and carries a high risk of suicide, especially in men. Imaging studies have increased our understanding of the biological mechanisms of depression in the elderly. Depression is sometimes difficult to diagnose in the elderly. It should be differentiated from apathetic states ( negative syndrome ), and its treatment requires knowledge of specific physiological changes that occur in this age group. Geriatric depression is more somatic and less ideational than depression in other age groups. Acute treatments with various antidepressant medications, augmentation strategies, electroconvulsive treatments, and psychotherapy must be coupled with maintenance strategies to prevent recurrences, which are common.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Comorbidity_MeSH P_Depression_MeSH S_diagnosis_MeSH Depression_diagnosis_MeSH S_epidemiology_MeSH Depression_epidemiology_MeSH S_therapy_MeSH Depression_therapy_MeSH M_Electroconvulsive_Therapy_MeSH M_Human_MeSH M_Psychotherapy_MeSH 
****** 12517682
----K 5
----T Different drug classes have variable effects on blood pressure depending on the time of day.
----A BACKGROUND: Blood pressure (BP) is controlled by a variety of systems, the activities of which vary throughout the day. As drugs are developed that selectively block these systems, the fall in BP may not be consistent over 24 h. METHODS: A total of 24 patients (aged >65 years) with systolic BP (SBP; >150 mm Hg) that had not been treated entered a substudy of a larger study performed in 74 patients. In a double blind, crossover study with a balanced design, they received placebo, atenolol 50 mg, perindopril 8 mg, felodipine 10 mg, or hydrochlorothiazide 50 mg. The study periods were 2 months. Ambulatory BP monitoring was performed at the end of each period, and was divided into awake periods (9:00 AM to 10:00 PM), sleep periods (12:00 AM to 6:00 AM), and morning periods (6:00 AM to 9:00 AM). Medication was taken at 9:00 AM. RESULTS: The four drug classes lowered 24-h mean SBP (P <.05), but the fall with atenolol was less than with the other drugs. The fall in awake BP with perindopril was less than with felodipine or hydrochlorothiazide. Atenolol caused no significant fall in sleep or morning SBP, and the falls with the other three drugs were significant and were greater than the fall with atenolol. The fall in sleep BP with perindopril was greater than with the other drug classes. The awake-sleep difference in SBP increased with perindopril, stayed the same with felodipine and hydrochlorothiazide, and was reduced by atenolol. CONCLUSIONS: In this study, the response to the different drug classes differed. The response to drugs that work relatively nonspecifically (diuretics, calcium blockers) was relatively consistent over 24 h. The response to beta blockers and to angiotensin converting enzyme inhibitors reflected the activity of control systems. This finding supports the concept of multiple drug therapy that may need to be tailored to the time of day.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Atenolol_MeSH S_administration_&_dosage_MeSH Atenolol_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Blood_Pressure_Monitoring__Ambulatory_MeSH M_Circadian_Rhythm_MeSH S_physiology_MeSH Circadian_Rhythm_physiology_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Felodipine_MeSH S_administration_&_dosage_MeSH Felodipine_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Perindopril_MeSH S_administration_&_dosage_MeSH Perindopril_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12521623
----K E
----T Effects of propranolol on recovery of heart rate variability following acute myocardial infarction and relation to outcome in the Beta-Blocker Heart Attack Trial.
----A This study evaluated the effects of propranolol on recovery of heart rate variability (HRV) after acute myocardial infarction and its relation to outcome in the Beta-blocker Heart Attack Trial (BHAT). Beta blockers improve mortality after acute myocardial infarction, but through an unknown mechanism. Depressed HRV, a measure of autonomic tone, predicts mortality after acute myocardial infarction. Whether beta blockers influence recovery of HRV after acute myocardial infarction, and thereby improve outcome, is unknown. We compared 24-hour HRV parameters at 1 week after acute myocardial infarction and after 6 weeks of treatment with propanolol (n = 88) or placebo (n = 96). The relation between 25-month outcome (death/acute myocardial infarction/congestive heart failure), propranolol treatment, and HRV was further analyzed. After 6 weeks, high-frequency (HF) power (log-normalized), an index of vagal tone, increased more in propranolol-treated patients (4.28 +/- 0.1 to 5.17 +/- 0.09 ms(2)) than in placebo-treated patients (4.26 +/- 0.09 to 4.77 +/- 0.1 ms(2), p <0.05). Sympathovagal balance measured by the low-frequency (LF) to HF ratio increased in placebo-treated patients (3.55 +/- 0.24 to 3.86 +/- 0.24) but decreased in those treated with propranolol (3.76 +/- 0.29 to 3.17 +/- 0.23, p <0.01). Other frequency-domain parameters increased over time but were not affected by propranolol. Propranolol blunted the morning increase in the LF/HF ratio. Recovery of HF, the strongest HRV predictor of outcome, and propranolol therapy independently predicted outcome. In summary, after acute myocardial infarction, propranolol therapy improves recovery of parasympathetic tone, which correlates with improved outcome, and decreases morning sympathetic predominance. These findings may elucidate the mechanisms by which beta blockers decrease mortality and reduce the early morning risk of sudden death after acute myocardial infarction.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Autonomic_Nervous_System_MeSH S_drug_effects_MeSH Autonomic_Nervous_System_drug_effects_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12521629
----K 3
----T Clinical outcomes in patients on beta-blocker therapy admitted with worsening chronic heart failure.
----A Beta blockers have been shown to reduce morbidity and mortality in patients with heart failure without evidence of overt congestion. No data are available describing outcomes of patients admitted with exacerbated chronic heart failure who are receiving beta blockade at the time of admission. The purpose of this analysis was to evaluate clinical outcomes in patients from the Outcomes of the Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study who were prescribed beta blockers on admission compared with patients who were not prescribed beta blockers at admission. In all, 212 patients were treated with beta blockers at admission and 737 patients were not. Baseline characteristics were similar between groups, except that patients prescribed beta blockers on admission had slightly higher ejection fractions, fewer New York Heart Association class IV symptoms, and lower heart rates. There was no difference in clinical events between patients who were treated with beta blockers at the time of admission and those who were not. Exploratory analyses suggested that patients whose beta-blocker therapy was discontinued had a higher risk of adverse outcomes, particularly in the subset of patients randomized to milrinone. The data from this nonrandom comparison suggest that continuation of pre-existing beta-blocker therapy is not associated with an increased risk of adverse clinical events in patients admitted with worsening heart failure. These results also suggest that caution should be taken when withdrawing beta blockade in this population.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_therapeutic_use_MeSH Cardiotonic_Agents_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Milrinone_MeSH S_therapeutic_use_MeSH Milrinone_therapeutic_use_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12523682
----K E
----T Lower plasma noradrenaline and blood viscosity on carvedilol vs atenolol in men with recent myocardial infarction.
----A The Carvedilol Acute Myocardial Infarction Study (CAMIS) investigates cardiac remodeling in patients (n = 250) randomized to carvedilol vs atenolol and treated for 12 months after acute myocardial infarction. In a sub-study, we compared sympathetic, hemorrheological and vascular effects in small but particularly well-matched groups of participants who had been on reasonably equipotent but unchanged doses of carvedilol (n = 10) or atenolol (n = 10) for at least 4 weeks. Blood pressures (p < 0.05), plasma adrenaline (p = 0.034), plasma vasopressin (p = 0.022) and whole blood viscosity at shear rate 0.5 cp (p = 0.050), 1.1 cp (p = 0.023), 5.8 cp (p = 0.049) and 201 cp (p = 0.060) taken in the laboratory at baseline before 2 h of using the hyperinsulinemic, isoglycemic glucose clamp were lower on carvedilol. Plasma noradrenaline was lower on carvedilol at baseline and throughout the clamp (p < 0.0005). Forearm vascular resistance as measured by plethysmography during the clamp tended to be lower on carvedilol (p = 0.074). No significant difference was found between the groups in glucose disposal rate measured by clamp, maximal forearm blood flow and minimal forearm vascular resistance after 10 min of ischemia, or in ambulatory blood pressure and heart rate taken a few days later. Thus, potential benefits of carvedilol vs atenolol were seen in these post-infarction patients in a laboratory setting. These findings suggest that the inhibitory effects on the sympathetic nervous system and related blood viscosity are stronger with carvedilol than with atenolol.
----P Clinical_Trial Journal_Article 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Blood_Viscosity_MeSH S_drug_effects_MeSH Blood_Viscosity_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH M_Female_MeSH M_Forearm_MeSH S_blood_supply_MeSH Forearm_blood_supply_MeSH M_Glucose_Clamp_Technique_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Regional_Blood_Flow_MeSH S_physiology_MeSH Regional_Blood_Flow_physiology_MeSH M_Vascular_Resistance_MeSH S_physiology_MeSH Vascular_Resistance_physiology_MeSH 
****** 12527626
----K 5
----T Treatment of systemic hypertension in patients with pulmonary disease: COPD and asthma.
----A We present a two-part review of the English-language literature pertaining to drug therapy for systemic high BP in patients with pulmonary diseases. Part I examines the literature pertaining to the use of antihypertensive drugs in patients with systemic hypertension and coexisting pulmonary conditions, especially COPD and asthma. Part II of the series reviews studies assessing the relationship between sleep-disordered breathing (including the role of the sympathetic nervous system) and systemic hypertension, and presents an approach to the management of these patients. It is the aim of both parts of this review to make qualified conclusions and recommendations applying a methodologic critique to assess the current literature. In the first part of this series, we review the demographics of hypertension in patients with COPD. This is followed by an extensive review of the use of specific classes of antihypertensive drug therapies in patients with pulmonary disease. The antihypertensive agents reviewed include diuretics, calcium antagonists, angiotensin-converting enzyme inhibitors, and angiotensin II receptor antagonists, beta-adrenergic blocking agents, and alpha-beta-blockers and other non-beta-blocker classes. Additionally, the renin angiotensin system is briefly reviewed, with a discussion of how angiotensin-converting enzyme inhibitors induce cough, especially in pulmonary and congestive heart failure patients.
----P Journal_Article Review Review__Academic 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Asthma_MeSH S_complications_MeSH Asthma_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Pulmonary_Disease__Chronic_Obstructive_MeSH S_complications_MeSH Pulmonary_Disease__Chronic_Obstructive_complications_MeSH 
****** 12528088
----K 2
----T Effect of selective and nonselective beta-blockers on resting energy production rate and total body substrate utilization in chronic heart failure.
----A BACKGROUND: In chronic heart failure (CHF) beta-blockers reduce myocardial oxygen consumption and improve myocardial efficiency by shifting myocardial substrate utilization from increased free fatty acid oxidation to increased glucose oxidation. The effect of selective and nonselective beta-blockers on total body resting energy production rate (EPR) and substrate utilization is not known. METHODS: Twenty-six noncachectic patients with moderately severe heart failure (New York Heart Association class II or III, left ventricular ejection fraction < 0.40) were treated with carvedilol (37.5 +/- 13.5 mg/12 h) or bisoprolol (5.4 +/- 3.0 mg/d) for 6 months. Indirect calorimetry was performed before and after 6 months of treatment. RESULTS: Resting EPR was decreased in carvedilol (5.021 +/- 0.803 to 4.552 +/- 0.615 kJ/min, P <.001) and bisoprolol group (5.230 +/- 0.828 to 4.978 +/- 0.640 kJ/min, P <.05; nonsignificant difference between groups). Lipid oxidation rate decreased in carvedilol and remained unchanged in bisoprolol group (2.4 +/- 1.4 to 1.5 +/- 0.9 mg m(2)/kg min versus 2.7 +/- 1.1 to 2.5 +/- 1.1 mg m(2)/kg min, P <.05). Glucose oxidation rate was increased only in carvedilol (2.6 +/- 1.4 to 4.4 +/- 1.6 mg m(2)/kg min, P <.05), but did not change in bisoprolol group. CONCLUSIONS: Both selective and nonselective beta-blockers reduce total body resting EPR in noncachectic CHF patients. Carvedilol compared to bisoprolol shifts total body substrate utilization from lipid to glucose oxidation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adipose_Tissue_MeSH S_drug_effects_MeSH Adipose_Tissue_drug_effects_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Basal_Metabolism_MeSH S_drug_effects_MeSH Basal_Metabolism_drug_effects_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Body_Weight_MeSH S_drug_effects_MeSH Body_Weight_drug_effects_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Epinephrine_MeSH S_blood_MeSH Epinephrine_blood_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_blood_MeSH Heart_Failure__Congestive_blood_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Patient_Compliance_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Severity_of_Illness_Index_MeSH M_Statistics_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Uric_Acid_MeSH S_blood_MeSH Uric_Acid_blood_MeSH M_Ventricular_Dysfunction__Left_MeSH S_blood_MeSH Ventricular_Dysfunction__Left_blood_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12529162
----K 5
----T Graves disease in childhood: a review of the options for diagnosis and treatment.
----A While diagnosing Graves disease in childhood and adolescence does not usually present specific problems, the treatment of hyperthyroidism is still controversial. In particular, with regard to the use of radioiodine therapy, strategies vary between many European and North American pediatric endocrinology centers. After the diagnosis is made, antithyroid drug treatment with methimazole (thiamazole), carbimazole, or propylthiouracil should be performed with caution, in particular, because of severe adverse effects, such as agranulocytosis or hepatitis, that are found in up to 1% of patients. Antithyroid drug treatment should not be continued long-term, particularly since definitive remission cannot be expected in more than 30-40% of patients. In contrast, the risk of severe adverse effects is still present, and the risk of thyroid carcinoma increases with time and appears to be considerably higher than after radioiodine treatment. To a great extent, the success of surgery depends on the skills of a trained surgeon. The question of whether to perform total or subtotal thyroidectomy is yet to be resolved. Surgery should be considered in patients with a large thyroid gland (>80g), severe ophthalmopathy, and a lack of remission on antithyroid drug treatment. Success rates have increased to up to 97%, while severe adverse effects (laryngeal nerve palsy, hypoparathyroidism) occur in approximately 4% of patients. Mortality is below 0.1%. Radioiodine treatment in children >5 years of age does not appear to be associated with an increased risk of thyroid carcinoma; however, long-term data are lacking. Compared with the surgical approach, success rates are lower, particularly if low doses of radioiodine are used. In general, adverse effects are less prevalent than in patients who have undergone surgery.
----P Journal_Article Review Review__Tutorial 
----M M_Adolescent_MeSH M_Antithyroid_Agents_MeSH S_administration_&_dosage_MeSH Antithyroid_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antithyroid_Agents_therapeutic_use_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Graves'_Disease_MeSH S_diagnosis_MeSH Graves'_Disease_diagnosis_MeSH S_therapy_MeSH Graves'_Disease_therapy_MeSH M_Human_MeSH M_Iodine_Radioisotopes_MeSH S_therapeutic_use_MeSH Iodine_Radioisotopes_therapeutic_use_MeSH M_Thyroidectomy_MeSH 
****** 12529904
----K 5
----T Cardiovascular disease prevention.
----A In this chapter, we have reviewed many of the steps necessary for effective CHD risk reduction. The first step in the office setting is to assess the individual CHD risk. This combines the evaluation of current CHD or a "secondary risk equivalent" with the counting of risk factors and in many cases, the absolute risk calculation. The next steps are to consider each of the major modifiable risk factors (hypertension, dyslipidemia, diabetes mellitus, smoking status) to set goals for each and then work to achieve those goals through lifestyle changes and medication therapy. We reviewed each of these risk factors in detail and then turned to a discussion of emerging risk factors that may help "fine-tune" the risk assessment in some borderline cases. We also discussed additional non-invasive testing that is available to the clinician to help refine the assessment of current burden of disease. Finally, we discuss some of the barriers that exist on both a global and local level to effective treatment of CHD risk factors.
----P Journal_Article 
----M M_Cardiovascular_Diseases_MeSH S_diagnosis_MeSH Cardiovascular_Diseases_diagnosis_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_diagnosis_MeSH Diabetes_Mellitus_diagnosis_MeSH S_therapy_MeSH Diabetes_Mellitus_therapy_MeSH M_Health_Behavior_MeSH M_Health_Promotion_MeSH M_Human_MeSH M_Life_Style_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Preventive_Health_Services_MeSH P_Primary_Prevention_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH 
****** 12540786
----K 3
----T Nadolol plus spironolactone in the prophylaxis of first variceal bleed in nonascitic cirrhotic patients: A preliminary study.
----A Treatment with beta-blockers fails to decrease portal pressure in nearly 40% of cirrhotic patients. Recent studies have suggested that treatment with spironolactone reduces pressure and flow in the portal and variceal systems. This trial was designed to assess if nadolol plus spironolactone is more effective than nadolol alone to prevent the first variceal bleeding. One hundred patients with medium and large varices who had never bled and were without ascites were included in a prospective, randomized, multicenter, double-blind, placebo-controlled trial. The patients were randomized into 2 groups: 51 received nadolol plus placebo (N + P) and 49 received nadolol plus spironolactone 100 mg/d (N + S). Hepatic venous pressure gradient (HVPG) and activity of the renin-aldosterone system (plasma renin activity/plasma aldosterone levels) were measured in 24 patients. There were no significant differences in the appearance of variceal bleeding and ascites between groups at a mean follow-up of 22 +/- 16 months. However, analyzing both complications together, the incidence was significantly higher in the N + P group than in the N + S group (39% vs. 20%; P <.04). Clinical ascites was also higher in patients in the N + P group than in the N + S group (21% vs. 6%; P <.04). Significant increases in plasma renin activity and plasma aldosterone levels were only observed in patients in the N + S group (P <.01). The cumulative probabilities of remaining free of bleeding and ascites were similar in both groups after 70 months of follow-up. In conclusion, these results suggest that nadolol plus spironolactone does not increase the efficacy of nadolol alone in the prophylaxis of the first variceal bleeding. However, when bleeding and ascites were considered together, the combined therapy effectively reduced the incidence of both portal-hypertensive complications.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nadolol_MeSH S_therapeutic_use_MeSH Nadolol_therapeutic_use_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Splanchnic_Circulation_MeSH S_drug_effects_MeSH Splanchnic_Circulation_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12540788
----K 4
----T Low doses of isosorbide mononitrate attenuate the postprandial increase in portal pressure in patients with cirrhosis.
----A Postprandial hyperemia is associated with a significant increase in portal pressure in cirrhosis, which may contribute to progressive dilation and rupture of gastroesophageal varices. In cirrhosis, an insufficient hepatic production of nitric oxide (NO) may impair the expected hepatic vasodilatory response to increased blood flow, further exaggerating the postprandial increase in portal pressure. This study was aimed at investigating whether low doses of an oral NO donor might counteract the postprandial peak in portal pressure. Twenty-three portal hypertensive cirrhotics, 8 of them under propranolol therapy, were randomized to receive orally 5-isosorbide mononitrate (ISMN; 10 mg; n = 11) or placebo (n = 12) and a standard liquid meal 15 minutes later. Hepatic venous pressure gradient (HVPG), mean arterial pressure (MAP), and hepatic blood flow (HBF) were measured at baseline and 15, 30, and 45 minutes after a meal. ISMN significantly attenuated the postprandial increase in portal pressure as compared with placebo (peak HVPG increase: 2.4 +/- 1.4 mm Hg vs. 5.2 +/- 2.1 mm Hg, P =.002). Percentual increases in HBF were similar in both groups. MAP decreased slightly in ISMN group (-7.5% +/-.5%; P <.01 vs. baseline). These effects were also observed in patients on chronic propranolol therapy. In conclusion, hepatic NO supplementation by low doses of ISMN effectively reduces the postprandial increase of portal pressure in cirrhosis, with only a mild effect on arterial pressure. The same was observed in patients receiving propranolol. Our results suggest that therapeutic strategies based on selective hepatic NO delivery may improve the treatment of portal hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Human_MeSH M_Isosorbide_Dinitrate_MeSH S_administration_&_dosage_MeSH Isosorbide_Dinitrate_administration_&_dosage_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH M_Liver_Cirrhosis_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitric_Oxide_Donors_MeSH S_administration_&_dosage_MeSH Nitric_Oxide_Donors_administration_&_dosage_MeSH M_Portal_Vein_MeSH S_physiopathology_MeSH Portal_Vein_physiopathology_MeSH P_Postprandial_Period_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilator_Agents_MeSH S_administration_&_dosage_MeSH Vasodilator_Agents_administration_&_dosage_MeSH 
****** 12544718
----K I
----T Efficacy of monotherapy compared with combined antianginal drugs in the treatment of chronic stable angina pectoris: a meta-analysis.
----A OBJECTIVE: To determine the relative efficacy of antianginal drugs administered as monotherapy or in combination in patients with chronic stable angina. METHODS: A meta-analysis was performed on randomized trials, published in English between 1980 and 1999, that directly compared combined treatment and monotherapy. Twenty-two articles were included, all on the comparison of -blocker monotherapies to their combination with a calcium antagonist and 10 on the comparison of calcium antagonist monotherapies to their combination with a -blocker. RESULTS: Time to 1 mm ST-segment depression, total exercise duration and time to onset of anginal pain were significantly increased with the combined therapy compared to -blocker alone (by 8, 5 and 12%, respectively). Only time to 1 mm ST-segment depression was significantly increased with the combined therapy compared to calcium antagonist alone (by 9%). For all these parameters, the adjusted differences were significant only within 6 h following drug intake and were not significant after 6 h. No analysis of safety data could be performed. CONCLUSION: As far as exercise testing is concerned, the combination of a calcium antagonist and a -blocker is statistically more effective than either monotherapy. Further studies are needed to confirm the higher efficacy after the first 6 h following drug intake.
----P Clinical_Trial Journal_Article Meta-Analysis Randomized_Controlled_Trial Review Review_of_Reported_Cases 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Comparative_Study_MeSH M_Coronary_Angiography_MeSH M_Cross-Over_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Reproducibility_of_Results_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 12544861
----K 5
----T The role of blood pressure lowering before and after stroke.
----A PURPOSE OF REVIEW: Elevated blood pressure is one of the most potent risk factors for first ever and recurrent stroke as well as influencing early outcome after acute stroke. There have been a number of significant randomized controlled trials which may influence management in each of these three categories. RECENT FINDINGS: For primary prevention, the recent information from the Heart Outcomes Prevention Evaluation, Losartan Intervention for Endpoint Reduction to Hypertension, Study on Cognition and Prognosis in the Elderly and Australian National Blood Pressure Study support the view that blood pressure lowering protects against stroke regardless of baseline blood pressure level. There is some evidence that blockade of the angiotensin system may give additional protection. For secondary prevention, evidence from the Perindopril Protection against Recurrent Stroke Study shows that blood pressure lowering with perindopril based therapy reduces fatal or non-fatal stroke events, again in hypertensive or normotensive individuals. There is uncertainty about blood pressure lowering in acute stroke, although presentation of the recent Acute Candesartan Cilexetil Evaluation in Stroke Survivors trial in which there was significant protection against vascular events using candesartan suggests that further studies should be undertaken. SUMMARY: Blood pressure lowering for primary prevention of stroke should be undertaken using a variety of therapeutic agents. For secondary stroke prevention perindopril based therapy should be used based on current evidence. Uncertainty still exists as to whether blood pressure lowering in the acute stroke setting is safe or improves outcomes.
----P Journal_Article Review Review_Literature 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cerebral_Infarction_MeSH S_drug_therapy_MeSH Cerebral_Infarction_drug_therapy_MeSH S_etiology_MeSH Cerebral_Infarction_etiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Perindopril_MeSH S_adverse_effects_MeSH Perindopril_adverse_effects_MeSH S_therapeutic_use_MeSH Perindopril_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Recurrence_MeSH M_Treatment_Outcome_MeSH 
****** 12542721
----K 5
----T Evidence-based treatment of hypertension in patients with diabetes mellitus.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diabetic_Nephropathies_MeSH S_physiopathology_MeSH Diabetic_Nephropathies_physiopathology_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH 
****** 12544508
----K 5
----T A microarray minisequencing system for pharmacogenetic profiling of antihypertensive drug response.
----A We aimed to develop a microarray genotyping system for multiplex analysis of a panel of single nucleotide polymorphisms (SNPs) in genes encoding proteins involved in blood pressure regulation, and to apply this system in a pilot study demonstrating its feasibility in the pharmacogenetics of hypertension. A panel of 74 SNPs in 25 genes involved in blood pressure regulation was selected from the SNP databases, and genotyped in DNA samples of 97 hypertensive patients. The patients had been randomized to double-blind treatment with either the angiotensin II type 1 receptor blocker irbesartan or the beta 1-adrenergic receptor blocker atenolol. Genotyping was performed using a microarray based DNA polymerase assisted 'minisequencing' single nucleotide primer extension assay with fluorescence detection. The observed genotypes were related to the blood pressure reduction using stepwise multiple regression analysis. The allele frequencies of the selected SNPs were determined in the Swedish population. The established microarray-based genotyping system was validated and allowed unequivocal multiplex genotyping of the panel of 74 SNPs in every patient. Almost 7200 SNP genotypes were generated in the study. Profiles of four or five SNP-genotypes that may be useful as predictors of blood pressure reduction after antihypertensive treatment were identified. Our results highlight the potential of microarray-based technology for SNP genotyping in pharmacogenetics.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_DNA_Primers_MeSH S_genetics_MeSH DNA_Primers_genetics_MeSH M_Databases__Genetic_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Gene_Expression_MeSH S_drug_effects_MeSH Gene_Expression_drug_effects_MeSH M_Gene_Expression_Profiling_MeSH M_Gene_Frequency_MeSH S_drug_effects_MeSH Gene_Frequency_drug_effects_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oligonucleotide_Array_Sequence_Analysis_MeSH S_methods_MeSH Oligonucleotide_Array_Sequence_Analysis_methods_MeSH M_Pharmacogenetics_MeSH S_methods_MeSH Pharmacogenetics_methods_MeSH M_Polymorphism__Single_Nucleotide_MeSH S_genetics_MeSH Polymorphism__Single_Nucleotide_genetics_MeSH M_Random_Allocation_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_metabolism_MeSH Receptors__Angiotensin_metabolism_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12545683
----K 4
----T Projected impact of travoprost versus both timolol and latanoprost on visual field deficit progression and costs among black glaucoma subjects.
----A PURPOSE: We compared differences associated with use of travoprost and latanoprost on both progression of perimetric loss over time and associated costs among black patients. METHODS: Patients with primary open-angle glaucome or ocular hypertension were randomly assigned to one of four arms in a 12-month, double-masked study: travoprost (0.004% or 0.0015%), latanoprost (0.005%), or timolol (0.5%). Forty-nine patients received 0.004% travoprost, 43 received latanoprost, and 40 received timolol. We applied algorithms found in published studies that link intraocular pressure (IOP) control to visual field progression and calculated the likelihood of visual field deterioration based on IOP data. This was used to estimate differences in medical care costs. RESULTS: The average IOP was lower for patients receiving travoprost than for patients receiving latanoprost or timolol (17.3 versus 18.7 versus 20.5 mm Hg respectively, P < .05). Travoprost-treated patients had a smaller predicted change in visual field defect score (VFDS) than latanoprost-treated patients and timolol-treated patients, and significantly fewer were expected to demonstrate visual field progression. Medical care costs would be higher for latanoprost-treated and timolol-treated patients. CONCLUSIONS: Recent studies have provided algorithms linking IOP control to changes in visual fields. We found that treatment with travoprost was associated with less visual field progression and potential cost savings.
----P Clinical_Trial Clinical_Trial__Phase_III Journal_Article Randomized_Controlled_Trial 
----M P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cloprostenol_MeSH S_analogs_&_derivatives_MeSH Cloprostenol_analogs_&_derivatives_MeSH S_economics_MeSH Cloprostenol_economics_MeSH S_therapeutic_use_MeSH Cloprostenol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Disease_Progression_MeSH M_Double-Blind_Method_MeSH M_Drug_Costs_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_economics_MeSH Glaucoma__Open-Angle_economics_MeSH S_ethnology_MeSH Glaucoma__Open-Angle_ethnology_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_economics_MeSH Ocular_Hypertension_economics_MeSH S_ethnology_MeSH Ocular_Hypertension_ethnology_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Prostaglandins_F__Synthetic_MeSH S_economics_MeSH Prostaglandins_F__Synthetic_economics_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_economics_MeSH Timolol_economics_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_United_States_MeSH M_Vision_Disorders_MeSH S_physiopathology_MeSH Vision_Disorders_physiopathology_MeSH M_Visual_Fields_MeSH S_drug_effects_MeSH Visual_Fields_drug_effects_MeSH 
****** 12549721
----K 5
----T Relieving migraine pain: sorting through the options.
----A Although triptans are a major advance in the treatment of migraine, the optimal approach for acute treatment involves a combination of lifestyle modifications, nonpharmacologic symptom relief, and drug therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Analgesics__Non-Narcotic_MeSH S_therapeutic_use_MeSH Analgesics__Non-Narcotic_therapeutic_use_MeSH M_Diagnosis__Differential_MeSH M_Drugs__Non-Prescription_MeSH S_therapeutic_use_MeSH Drugs__Non-Prescription_therapeutic_use_MeSH M_Ergotamine_MeSH S_therapeutic_use_MeSH Ergotamine_therapeutic_use_MeSH M_Headache_Disorders_MeSH S_diagnosis_MeSH Headache_Disorders_diagnosis_MeSH M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_etiology_MeSH Migraine_etiology_MeSH S_therapy_MeSH Migraine_therapy_MeSH M_Patient_Education_MeSH M_Referral_and_Consultation_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12549727
----K 5
----T Thyrotoxicosis and the cardiovascular system: subtle but serious effects.
----A Thyrotoxicosis is associated with increased cardiovascular morbidity and mortality, primarily due to heart failure and thromboembolism. However, its signs and symptoms may be subtle and can easily be missed. Therefore, one should suspect thyrotoxicosis in patients with palpitations, exercise intolerance, dyspnea on exertion, and other cardiovascular signs.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_adverse_effects_MeSH Amiodarone_adverse_effects_MeSH M_Antithyroid_Agents_MeSH S_therapeutic_use_MeSH Antithyroid_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH M_Contrast_Media_MeSH S_adverse_effects_MeSH Contrast_Media_adverse_effects_MeSH M_Human_MeSH M_Thyrotoxicosis_MeSH S_complications_MeSH Thyrotoxicosis_complications_MeSH S_drug_therapy_MeSH Thyrotoxicosis_drug_therapy_MeSH S_etiology_MeSH Thyrotoxicosis_etiology_MeSH 
****** 12549986
----K 5
----T Pharmacotherapy of diabetes mellitus: implications for the prevention and treatment of cardiovascular disease.
----A Diabetes mellitus in adults is associated with an increased risk of premature vascular disease and a higher mortality rate. The presence of other risk factors, often seen in diabetic patients, such as systemic hypertension, augments the rate of vascular diseases. Evidence is growing that tight control of hyperglycemia using insulin and/or oral hypoglycemic agents will modify this risk. More aggressive control of concomitant hypertension and/or hyperlipidemia is also required. Diabetic patients who have myocardial infarctions do worse than nondiabetic patients. Various strategies to improve outcomes include the use of tight blood glucose control, and various coronary interventions are currently under clinical study.
----P Journal_Article Review Review__Academic 
----M M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Diabetic_Angiopathies_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypoglycemic_Agents_MeSH S_adverse_effects_MeSH Hypoglycemic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Insulin_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Risk_Factors_MeSH M_Thrombophilia_MeSH S_drug_therapy_MeSH Thrombophilia_drug_therapy_MeSH 
****** 12556656
----K 5
----T Meta-analysis, meta-regression, and meta-physics.
----A 
----P Comment Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Controlled_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Meta-Analysis_MeSH M_Metaphysics_MeSH M_Regression_Analysis_MeSH 
****** 12556657
----K 5
----T Benefits of antihypertensive pharmacologic therapy and blood pressure reduction in outcome trials.
----A In a quantitative overview of published trials, we investigated whether pharmacologic properties of antihypertensive drugs, as opposed to reduction in blood pressure, explain cardiovascular outcomes in hypertensive or high-risk patients. We used meta-regression to investigate the association between the odds ratios of outcome (experimental vs. reference treatment) and the corresponding blood pressure differences between study groups. Thus, we correlated odds ratios with between-group differences in systolic pressure. We then compared odds ratios of benefit observed in recent trials with those predicted by meta-regression on the basis of the differences in systolic pressure between randomized groups. Among nine actively-controlled trials in hypertension, significant differences in systolic pressure (follow-up minus baseline) between randomized groups (experimental minus reference) were observed in the ALLHAT, CAPPP, MIDAS, and NORDIL trials. Furthermore, the differences in achieved systolic and/or diastolic pressure between study groups were also significant in the hypertension trials and studies in high-risk patients, which involved untreated control patients. The differences between the observed odds ratios and those predicted by meta-regression did not reach statistical significance except for NORDIL and the single-drug therapy subgroup of the PROGRESS trial. In NORDIL, the risk of stroke was lower on diltiazem than on the older drug classes despite a 3.1 mm Hg higher systolic pressure on the calcium channel blocker. In PROGRESS, perindopril alone reduced blood pressure by 5/3 mm Hg, but did not affect the incidence of all cardiovascular events or the recurrence of stroke. In conclusion, the finding that in the reviewed trials blood pressure reduction largely accounted for outcome emphasizes the desirability of tight blood pressure control. The hypothesis that blood pressure-lowering medications might influence cardiovascular prognosis over and beyond their antihypertensive effect remains to a large extent unproved.
----P Journal_Article Meta-Analysis 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Odds_Ratio_MeSH M_Randomized_Controlled_Trials_MeSH M_Regression_Analysis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH M_Treatment_Outcome_MeSH 
****** 12561007
----K 5
----T Variceal bleeding and portal hypertension: has there been any progress in the last 12 months?
----A A review of the literature on the management of esophagogastric varices published in the last 12 months shows that the data are still quite conflicting. In the primary and secondary prophylaxis of variceal bleeding, beta-blockers are still the mainstay of pharmacotherapy. Measurement of the hepatic portal venous pressure gradient is considered to be a reliable parameter for successful reduction of portal pressure using medical therapy. However, intolerance of propranolol requiring discontinuation of therapy has been observed in approximately 30 % of patients. Patients' compliance with medication may represent another drawback of medical therapy.The role of endoscopic band ligation in secondary prophylaxis is now indisputable, especially in comparison with sclerotherapy. In the primary prevention of variceal bleeding, band ligation is beginning to have a competitive edge over pharmacological therapy.Acute variceal bleeding is no longer a frequent morbid emergency. Most cases of bleeding can now be managed successfully with band ligation and N-butyl-2-cyanoacrylate obliteration. N-butyl-2-cyanoacrylate has come into increasingly widespread use in the treatment of bleeding gastric fundal varices in which surgery or transjugular intrahepatic portosystemic shunting were previously regarded as the preferred therapies.
----P Journal_Article Review Review_Literature 
----M M_Acute_Disease_MeSH M_Enbucrilate_MeSH S_analogs_&_derivatives_MeSH Enbucrilate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Enbucrilate_therapeutic_use_MeSH M_Endoscopy__Digestive_System_MeSH M_Endosonography_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH S_ultrasonography_MeSH Esophageal_and_Gastric_Varices_ultrasonography_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Hemostatics_MeSH S_therapeutic_use_MeSH Hemostatics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH S_therapy_MeSH Hypertension__Portal_therapy_MeSH S_ultrasonography_MeSH Hypertension__Portal_ultrasonography_MeSH M_Laser_Coagulation_MeSH M_Octreotide_MeSH S_therapeutic_use_MeSH Octreotide_therapeutic_use_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH M_Tissue_Adhesives_MeSH S_therapeutic_use_MeSH Tissue_Adhesives_therapeutic_use_MeSH 
****** 12558470
----K 3
----T Cost-minimisation study of dorzolamide versus brinzolamide in the treatment of ocular hypertension and primary open-angle glaucoma: in four European countries.
----A OBJECTIVE: Cost is an issue when prescribing two drugs with equivalent efficacy. We compared the direct medical costs of topical brinzolamide 1% (twice a day or three times daily) with topical dorzolamide 2% (twice a day or three times daily) in France, Italy, Portugal and Spain in patients with ocular hypertension or primary open-angle glaucoma. DESIGN AND SETTING: Three double-blind, controlled, randomised trials (with a study duration of 3 months) compared the response rate of brinzolamide twice a day or three times daily versus dorzolamide three times daily, and the response rate of brinzolamide-timolol twice a day versus a dorzolamide-timolol combination twice a day. A fourth double-blind randomised trial (with a duration of 12 months) compared brinzolamide twice a day and three times daily with timolol monotherapy. Local tolerance was compared in two dedicated studies. Rates of switching to a new medication regimen were evaluated through a US health maintenance organisation database. In case of treatment failure, the patients were treated with latanoprost. A model was developed to value direct medical costs over 3 months. The economic perspective was that of the third-party payer and the patient, and included direct medical costs (reimbursed part plus co-payment). PATIENTS: Patients with ocular hypertension and/or primary open-angle glaucoma who had not responded to or could not tolerate beta-blocker therapy. OUTCOME MEASURE: The daily direct medical costs of therapy with the two drugs. RESULTS: As monotherapy, brinzolamide twice daily and three times daily was found to be as efficacious as dorzolamide three times a day. Brinzolamide twice daily plus timolol was also as efficacious as a combination of dorzolamide and timolol twice a day. Stinging of the eye upon instillation with brinzolamide was experienced by fewer patients than with dorzolamide (p < 0.0001). The likelihood of patients treated with dorzolamide changing therapy was 1.28 times greater than that for those treated with brinzolamide. The size of the brinzolamide drop is 18.7% smaller than that of dorzolamide allowing seven more therapy days per bottle with brinzolamide twice daily than with dorzolamide monotherapy, and five more days when brinzolamide is used three times a day. The direct medical costs for patients treated with brinzolamide were lower in all four European countries when drop size was taken into account than for those treated with dorzolamide. Sensitivity analyses confirmed the robustness of our findings. CONCLUSION: Because brinzolamide can be prescribed twice daily in monotherapy and because fewer patients treated with brinzolamide switch therapy due to local intolerance, our model suggests that brinzolamide is a cost-saving alternative to dorzolamide.
----P Journal_Article 
----M M_Administration__Topical_MeSH M_Carbonic_Anhydrase_Inhibitors_MeSH S_economics_MeSH Carbonic_Anhydrase_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Carbonic_Anhydrase_Inhibitors_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH P_Economics__Pharmaceutical_MeSH M_Europe_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_economics_MeSH Glaucoma__Open-Angle_economics_MeSH M_Human_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_economics_MeSH Ocular_Hypertension_economics_MeSH M_Randomized_Controlled_Trials_MeSH M_Sulfonamides_MeSH S_economics_MeSH Sulfonamides_economics_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiazines_MeSH S_economics_MeSH Thiazines_economics_MeSH S_therapeutic_use_MeSH Thiazines_therapeutic_use_MeSH M_Thiophenes_MeSH S_economics_MeSH Thiophenes_economics_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH 
****** 12559536
----K 3
----T Effects of verapamil and metoprolol on recovery from atrial electrical remodeling after cardioversion of long-lasting atrial fibrillation.
----A The aim of this prospective, randomized study was to investigate the effect of pretreatment with two different intracellular calcium-lowering drugs (verapamil and metoprolol) on recovery from atrial effective refractory period (AERP) shortening after internal electrical cardioversion (EC) of persistent atrial fibrillation (AF) in patients on amiodarone. Twenty-one patients on amiodarone for at least 30 days were referred to our hospital for internal EC of a persistent AF refractory to external EC. They were randomized to receive only amiodarone (group AMI, n=7), or amiodarone and verapamil 240 mg/day (group VER, n=7), or amiodarone and metoprolol 100 mg/day (group MET, n=7). Left AERP was measured 10 min and 24 h after EC. AERP was also determined in 13 controls. The AERP after 10 min was significantly shorter in group AMI (201 (31) ms, P<0.02) and group MET (203 (34) ms, P<0.03) than in controls (249 (45) ms), but not in group VER (237 (51) ms, P=NS). The AERP after 24 h was still significantly shorter in group AMI (204 (38) ms, P<0.04) than in controls, but not in group MET (225 (52) ms, P=NS) or in group VER (290 (36) ms, P=NS). Pretreatment with amiodarone and verapamil prevents AERP shortening, while pretreatment with amiodarone and metoprolol only accelerated AERP recovery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Analysis_of_Variance_MeSH M_Atrial_Fibrillation_MeSH S_diagnosis_MeSH Atrial_Fibrillation_diagnosis_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Atrial_Function_MeSH S_drug_effects_MeSH Atrial_Function_drug_effects_MeSH S_physiology_MeSH Atrial_Function_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Echocardiography__Doppler_MeSH M_Electric_Countershock_MeSH S_methods_MeSH Electric_Countershock_methods_MeSH M_Electrophysiology_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Probability_MeSH M_Prospective_Studies_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH M_Verapamil_MeSH S_administration_&_dosage_MeSH Verapamil_administration_&_dosage_MeSH 
****** 12566015
----K 4
----T Timolol 0.5%/dorzolamide 2% fixed combination vs timolol maleate 0.5% and unoprostone 0.15% given twice daily to patients with primary open-angle glaucoma or ocular hypertension.
----A OBJECTIVE: To compare the efficacy and safety of timolol 0.5%/dorzolamide 2% fixed combination vs timolol maleate 0.5% and unoprostone 0.15% given twice daily. DESIGN: Prospective multicenter, randomized, double-masked, crossover comparison study. METHODS: Primary open-angle glaucoma or ocular hypertension patients were randomly assigned to one of the treatment groups for a 6-week treatment period and then crossed over to the opposite treatment. Diurnal curve testing was performed at 8:00 AM, 10:00 AM, 4:00 PM, 6:00 PM, and 8:00 PM at baseline and the end of each treatment period. The run-in medicine was timolol twice daily for 28 days. RESULTS: Thirty-two patients completed this trial. The baseline trough pressure was 24.3 +/- 3.0 mm Hg, and the diurnal curve was 23.4 +/- 3.2 mm Hg. For the fixed combination the treatment trough pressure was 20.8 +/- 4.1 mm Hg and the diurnal curve was 19.6 +/- 3.6 mm Hg, whereas timolol and unoprostone concomitant therapy showed a treatment trough pressure of 20.1 +/- 4.5 mm Hg and a diurnal pressure of 19.8 +/- 4.1 mm Hg. There was no significant difference between treatment groups at any time point, for the diurnal curve, or in the extended reduction from baseline. There was no difference between treatment groups regarding ocular and systemic unsolicited or solicited adverse events. Burning, stinging, and conjunctival hyperemia were the adverse events most noted. There were no serious adverse events during this trial. CONCLUSIONS: This study suggests that both timolol/dorzolamide 2% fixed combination and concomitant timolol maleate 0.5% and unoprostone 0.15% therapy provide similar efficacy and safety throughout the daytime diurnal curve.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Dinoprost_MeSH S_adverse_effects_MeSH Dinoprost_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Dinoprost_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Dinoprost_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Visual_Acuity_MeSH 
****** 12566891
----K 4
----T Timolol 0.1% gel (Nyogel 0.1% once daily versus conventional timolol 0.5% solution twice daily: a comparison of efficacy and safety.
----A In a prospective, randomised, double-masked, parallel-group, multi-centre study, 210 patients with primary open angle glaucoma or ocular hypertension were enrolled of whom 167 (timolol 0.1% gel 82, timolol 0.5% 85) completed the study as per protocol. The change in intraocular pressure between baseline and week 12 in the worse eye ('at trough') was 6.3 (SD 3.3) mm Hg on timolol 0.1% gel and 7.0 (2.9) mm Hg on timolol 0.5%; this difference was not statistically significant (p = 0.19). The difference between the two study groups in the change of intraocular pressure from baseline was 0.62 mm Hg; the 90% CI of -0.09 to +1.33 mm Hg was within the pre-specified limits of -1.5 to +1.5 mm Hg demonstrating equivalence between timolol 0.1% gel and timolol 0.5%. The plasma levels of timolol (ng/ml) at 12 weeks in the timolol 0.1% gel group were significantly less than that with timolol 0.5% both before instillation (mean 0.057, SD 0.131 and mean 0.470, SD 0.519 respectively, p = 0.025) and after instillation (mean 0.552, SD 0.992 and mean 2.473, SD 1.780 respectively, p = 0.008). Both treatments were well tolerated with no statistically significant difference between the groups in the occurrence of ocular or systemic adverse events.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Gels_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Visual_Acuity_MeSH S_drug_effects_MeSH Visual_Acuity_drug_effects_MeSH 
****** 12566870
----K 4
----T Comparison of efficacy and tolerability between two gel-forming timolol maleate ophthalmic solutions in patients with glaucoma or ocular hypertension.
----A PURPOSE: To compare two gel-forming timolol maleate ophthalmic solutions, Timoptol XE and Lizmon TG, in regard to efficacy and tolerability in patients with glaucoma or ocular hypertension by means of a patient-masked prospective randomized crossover study. SUBJECTS AND METHODS: A total of 37 patients with glaucoma or ocular hypertension under treatment with antiglaucoma ophthalmic solutions including 0.5% twice-daily timolol maleate participated in this study. Only timolol maleate was withdrawn and either Timoptol XE or Lizmon TG was randomly allocated. After instillation for 1 month, the other ophthalmic solution was subsequently instilled for another month. Routine ophthalmic examination including slit-lamp examination and intraocular pressure (IOP) monitoring was conducted before instillation of gel-forming ophthalmic solutions and just after completing the instillation of each ophthalmic solution. Patient questionnaire surveys were also performed just after completing the instillation of each ophthalmic solution. RESULTS: Mean IOP, just before the withdrawal of timolol ophthalmic solution, was 16.4 +/- 2.9 mm Hg. At the end of Timoptol XE or Lizmon TG instillation, mean IOPs were 16.3 +/- 2.5 or 16.3 +/- 3.0 mm Hg, respectively. The results of the questionnaire survey showed no significant difference between Timoptol XE and Lizmon TG in regard to all survey items. Twenty-nine patients (78.4%) preferred to use gel-forming timolol solutions rather than twice-daily timolol ophthalmic solution. The presence of concurrently used ophthalmic solutions did not effect the incidences of subjective symptoms. The incidences of objective adverse effects were not significantly different between two gel-forming timolol ophthalmic solutions. CONCLUSION: Both gel-forming timolol ophthalmic solutions could be good choices for glaucoma treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cross-Over_Studies_MeSH M_Female_MeSH M_Gels_MeSH M_Glaucoma__Angle-Closure_MeSH S_drug_therapy_MeSH Glaucoma__Angle-Closure_drug_therapy_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Patient_Compliance_MeSH M_Patient_Satisfaction_MeSH M_Prospective_Studies_MeSH M_Questionnaires_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Visual_Acuity_MeSH 
****** 12570793
----K 5
----T Angiotensin-converting enzyme inhibitors: mechanisms of action and implications in anesthesia practice.
----A This review summarizes physiology of circulating and local renin-angiotensin system (RAS), enzymatic properties and mechanism of action of angiotensin I converting enzyme inhibitors (ACEIs) on RAS, and implications of ACEIs in anesthetic management of patients treated with these drugs. ACEIs, through their effect on RAS, may improve cardiovascular functions, pulmonary dynamics, and body fluid homeostasis. Thus, ACEIs have become an integral part of management of patients with hypertension, congestive heart failure (CHF) and chronic renal disease. ACEIs, due to differences in their chemical structure, exert different pharmacological actions and can have protective or occasional damaging effects on different organs. The anesthesiologists are commonly involved in the management of patients treated with ACEIs. Thus, the role of ACEIs and their possible interaction with anesthetic agents must be an integral part of clinical decision-making during anesthesia Hemodynamic variation during anesthesia is mainly related to specific effects of anesthetic agents on sympathetic nervous system. Those with preoperative fasting, volume depletion and extended sympathetic blockade can have reduced vascular capacitance resulting in decreased venous return, reduced cardiac output and severe arterial hypotension. Angiotensin II (ANG2) a potent vasoconstrictor may counterbalance such hypotensive effect. During ACE inhibition ANG2 cannot counterbalance this hypotension. Thus, induction of anesthesia may cause severe hypotension in hypovolemic patients specifically in those receiving diuretics as a complement to ACEIs. Recent advances in RAS and the pharmacology of ACEIs have identified some predisposing factors and risks associated with anesthesia in patients treated with ACEIs. Practitioners should be vigilant, and readily have vasopressors, necessary fluids and other resuscitative measures for treatment of unexpected hemodynamic instability during anesthesia and surgery.
----P Journal_Article Review Review__Tutorial 
----M M_Anesthesia_MeSH S_methods_MeSH Anesthesia_methods_MeSH M_Angiotensin_I_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_I_antagonists_&_inhibitors_MeSH S_physiology_MeSH Angiotensin_I_physiology_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH S_physiology_MeSH Angiotensin_II_physiology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Human_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH 
****** 12574534
----K 5
----T Angiotensin-converting enzyme inhibitors for stroke prevention: is there HOPE for PROGRESS After LIFE?
----A 
----P Editorial Review Review__Tutorial 
----M M_Angiotensin_II_MeSH S_physiology_MeSH Angiotensin_II_physiology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Benzoates_MeSH S_therapeutic_use_MeSH Benzoates_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Clinical_Trials_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Life_Style_MeSH M_Practice_Guidelines_MeSH M_Ramipril_MeSH S_adverse_effects_MeSH Ramipril_adverse_effects_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Risk_MeSH M_Risk_Factors_MeSH 
****** 12574539
----K 5
----T Prevention and health services delivery.
----A 
----P Editorial Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antioxidants_MeSH S_administration_&_dosage_MeSH Antioxidants_administration_&_dosage_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH S_therapy_MeSH Cerebrovascular_Accident_therapy_MeSH M_Dietary_Supplements_MeSH M_Estrogen_Replacement_Therapy_MeSH M_Food_Habits_MeSH M_Fruit_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Nutrition_Surveys_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH P_Primary_Prevention_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Risk_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_Vegetables_MeSH 
****** 12580985
----K 3
----T Blood pressure response to conventional and low-dose enalapril in chronic renal failure.
----A AIMS: In chronic renal failure, the clearance of most ACE inhibitors including enalapril is reduced. Hence, with conventional dosage, plasma enalaprilat may be markedly elevated. It is unclear whether this excess of drug exposure affords an improved control of blood pressure. The aim of the present study was to evaluate short-term blood pressure response to two different plasma levels of enalaprilat. METHODS: As part of an open, randomized, controlled trial of the effect of high and low dosage of enalapril on the progression of renal failure, short-term blood pressure response was evaluated. Data were analysed in all patients completing 3 months of follow-up. The patients were allocated to two trough plasma concentrations of enalaprilat, either above 50 ng ml(-1) (high) (n = 17) or below 10 ng ml(-1) (low) (n = 18), and the daily dose of enalapril titrated accordingly. RESULTS: Median (range) glomerular filtration rate (GFR) at baseline was 18 (7.9) in the high enalaprilat concentration group and 17 (7.3) ml min(-1) 1.73 m(2) in the low concentration group (NS). Nine patients in each group were on treatment with enalapril at baseline with a median daily dose of 5 mg in both the high (5-10) and low (2.5-20) concentration group. At 3 months' follow-up, the dose was 10 (2.5-30) and 1.9 (1.25-5) mg (P < 0.0001), respectively. After 3 months median trough concentrations of enalaprilat were 82.5 (22-244) ng ml(-1) and 9.1 (2.5-74.8) ng ml(-1) (P < 0.002). At baseline the median systolic blood pressures in the two groups were 140 (110-200) and 133 (110-165), in the high and low enalaprilat concentration groups, respectively, and after 3 months they were 135 (105-170) and 130 (105-170) mmHg (NS). Median diastolic blood pressure was 80 mmHg in each group both at baseline (65-100) and at follow-up (60-95) (NS). There was no difference between the groups in concomitant antihypertensive treatment (number of patients treated, mean daily dose) during the observation period. Proteinuria remained stable during the study period in both groups; patients in the high concentration group had higher plasma potassium concentrations at day 90 and patients in the low group experienced a slight increase in GFR. CONCLUSIONS: In moderate to severe chronic renal insufficiency the same degree of blood pressure control was achieved on low as well as moderate daily doses of enalapril. This was irrespective of concomitant antihypertensive treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_blood_MeSH Angiotensin-Converting_Enzyme_Inhibitors_blood_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Glomerular_Filtration_Rate_MeSH S_drug_effects_MeSH Glomerular_Filtration_Rate_drug_effects_MeSH M_Hemoglobins_MeSH S_analysis_MeSH Hemoglobins_analysis_MeSH M_Human_MeSH M_Kidney_Failure__Chronic_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Proteinuria_MeSH S_physiopathology_MeSH Proteinuria_physiopathology_MeSH 
****** 12584370
----K 5
----T Initial treatment of hypertension.
----A 
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diet__Reducing_MeSH M_Diet__Sodium-Restricted_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Life_Style_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_complications_MeSH Obesity_complications_MeSH S_diet_therapy_MeSH Obesity_diet_therapy_MeSH M_Practice_Guidelines_MeSH M_Smoking_Cessation_MeSH 
****** 12585949
----K I
----T Effects of initiating carvedilol in patients with severe chronic heart failure: results from the COPERNICUS Study.
----A CONTEXT: Beta-blockers remain underused despite their established utility for improving outcome in heart failure. Concerns that initiation of treatment produces few immediate benefits and may have important risks may be deterring widespread use. OBJECTIVE: To evaluate the early effects of the beta-blocker carvedilol in patients with severe heart failure. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind, placebo-controlled trial conducted from October 28, 1997, to March 20, 2000, at 334 hospital centers in 21 countries among 2289 patients with symptoms of heart failure at rest or with minimal exertion who were clinically euvolemic and had a left ventricular ejection fraction of less than 25%. INTERVENTION: Patients were randomly assigned to receive carvedilol, with start dosage of at 3.125 mg twice daily with uptitration to a target dosage of 25 mg twice daily (n = 1156), or placebo (n = 1133), in addition to their usual medications for heart failure. MAIN OUTCOME MEASURES: Death, hospitalization, or permanent withdrawal from study drug, as well as adverse events during the first 8 weeks of treatment. RESULTS: The carvedilol group experienced no increase in cardiovascular risk but instead had fewer patients who died (19 vs 25; hazard ratio [HR], 0.75; 95% confidence interval [CI], 0.41-1.35); who died or were hospitalized (134 vs 153; HR, 0.85; 95% CI, 0.67-1.07); or who died, were hospitalized, or were permanently withdrawn from treatment (162 vs 188; HR, 0.83; 95% CI, 0.68-1.03). These effects were similar in direction and magnitude to those observed during the entire study, and were apparent particularly in the 624 patients with recent or recurrent decompensation or a very depressed left ventricular ejection fraction. Differences in favor of carvedilol became apparent as early as 14 to 21 days following initiation of treatment. Worsening heart failure was the only serious adverse event with a frequency greater than 2% and was reported with similar frequency in the placebo and carvedilol groups (6.4% vs 5.1%). CONCLUSIONS: These data suggest that, in clinically euvolemic patients, the relation of benefit to risk during initiation of treatment with carvedilol is similar to that seen during long-term therapy with the drug. Our findings should provide the reassurance needed to encourage the high levels of use that are warranted by the results of long-term clinical trials.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Risk_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12586182
----K 4
----T Comparison of the intraocular pressure lowering effect of latanoprost and carteolol-pilocarpine combination in newly diagnosed glaucoma.
----A PURPOSE: To evaluate the comparative efficacy of latanoprost monotherapy versus combined carteolol and pilocarpine therapy in patients with newly diagnosed glaucoma. METHODS: Masked randomized prospective trial. This study included 51 patients (64 eyes) with newly diagnosed glaucoma or ocular hypertension. The cases were randomly divided into two treatment groups for administration of latanoprost 0.005% once daily, or of carteolol 2% twice daily and pilocarpine 2% twice daily. Mean diurnal intraocular pressure (IOP) was measured at baseline, week 2, week 4, and month 3 after the beginning of treatment. Changes in mean IOP from baseline to the 3-month visit were determined by an analysis of variance. RESULTS: Mean diurnal IOP values were 25.1 +/- 3.1 mm Hg and 25.5 +/- 2.5 mm Hg at baseline in the latanoprost monotherapy group and in the carteolol-plus-pilocarpine group, respectively. Diurnal IOP was significantly decreased from baseline to 3 months in both groups (P <.001). At this time point, latanoprost monotherapy had reduced mean diurnal IOP by 7.2 +/- 2.5 mm Hg (28.7%) and carteolol plus pilocarpine had reduced mean diurnal IOP by 7.4 +/- 2.7 mm Hg (29%). There was no difference between the groups in terms of their IOP reduction effect (P =.51). Decreased visual acuity and twilight vision, blurred vision, and headache were more frequent in the carteolol-plus-pilocarpine group than in the latanoprost group (P <.05). CONCLUSIONS: We concluded that latanoprost monotherapy was at least as effective as the carteolol-pilocarpine combination therapy in reducing mean diurnal IOP in newly diagnosed glaucoma or ocular hypertension.
----P Clinical_Trial Evaluation_Studies Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Carteolol_MeSH S_adverse_effects_MeSH Carteolol_adverse_effects_MeSH S_therapeutic_use_MeSH Carteolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Evaluation_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Pilocarpine_MeSH S_adverse_effects_MeSH Pilocarpine_adverse_effects_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Visual_Acuity_MeSH 
****** 12590013
----K 5
----T The prevention of type 2 diabetes--lifestyle change or pharmacotherapy? A challenge for the 21st century.
----A Diabetes mellitus is occurring in epidemic proportions in many countries. In Australia 7.4% of people over 25 years of age have diabetes (mostly type 2) and comparable or higher prevalences have been reported in the United States and a number of Asian countries. The enormous economic and social cost of this disease makes a compelling case for prevention. Epidemiological studies have shown clearly that type 2 diabetes results from an interaction between a genetic predisposition and lifestyle factors including obesity, sedentary behaviour and both calorie excess and various dietary constituents. The natural history of type 2 diabetes includes a preceding period of impaired glucose tolerance (IGT)/impaired fasting glucose (IFG) which provides an opportunity for targeted intervention within large communities. Lifestyle intervention studies have consistently shown that quite modest changes can reduce the progression from IGT to diabetes by 50-60%. It may, however, not be possible to translate these successful findings to larger cohorts or maintain the lifestyle changes longer term. This has lead to consideration of pharmacotherapy. While small studies with sulphonylureas are inconclusive, benefits have been found for metformin, acarbose and troglitazone. Big intervention studies with ramipril, rosiglitazone, valsartan and nateglinide are underway. Pharmacological intervention raises a whole range of ethical, economic and practical issues not the least of which is the problem of long term therapy of the 'otherwise well'.
----P Journal_Article Review Review_Literature 
----M M_Clinical_Trials_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus__Type_II_prevention_&_control_MeSH M_Human_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH P_Risk_Reduction_Behavior_MeSH 
****** 12594150
----K 5
----T Long QT syndrome and anaesthesia.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Action_Potentials_MeSH S_physiology_MeSH Action_Potentials_physiology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anesthesia_MeSH S_methods_MeSH Anesthesia_methods_MeSH M_Cardiac_Pacing__Artificial_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH M_Electric_Countershock_MeSH S_methods_MeSH Electric_Countershock_methods_MeSH M_Gene_Therapy_MeSH S_methods_MeSH Gene_Therapy_methods_MeSH M_Human_MeSH M_Ion_Channels_MeSH S_physiology_MeSH Ion_Channels_physiology_MeSH M_Long_QT_Syndrome_MeSH S_congenital_MeSH Long_QT_Syndrome_congenital_MeSH S_diagnosis_MeSH Long_QT_Syndrome_diagnosis_MeSH S_physiopathology_MeSH Long_QT_Syndrome_physiopathology_MeSH S_therapy_MeSH Long_QT_Syndrome_therapy_MeSH M_Long-Term_Care_MeSH S_methods_MeSH Long-Term_Care_methods_MeSH M_Potassium_Channels_MeSH S_physiology_MeSH Potassium_Channels_physiology_MeSH M_Sodium_Channels_MeSH S_physiology_MeSH Sodium_Channels_physiology_MeSH M_Sympathectomy_MeSH S_methods_MeSH Sympathectomy_methods_MeSH M_Torsades_de_Pointes_MeSH S_drug_therapy_MeSH Torsades_de_Pointes_drug_therapy_MeSH 
****** 12595838
----K E
----T Double-blind, placebo-controlled, randomized trial of prophylactic metoprolol for reduction of hospital length of stay after heart surgery: the beta-Blocker Length Of Stay (BLOS) study.
----A BACKGROUND: Atrial fibrillation (AF) is a common complication of heart surgery. Previous studies have shown that there is an association between postoperative AF and prolongation of hospital length of stay. No previous trials have been primarily directed at demonstrating that the use of drugs that prevent AF would shorten length of stay and reduce the costs of postoperative care. METHODS: A randomized, double-blind, placebo-controlled trial of metoprolol was performed in patients immediately after nonemergent heart surgery. Metoprolol was given orally at a dose of 100 mg per day after the patient's arrival in the intensive care unit until hospital discharge or 14 days, whichever was sooner. This dose was increased to 150 mg per day after the enrollment of 411 patients. The primary outcome measure of the study was hospital length of stay from admission to intensive care unit until hospital discharge. There were 1000 patients enrolled, evenly distributed to the metoprolol and placebo groups. RESULTS: There was a 20% reduction in the risk of AF developing with metoprolol, from 39% of patients to 31% of patients (P =.01). There was no effect of treatment on hospital length of stay, which was 152 +/- 61 hours for placebo and 155 +/- 90 hours for metoprolol (P = 0.79). The cost of postoperative care in the 2 treatment groups was similar. CONCLUSION: Prophylactic metoprolol reduces the risk of AF after heart surgery. It does not reduce hospital length of stay. Although it is cost effective for the reduction of AF, it did not reduce the overall cost of care.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_economics_MeSH Atrial_Fibrillation_economics_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH P_Coronary_Artery_Bypass_MeSH M_Costs_and_Cost_Analysis_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Valve_Diseases_MeSH S_surgery_MeSH Heart_Valve_Diseases_surgery_MeSH M_Human_MeSH P_Length_of_Stay_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_economics_MeSH Metoprolol_economics_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_economics_MeSH Postoperative_Complications_economics_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12599843
----K 1
----T [The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with hypertension and ECG-verified left ventricular hypertrophy in the LIFE-study]
----A INTRODUCTION: Left ventricular hypertrophy is a strong independent predictor of risk of cardiovascular morbidity and death. The aim of the LIFE-study was to establish whether treatment with the angiotensin-II AT 1-receptor antagonist, losartan, reduced cardiovascular events more effectively than treatment with the betablocker atenolol in patients with hypertension and left ventricular hypertrophy. MATERIAL AND METHODS: The LIFE-study included 9193 patients with essential hypertension and ECG-verified left ventricular hypertrophy, age range 55-80 years, systolic blood pressure in sitting position 160-200 mmHg and/or diastolic blood pressure 95-115 mmHg. Patients were randomized to double-blind treatment with losartan versus atenolol. They were followed for at least four years and until 1040 patients had a primary cardiovascular event (cardiovascular death, myocardial infarction or stroke). RESULTS: Blood pressure fell by 30.2/16.6 and 29.1/16.8 mmHg in the losartan and the atenolol group, respectively. The primary composite endpoint occurred in 508 losartan and 588 atenolol patients (relative risk 0.87, p = 0.021). A total of 232 and 309, respectively, had fatal or non-fatal stroke (relative risk 0.75, p = 0.001). There was no difference in myocardial infarction. New-onset diabetes was 25% less frequent on losartan. Side effects were less on losartan compared to atenolol. DISCUSSION: Losartan prevents to a higher degree cardiovascular morbidity and death than atenolol for a similar reduction in blood pressure and is better tolerated.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_diagnosis_MeSH Hypertrophy__Left_Ventricular_diagnosis_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH 
****** 12599844
----K 1
----T [The effect of losartan versus atenolol on cardiovascular morbidity and mortality in patients with diabetes mellitus in the LIFE-study]
----A INTRODUCTION: The most suitable antihypertensive drug to reduce the risk of cardiovascular disease in patients with hypertension and diabetes is unclear. In a prespecified analysis of the LIFE-study we compared the effects of losartan and atenolol on cardiovascular morbidity and mortality in diabetic patients. MATERIAL AND METHODS: A total of 1195 patients in the LIFE-study had diabetes at the time of the randomisation. The patients were randomised for double-blind treatment with losartan versus atenolol. The patients had ECG-verified left ventricular hypertrophy, mean age 67 years, blood pressure 177/96 mmHg after two weeks placebo run-in period. Patients were followed for at least four years (mean 4.7 years). The primary composite endpoint was cardiovascular death, stroke or myocardial infarction. RESULTS: Blood pressure was reduced to 146/79 and 148/79 in losartan-treated patients and atenolol-treated patients, respectively. The primary endpoint occurred in 103 patients assigned losartan (n = 586) and 139 assigned atenolol (n = 609). Relative risk reduction 24% (p < 0.031). Cardiovascular mortality was reduced by 37% in favour of losartan (p < 0.028), and all cause mortality by 39% (p < 0.002). DISCUSSION: Losartan was very effective in reducing cardiovascular morbidity and mortality as compared to atenolol. These results will have a major impact on the choice of anti-hypertensive treatment for patients with hypertension and diabetes.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH M_Double-Blind_Method_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH 
****** 12600135
----K 5
----T Asthma in the school-aged child.
----A Understanding the role of inflammation in childhood asthma has led to major changes in the approach to management of this disease. Based on the guidelines from the NIH, inhaled long-term control medications that target the underlying inflammatory processes in asthma are now recommended as the mainstay of drug treatment. Long-term control medications are recommended for all children who have asthma symptoms that occur more frequently than twice weekly or nocturnal symptoms more than twice monthly. Environmental control measures to decrease allergen exposure are important, as is attention to sinusitis and GER. The main impediment to improved asthma care is poor patient compliance. Many patients do not understand the role and importance of prophylactic medications in asthma treatment. Further, inconvenient dosing regimens, difficulties with metered-dose inhalers, and fear of potential side effects have all contributed to poor patient compliance. Increased efforts at patient education are needed to improve adherence to asthma plans. These efforts at improving patient compliance, along with improved physician adherence to the guidelines from the NIH, are needed to decrease the morbidity and mortality of childhood asthma.
----P Journal_Article Review Review__Tutorial 
----M M_Asthma_MeSH S_drug_therapy_MeSH Asthma_drug_therapy_MeSH M_Child_MeSH M_Human_MeSH M_Patient_Compliance_MeSH 
****** 12602461
----K E
----T Relationships between the antihypertensive effects of bisoprolol and levels of plasma atrial natriuretic peptide in hypertensive patients.
----A Previous studies have demonstrated that beta-blockade increases the levels of plasma atrial natriuretic peptide (ANP), but relationships between this effect and the antihypertensive action of beta-blockade remain unknown. In this study we investigated the amplitude and determinants of bisoprolol-induced ANP increase and the relationships between this increase and the antihypertensive effect of bisoprolol. Nineteen patients with mild to moderate hypertension were included in the study. In the first phase of the study (cross-over, placebo controlled, randomized phase), the effects of 10 mg bisoprolol on plasma ANP at rest and during exercise were compared to placebo. The antihypertensive action of bisoprolol was then evaluated after a 2-week period of treatment (10 mg/day) using ambulatory blood pressure monitoring. Bisoprolol significantly increased plasma ANP level at rest (from 30.6 +/- 20.5 to 42.8 +/- 35.6; P < 0.05) and also during exercise (from 54.7 +/- 44.3 to 119.1 +/- 159.9; pg/mL +/- SD; P < 0.05). Plasma ANP at rest was not significantly correlated with left ventricular mass. After the 15 days of treatment, the bisoprolol-induced daytime diastolic blood pressure reduction was significantly correlated to the initial bisoprolol-induced plasma ANP increase (r = 0.49, P = 0.035). These results suggest that the antihypertensive effect of beta-blocking agents could be partly mediated by an increase of ANP release.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Bisoprolol_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Echocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 12605566
----K 5
----T Antiarrhythmic drugs: new agents and evolving concepts.
----A Properties of several new antiarrhythmic drugs are summarised in this review article. Recent concepts concerning their safety and efficacy of antiarrhythmics are discussed. A brief perspective on possible future strategies for pharmacotherapy of arrhythmias is provided.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_classification_MeSH Anti-Arrhythmia_Agents_classification_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_genetics_MeSH Arrhythmia_genetics_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Clinical_Trials_MeSH M_Gene_Therapy_MeSH M_Heart_Atria_MeSH S_drug_effects_MeSH Heart_Atria_drug_effects_MeSH M_Human_MeSH M_Ion_Channels_MeSH S_antagonists_&_inhibitors_MeSH Ion_Channels_antagonists_&_inhibitors_MeSH M_Pharmacogenetics_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 12605568
----K 5
----T Treatment of scleroderma: an update.
----A The goal of this article is to update the reader and focus on novel therapies and clinical trials published since our last review [6]. Evidence suggests that drug intervention should target one or all of three biological processes: vascular disease, autoimmunity and tissue fibrosis. Efforts should be made to classify the subtype of scleroderma, to determine the activity of the disease process and the degree of specific organ involvement before specific treatment decisions are made. Cyclophosphamide in fibrosing alveolitis, intravenous prostaglandins and other vasodilators for the vascular disease, endothelin-1 inhibition in pulmonary hypertension and immunosuppressive therapy for early inflammatory disease, all appear to have benefit. Several agents used in vitro and in animal models of fibrosis also show promise including anti-transforming growth factor-beta, the statins and anti-integrins. More experience in well-designed clinical trials is needed to define the role of these agents in treating scleroderma.
----P Journal_Article Review Review__Tutorial 
----M M_Clinical_Trials_MeSH M_Human_MeSH M_Immunosuppressive_Agents_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH M_Scleroderma__Systemic_MeSH S_drug_therapy_MeSH Scleroderma__Systemic_drug_therapy_MeSH S_radiotherapy_MeSH Scleroderma__Systemic_radiotherapy_MeSH S_therapy_MeSH Scleroderma__Systemic_therapy_MeSH M_Stem_Cell_Transplantation_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ultraviolet_Rays_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12613089
----K 5
----T Exercise considerations in hypertension, obesity, and dyslipidemia.
----A Sports medicine practitioners who care for a wide array of athletes and active individuals will consistently face issues regarding chronic cardiovascular diseases and their associated risk factors. Among these, hypertension, obesity, and dyslipidemia are common clinical conditions that may be encountered even amongst elite caliber athletes. Consequently, those entrusted with the care of this active population must recognize the presence of these disorders and feel comfortable with their management in the face of continued sports or exercise participation. This article reviews the pathophysiology of these conditions as they relate to athletes and outlines the value of continued exercise in the management of each of these entities while addressing the specific and unique treatment needs of active individuals.
----P Journal_Article Review Review__Tutorial 
----M P_Exercise_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_prevention_&_control_MeSH Hyperlipidemia_prevention_&_control_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Obesity_MeSH S_prevention_&_control_MeSH Obesity_prevention_&_control_MeSH 
****** 12616463
----K 5
----T Sexual dysfunction in men and women with chronic kidney disease and end-stage kidney disease.
----A Sexual dysfunction is a common finding in both men and women with chronic kidney failure. Common disturbances include erectile dysfunction in men, menstrual abnormalities in women, and decreased libido and fertility in both sexes. These abnormalities are primarily organic in nature and are related to uremia as well as the other comorbid conditions that frequently occur in the chronic kidney failure patient. Fatigue and psychosocial factors related to the presence of a chronic disease are also contributory factors. Disturbances in the hypothalamic-pituitary-gonadal axis can be detected before the need for dialysis but continue to worsen once dialytic therapy is initiated. Impaired gonadal function is prominent in uremic men, whereas the disturbances in the hypothalamic-pituitary axis are more subtle. By contrast, central disturbances are more prominent in uremic women. Therapy is initially directed toward optimizing the delivery of dialysis, correcting anemia with recombinant erythropoietin, and controlling the degree of secondary hyperparathyroidism with vitamin D. For many practicing nephrologists, sildenafil has become the first line therapy in the treatment of impotence. In the hypogonadal man whose only complaint is decreased libido, testosterone may be of benefit. Regular gynecologic follow-up is required in uremic women to guard against potential complications of unopposed estrogen effect. Uremic women should be advised against pregnancy while on dialysis. Successful transplantation is the most effective means of restoring normal sexual function in both men and women with chronic kidney failure.
----P Journal_Article Review Review_Literature 
----M M_Female_MeSH M_Human_MeSH M_Kidney_Failure__Chronic_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Male_MeSH M_Sex_Disorders_MeSH S_etiology_MeSH Sex_Disorders_etiology_MeSH S_physiopathology_MeSH Sex_Disorders_physiopathology_MeSH S_therapy_MeSH Sex_Disorders_therapy_MeSH 
****** 12615283
----K 5
----T Cosegregation of the Marfan syndrome and the long QT syndrome in the same family leads to a severe cardiac phenotype.
----A 
----P Case_Reports Journal_Article 
----M M_Abnormalities__Multiple_MeSH S_diagnosis_MeSH Abnormalities__Multiple_diagnosis_MeSH M_Adolescent_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Echocardiography__Doppler_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Genetic_Predisposition_to_Disease_MeSH M_Human_MeSH M_Long_QT_Syndrome_MeSH S_complications_MeSH Long_QT_Syndrome_complications_MeSH S_diagnosis_MeSH Long_QT_Syndrome_diagnosis_MeSH S_genetics_MeSH Long_QT_Syndrome_genetics_MeSH M_Male_MeSH M_Marfan_Syndrome_MeSH S_complications_MeSH Marfan_Syndrome_complications_MeSH S_diagnosis_MeSH Marfan_Syndrome_diagnosis_MeSH S_genetics_MeSH Marfan_Syndrome_genetics_MeSH M_Pedigree_MeSH P_Phenotype_MeSH M_Prognosis_MeSH M_Risk_Assessment_MeSH M_Sampling_Studies_MeSH M_Severity_of_Illness_Index_MeSH 
****** 12615783
----K 5
----T Contemporary management of paroxysmal supraventricular tachycardia.
----A BACKGROUND: Abdominal aortic aneurysms (AAA) are characterized by extensive transmural inflammation and C-reactive protein (CRP) has emerged as an independent risk factor for the development of cardiovascular disease. Therefore, we evaluated a possible association between serum CRP and aneurysm dimension in patients with asymptomatic AAA. Furthermore, the possibility of CRP production by aneurysmal tissue has been examined. METHODS AND RESULTS: Serum CRP was determined highly sensitive (hsCRP) and aneurysmal size was measured in 39 patients with AAA. The presence of CRP mRNA was assessed in the aneurysmal tissue of 16 patients. Mean (SD) hsCRP was 3.23 (2.96) mg/L. After log-transformation, hsCRP correlated significantly with aneurysmal size (r=0.477, P=0.002). When the patients were divided into 3 equally sized groups according to hsCRP level, aortic diameter increased from lowest to upper hsCRP-tertile (49 mm, 61 mm, and 67 mm, respectively; P<0.05 for 3rd versus 1st tertile). This association persisted after correction for risk factors. CRP mRNA was found in 25% of aneurysmal aortic tissues. CONCLUSIONS: This is the first report showing that serum hsCRP is associated with aneurysmal size and that-in at least some patients-CRP may be produced by aneurysmal tissue. These data underscore the inflammatory nature of AAA formation, suggesting that serum hsCRP may serve as a marker of AAA disease and that CRP produced in vascular tissue might contribute to aneurysm formation.
----P Case_Reports Journal_Article 
----M M_Acute_Disease_MeSH M_Adolescent_MeSH M_Algorithms_MeSH M_Catheter_Ablation_MeSH M_Female_MeSH M_Human_MeSH M_Models__Cardiovascular_MeSH M_Tachycardia__Supraventricular_MeSH S_diagnosis_MeSH Tachycardia__Supraventricular_diagnosis_MeSH S_etiology_MeSH Tachycardia__Supraventricular_etiology_MeSH S_therapy_MeSH Tachycardia__Supraventricular_therapy_MeSH 
****** 12615784
----K 5
----T Antiadrenergic therapy of chronic heart failure: surprises and new opportunities.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Clinical_Trials_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_genetics_MeSH Heart_Failure__Congestive_genetics_MeSH M_Human_MeSH M_Polymorphism_(Genetics)_MeSH M_Receptors__Adrenergic_MeSH S_genetics_MeSH Receptors__Adrenergic_genetics_MeSH M_Sympatholytics_MeSH S_adverse_effects_MeSH Sympatholytics_adverse_effects_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH 
****** 12617406
----K 5
----T Thyrotoxicosis.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Antithyroid_Agents_MeSH S_adverse_effects_MeSH Antithyroid_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antithyroid_Agents_therapeutic_use_MeSH M_Carbimazole_MeSH S_administration_&_dosage_MeSH Carbimazole_administration_&_dosage_MeSH S_therapeutic_use_MeSH Carbimazole_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Female_MeSH P_Graves'_Disease_MeSH S_complications_MeSH Graves'_Disease_complications_MeSH S_diagnosis_MeSH Graves'_Disease_diagnosis_MeSH S_drug_therapy_MeSH Graves'_Disease_drug_therapy_MeSH S_radiotherapy_MeSH Graves'_Disease_radiotherapy_MeSH M_Heart_Diseases_MeSH S_etiology_MeSH Heart_Diseases_etiology_MeSH M_Human_MeSH M_Iodine_Radioisotopes_MeSH S_therapeutic_use_MeSH Iodine_Radioisotopes_therapeutic_use_MeSH M_Male_MeSH M_Potassium_Iodide_MeSH S_administration_&_dosage_MeSH Potassium_Iodide_administration_&_dosage_MeSH S_therapeutic_use_MeSH Potassium_Iodide_therapeutic_use_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications_MeSH S_drug_therapy_MeSH Pregnancy_Complications_drug_therapy_MeSH M_Propylthiouracil_MeSH S_administration_&_dosage_MeSH Propylthiouracil_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propylthiouracil_therapeutic_use_MeSH M_Puerperal_Disorders_MeSH S_drug_therapy_MeSH Puerperal_Disorders_drug_therapy_MeSH M_Radiotherapy_Dosage_MeSH M_Thyroid_Crisis_MeSH S_drug_therapy_MeSH Thyroid_Crisis_drug_therapy_MeSH M_Thyroid_Function_Tests_MeSH M_Thyroidectomy_MeSH P_Thyrotoxicosis_MeSH S_complications_MeSH Thyrotoxicosis_complications_MeSH S_diagnosis_MeSH Thyrotoxicosis_diagnosis_MeSH S_drug_therapy_MeSH Thyrotoxicosis_drug_therapy_MeSH S_etiology_MeSH Thyrotoxicosis_etiology_MeSH S_radiotherapy_MeSH Thyrotoxicosis_radiotherapy_MeSH M_Time_Factors_MeSH 
****** 12619016
----K 5
----T Transjugular intrahepatic portosystemic shunts: an update.
----A Transjugular intrahepatic portosystemic shunts (TIPS) have been used in the treatment of complications of portal hypertension. TIPS is used for the control of acute variceal bleeding and for the prevention of vericeal rebleeding when pharmacologic therapy and endoscopic therapy have failed. Patients with refractory ascites with adequate hepatic reserve and renal function who fail to respond to large volume paracentesis may be reasonable candidates for TIPS. Promising indications for TIPS are Budd-Chiari syndrome uncontrolled by medical therapy, severe portal hypertensive gastropathy, refractory hepatic hydrothorax, and hepatorenal syndrome. TIPS cannot be recommended for preoperative portal decompression solely to facilitate liver transplantation. Special care should be taken to insure proper placement of the stent to avoid increasing the technical difficulty of the transplantation procedure. The major limiting factors for TIPS success are shunt dysfunction and hepatic encephalopathy. Because shunt stenosis is the most important cause of recurrent complications of portal hypertension, a surveillance program to monitor shunt patency is mandatory. The MELD score may be useful in predicting post-TIPS survival, and also in counseling patients and their families.
----P Journal_Article Review Review_Literature 
----M M_Hepatic_Vein_Thrombosis_MeSH S_surgery_MeSH Hepatic_Vein_Thrombosis_surgery_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_surgery_MeSH Hypertension__Portal_surgery_MeSH M_Portasystemic_Shunt__Transjugular_Intrahepatic_MeSH S_methods_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_methods_MeSH S_trends_MeSH Portasystemic_Shunt__Transjugular_Intrahepatic_trends_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12619740
----K 5
----T Case report: prescribing caution. When a simple disease isn't so simple.
----A 
----P Case_Reports Journal_Article 
----M M_Adult_MeSH M_Anti-Infective_Agents__Urinary_MeSH S_contraindications_MeSH Anti-Infective_Agents__Urinary_contraindications_MeSH S_pharmacology_MeSH Anti-Infective_Agents__Urinary_pharmacology_MeSH M_Drug_Information_Services_MeSH M_Drug_Interactions_MeSH M_Female_MeSH M_Human_MeSH M_Myasthenia_Gravis_MeSH S_complications_MeSH Myasthenia_Gravis_complications_MeSH S_drug_therapy_MeSH Myasthenia_Gravis_drug_therapy_MeSH M_Norfloxacin_MeSH S_contraindications_MeSH Norfloxacin_contraindications_MeSH S_pharmacology_MeSH Norfloxacin_pharmacology_MeSH P_Polypharmacy_MeSH M_Urinary_Tract_Infections_MeSH S_complications_MeSH Urinary_Tract_Infections_complications_MeSH S_drug_therapy_MeSH Urinary_Tract_Infections_drug_therapy_MeSH 
****** 12620132
----K 5
----T Neuropsychiatric effects of cardiovascular drug therapy.
----A Various cardiovascular drugs have been shown to have neuropsychiatric effects that can be harmful or therapeutically beneficial to patients. As an example, both sedation and mental depression have been described in patients receiving centrally acting antihypertensive drugs and beta-adrenergic blockers, related to their antiadrenergic actions. In contrast, because of these antiadrenergic actions, agents like clonidine have been used to treat opiate, alcohol, and nicotine withdrawal, while beta blockers have been used to treat symptoms of performance anxiety, migraine, and psychocardiac disorders. Some antiarrhythmic drugs have been associated with delirium, and digitalis toxicity has been shown to cause hallucinations, mania, euphoria, and depression. The calcium-channel blocker verapamil has been used as an adjunctive treatment in patients with bipolar disorders. Since neuropsychiatric symptoms are seen in patients with cardiovascular disease, clinicians should be aware of the possible relationship between these symptoms and concurrent cardiovascular drug therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anticholesteremic_Agents_MeSH S_adverse_effects_MeSH Anticholesteremic_Agents_adverse_effects_MeSH M_Cardiovascular_Agents_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Central_Nervous_System_MeSH S_drug_effects_MeSH Central_Nervous_System_drug_effects_MeSH M_Diuretics_MeSH S_adverse_effects_MeSH Diuretics_adverse_effects_MeSH M_Human_MeSH M_Mental_Disorders_MeSH S_chemically_induced_MeSH Mental_Disorders_chemically_induced_MeSH S_drug_therapy_MeSH Mental_Disorders_drug_therapy_MeSH 
****** 12622571
----K 5
----T Antihypertensive drugs and renal protection.
----A 
----P Comment Letter 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH 
****** 12624713
----K 5
----T Treatment of migraine with aura: comments and perspectives.
----A Migraine with aura (MwA) is a primary headache that affects about 30% of migraine sufferers. The main questions for the physician caring for the patient who has MwA are: when to use preventive medications, what medications to use in acute and preventive treatment, and whether the aura should be treated. The aim of this paper is to review the various therapeutic options for MwA proposed in the current literature and to evaluate their efficacy.
----P Journal_Article Review Review__Tutorial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Classic_Migraine_MeSH S_drug_therapy_MeSH Classic_Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Classic_Migraine_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12623832
----K 6
----T Dorzolamide/timolol combination versus concomitant administration of brimonidine and timolol: six-month comparison of efficacy and tolerability.
----A PURPOSE: To compare the efficacy and tolerability of the 2% dorzolamide/0.5% timolol combination ophthalmic solution twice daily to the concomitant administration of 0.2% brimonidine ophthalmic solution twice daily and 0.5% timolol ophthalmic solution twice daily. DESIGN: Randomized, multicenter, observer-masked, parallel-group study. PARTICIPANTS: Two hundred ninety-three patients with ocular hypertension or primary open-angle glaucoma participated. INTERVENTION: After an open-label 3-week 0.5% timolol run-in period, patients with an hour 2 intraocular pressure (IOP) of > or = 22 mmHg were randomly assigned to receive either the dorzolamide/timolol combination twice daily or the concomitant use of brimonidine twice daily and timolol twice daily (brimonidine + timolol) for 6 months. MAIN OUTCOME MEASURES: The IOP-lowering effects at hour 0 and hour 2 were collected at 1, 3, and 6 months. We hypothesized that both treatment regimens would have comparable hour 2 IOP-lowering effects at month 3. The treatments were considered comparable if the two-sided 95% confidence interval of the treatment difference was within +/- 1.5 mmHg. Tolerability data were also collected at 1, 3, and 6 months. RESULTS: The primary efficacy analysis was based on the modified intent-to-treat population. At month 3, hour 2, the dorzolamide/timolol group had an adjusted mean (standard error) change in IOP of -5.04 (0.30) mmHg versus -5.41 (0.30) mmHg in the brimonidine + timolol group, with a treatment difference of 0.36 (0.40) mmHg (95% confidence interval [CI] of -0.42-1.14 mmHg). At month 3, hour 0, the dorzolamide/timolol group had a change in IOP of -3.66 (0.29) mmHg versus -4.15 (0.28) mmHg in the brimonidine + timolol group, with a treatment difference of 0.49 (0.39) mmHg (95% CI of -0.27-1.25 mmHg). Likewise, at all other observed time points, the 95% confidence interval of the treatment difference was within +/- 1.5 mmHg. Ninety-three patients (64%) in the dorzolamide/timolol group and 88 patients (60%) in the brimonidine + timolol group had adverse experiences that were deemed drug related by the investigator, for which 7 patients (5%) in the dorzolamide/timolol group and 8 patients (5%) in the brimonidine + timolol group were discontinued from the study. CONCLUSIONS: The efficacy of the dorzolamide/timolol combination and the concomitant administration of brimonidine and timolol were comparable. The incidence of drug-related adverse experiences and the incidence of discontinuations caused by drug-related adverse experiences were similar between groups.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Quinoxalines_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Sulfonamides_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Visual_Acuity_MeSH M_Visual_Fields_MeSH 
****** 12624564
----K 5
----T ALLHAT and AFFIRM.
----A 
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Coronary_Disease_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Double-Blind_Method_MeSH M_Follow-Up_Studies_MeSH M_Heart_Conduction_System_MeSH S_physiology_MeSH Heart_Conduction_System_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH 
****** 12482765
----K 3
----T Effects of nonspecific beta-adrenergic stimulation and blockade on blood coagulation in hypertension.
----A A hypercoagulable state might contribute to increased atherothrombotic risk in hypertension. The sympathetic nervous system is hyperactive in hypertension, and it regulates hemostatic function. We investigated the effect of nonspecific beta-adrenergic stimulation (isoproterenol) and blockade (propranolol) on clotting diathesis in hypertension. Fifteen hypertensive and 21 normotensive subjects underwent isoproterenol infusion in two sequential, fixed-order doses of 20 and then 40 ng. kg(-1). min(-1) for 15 min/dose. Thirteen subjects were double-blind studied after receiving placebo or propranolol (100 mg/day) for 5 days each. In hypertensive subjects, isoproterenol elicited a dose-dependent increase in plasma von Willebrand factor (vWF) antigen [F(2,34) = 5.02; P = 0.032] and a decrease in D-dimer [F(2,34) = 4.57; P = 0.040], whereas soluble tissue factor remained unchanged. Propranolol completely abolished the increase in vWF elicited by isoproterenol [F(1,12) = 10.25; P = 0.008] but had no significant effect on tissue factor and D-dimer. In hypertension, vWF is readily released from endothelial cells by beta-adrenergic stimulation, which might contribute to increased cardiovascular risk. However, beta-adrenergic stimulation alone may not be sufficient to trigger fibrin formation in vivo.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_Adrenergic_beta-Agonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Agonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Agonists_pharmacology_MeSH M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Blood_Coagulation_MeSH S_drug_effects_MeSH Blood_Coagulation_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Fibrin_Fibrinogen_Degradation_Products_MeSH S_metabolism_MeSH Fibrin_Fibrinogen_Degradation_Products_metabolism_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH M_Isoproterenol_MeSH S_administration_&_dosage_MeSH Isoproterenol_administration_&_dosage_MeSH S_pharmacology_MeSH Isoproterenol_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_von_Willebrand_Factor_MeSH S_antagonists_&_inhibitors_MeSH von_Willebrand_Factor_antagonists_&_inhibitors_MeSH S_metabolism_MeSH von_Willebrand_Factor_metabolism_MeSH 
****** 12628894
----K 5
----T Adult toxicology in critical care: Part II: specific poisonings.
----A OBJECTIVE: Multivariable modeling techniques are appearing in today's medical literature with increasing frequency. Improper reporting of these statistical models can potentially make the results of a study inaccurate, misleading, or difficult to interpret. We performed a manual literature search of five international pulmonary and critical care journals to determine the accuracy in the reporting of logistic regression modeling strategies. DESIGN: We examined all of the published manuscripts for 12 potential limitations in the reporting of important statistical methodologies over a 6-month period from July 1, 2000, until December 31, 2000. RESULTS: Of the 81 articles that included multivariable logistic regression analyses, only 65% (53 analyses) properly reported the coding classification of pertinent independent variables that were included in the final model. An odds ratio and confidence interval were reported for the independent variables included in the final model for 79% (64 analyses) and 74% (60 analyses), respectively. Only 12% (10 articles) referenced whether interaction terms or effect modifications were examined, 1% (1 article) reported testing for collinearity, and only 16% (13 articles) included a goodness-of-fit analysis of the logistic model. The type of statistical package was reported in 69% (56 articles). Finally, approximately 39% of the articles (22 of 57) may have overfit the logistic regression model, leading to potentially unreliable regression coefficients and odds ratios. CONCLUSIONS: Our results indicate that the reporting of multivariable logistic regression analyses in the pulmonary and critical care literature is often incomplete, therefore making it difficult for the reader to accurately interpret the manuscript. We recommend the implementation of adequate guidelines that will lead to overall improvements in the reporting and possibly to the conducting of multivariable analyses in the pulmonary medicine and critical care medicine literature.
----P Journal_Article Review Review__Tutorial 
----M M_Acetaminophen_MeSH S_poisoning_MeSH Acetaminophen_poisoning_MeSH M_Alcohols_MeSH S_poisoning_MeSH Alcohols_poisoning_MeSH M_Cyanides_MeSH S_poisoning_MeSH Cyanides_poisoning_MeSH M_Drug_Toxicity_MeSH S_diagnosis_MeSH Drug_Toxicity_diagnosis_MeSH S_physiopathology_MeSH Drug_Toxicity_physiopathology_MeSH S_therapy_MeSH Drug_Toxicity_therapy_MeSH M_Emergencies_MeSH M_Human_MeSH M_Insecticides_MeSH S_poisoning_MeSH Insecticides_poisoning_MeSH P_Poisoning_MeSH S_diagnosis_MeSH Poisoning_diagnosis_MeSH S_physiopathology_MeSH Poisoning_physiopathology_MeSH S_therapy_MeSH Poisoning_therapy_MeSH M_Street_Drugs_MeSH S_poisoning_MeSH Street_Drugs_poisoning_MeSH 
****** 12630981
----K 5
----T Planning and monitoring of placebo-controlled survival trials: comparison of the triangular test with usual interim analyses methods.
----A AIMS: For ethical and economic reasons, interim analysis of phase III clinical trials is essential. This study was conducted to compare the efficiency of two interim analysis procedures, which could be used to allow early termination of a clinical trial. METHODS: We made a post hoc application of two interim analysis methods (Lan & DeMets with O'Brien-Flemming modification, and the triangular test according to Whitehead) by using individual patient data from four published placebo-controlled survival trials. We determined the date the trial would have been stopped had each method been used, and we estimated consequent results in terms of events and patient numbers included in the trial, the duration of the trial, and on treatment effect. RESULTS: The triangular test provided the lowest number of events required to reach a conclusion of the trials while providing an accurate estimate of experimental treatment effects. The triangular test thus indicated the smallest number of patients that would have been enrolled, and the shortest trial duration. The difference between the methods was most important with a detrimental effect of experimental treatment: the number of required events was reduced by 75% and the trial duration was shortened by 48% with the triangular test compared to the Lan & DeMets method. CONCLUSIONS: Stopping a trial early must depend on the clinical context. It is most important to stop a placebo-controlled trial as soon as possible when the experimental treatment can be shown deleterious. In such a situation the triangular test is more appropriate than the Lan & DeMets method. When a treatment effect is no different from, or better than, placebo the triangular test is also superior but the importance of premature termination of the trial in such cases has to be balanced against the inevitable reduction of information that the trial can provide.
----P Journal_Article 
----M M_Clinical_Trials__Phase_III_MeSH S_methods_MeSH Clinical_Trials__Phase_III_methods_MeSH M_Comparative_Study_MeSH M_Controlled_Clinical_Trials_MeSH S_methods_MeSH Controlled_Clinical_Trials_methods_MeSH M_Data_Interpretation__Statistical_MeSH M_Meta-Analysis_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12636467
----K 5
----T Headache assessment and management.
----A 
----P Journal_Article 
----M P_Headache_MeSH S_diagnosis_MeSH Headache_diagnosis_MeSH S_etiology_MeSH Headache_etiology_MeSH S_therapy_MeSH Headache_therapy_MeSH P_Headache_Disorders_MeSH S_diagnosis_MeSH Headache_Disorders_diagnosis_MeSH S_etiology_MeSH Headache_Disorders_etiology_MeSH S_therapy_MeSH Headache_Disorders_therapy_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12639076
----K 3
----T Implantable cardioverter defibrillators in primary and secondary prevention: a systematic review of randomized, controlled trials.
----A BACKGROUND: Sudden cardiac death is common in persons with cardiovascular disease. PURPOSE: To assess the efficacy of implantable cardioverter defibrillators (ICDs) in persons at increased risk for sudden cardiac death. DATA SOURCES: MEDLINE (1980-2002), EMBASE (1980-2002), Cochrane Controlled Clinical Trial Registry (2002, Volume 3), other databases, and conference proceedings. Primary study authors and device manufacturers were contacted, and bibliographies of relevant papers were hand searched. STUDY SELECTION: Randomized, controlled clinical trials evaluating ICDs versus usual care were selected. DATA EXTRACTION: Two reviewers extracted data independently. DATA SYNTHESIS: Eight trials were included in the final analysis (4909 patients, 1154 deaths). Compared with usual care (most commonly amiodarone therapy), ICDs significantly reduced sudden cardiac death (relative risk [RR], 0.43 [95% CI, 0.35 to 0.53]) and all-cause mortality (RR, 0.74 [CI, 0.67 to 0.82]). The included trials were divided a priori into two categories: secondary prevention (involving patients resuscitated after cardiac arrest or unstable ventricular tachycardia or ventricular fibrillation [ n = 1963]) and primary prevention (involving patients at increased risk for sudden cardiac death but without documented cardiac arrest, ventricular fibrillation, or ventricular tachycardia [ n = 2946]). Regardless of baseline risk, ICDs were equally efficacious in preventing sudden cardiac death in both types of trials (RR, 0.50 [CI, 0.38 to 0.66] for secondary prevention vs. 0.37 [CI, 0.27 to 0.50] for primary prevention). However, the magnitude of benefit in total mortality varied within the primary prevention trials depending on baseline risk for sudden cardiac death. CONCLUSIONS: Implantable cardioverter defibrillators prevent sudden cardiac death regardless of baseline risk. However, their impact on total mortality is sensitive to baseline risk for arrhythmic death. Decisions about resource allocation for ICDs depend on accurate stratification of patients according to risk.
----P Journal_Article Meta-Analysis Review Review__Academic 
----M M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH P_Defibrillators__Implantable_MeSH M_Human_MeSH M_Mortality_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12639086
----K 5
----T Cardiac events in patients undergoing noncardiac surgery: shifting the paradigm from noninvasive risk stratification to therapy.
----A Internists and cardiologists are often asked to estimate the risk for perioperative myocardial infarction or cardiac death in patients being considered for noncardiac surgery. Estimating this risk in an individual patient is difficult and complex. Although noninvasive imaging tests are often used for this purpose, a review of the literature reveals that the positive predictive value of noninvasive imaging tests is uniformly low and that they do not provide information beyond that obtained by assessing simple clinical risk variables. Moreover, no evidence exists that noninvasive imaging tests lead to a therapeutic strategy that reduces the risk for perioperative myocardial infarction or cardiac death. Since the publication of guidelines for preoperative risk stratification by the American College of Cardiology/American Heart Association in 1996 and the American College of Physicians in 1997, three clinical trials have shown that beta-blocker therapy reduces the risk for perioperative cardiac events. This paper focuses on the relationship between risk stratification and subsequent therapy to minimize or eliminate risk. In short, the paradigm is shifting from predicting which patient is at high risk for having a perioperative cardiac event to minimizing the likelihood of such an event with specific perioperative pharmacologic therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Algorithms_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Heart_Function_Tests_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH P_Postoperative_Complications_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Risk_Assessment_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12640278
----K 5
----T Amiodarone-an "old" drug with new recommendations.
----A Amiodarone has gained recognition as an antiarrhythmic medication after recent publication of the newly revised American Heart Association guidelines for pediatric resuscitation. Although support for the widespread use of amiodarone in adults has been supported by research, the few pediatric studies demonstrate limited efficacy and highlight the need for additional data. Because of the nature of the need for this type of resuscitation medication, controlled prospective studies will be difficult to obtain if not morally contraindicated. This article reviews the properties of amiodarone and the pertinent pediatric studies to provide healthcare providers supplemental information regarding amiodarone when choosing antiarrhythmics for acute resuscitation. Individual providers need to discern whether the pediatric data available supports widespread acceptance into current treatment regimens.
----P Journal_Article Review Review__Tutorial 
----M M_Action_Potentials_MeSH M_Amiodarone_MeSH S_adverse_effects_MeSH Amiodarone_adverse_effects_MeSH S_pharmacology_MeSH Amiodarone_pharmacology_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_classification_MeSH Anti-Arrhythmia_Agents_classification_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Child_MeSH M_Heart_Conduction_System_MeSH S_drug_effects_MeSH Heart_Conduction_System_drug_effects_MeSH M_Human_MeSH M_Tachycardia__Ectopic_Junctional_MeSH S_drug_therapy_MeSH Tachycardia__Ectopic_Junctional_drug_therapy_MeSH M_Tachycardia__Supraventricular_MeSH S_drug_therapy_MeSH Tachycardia__Supraventricular_drug_therapy_MeSH S_physiopathology_MeSH Tachycardia__Supraventricular_physiopathology_MeSH 
****** 12643877
----K E
----T The LIFE study: the straw that should break the camel's back.
----A 
----P Editorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12643883
----K 5
----T Outcome beyond blood pressure control?
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Clinical_Trials_MeSH M_Drug_Costs_MeSH M_Forecasting_MeSH M_Human_MeSH M_Hypertension_MeSH S_economics_MeSH Hypertension_economics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Meta-Analysis_MeSH M_Middle_Aged_MeSH M_Prescriptions__Drug_MeSH S_economics_MeSH Prescriptions__Drug_economics_MeSH S_statistics_&_numerical_data_MeSH Prescriptions__Drug_statistics_&_numerical_data_MeSH M_Risk_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 12643886
----K I
----T The value of routine non-invasive tests to predict clinical outcome in stable angina.
----A BACKGROUND: Chronic stable angina is a common condition, but considerable differences exist in the likelihood of acute coronary events such as CHD death, non-fatal myocardial infarction (MI) and unstable angina between individual patients. Effective risk prediction is necessary for optimum management. The aim of this study was to identify clinical features and non-invasive test parameters associated with high risk of these coronary events in stable angina and compose a clinically useful model to predict adverse outcomes in this population. METHODS: Six hundred and eighty-two patients with stable angina and a positive exercise test (1mm ST depression) from the Total Ischaemic Burden European Trial (TIBET) study, were studied. Resting ECG, exercise tolerance testing and echocardiography were performed at baseline, off anti-anginal therapy. The patients were then randomised to treatment with atenolol, nifedipine or a combination of both. Clinical follow up continued for an average of 2 years (range 1-3 years). RESULTS AND CONCLUSIONS: Prior MI or prior CABG were the clinical parameters associated with adverse outcome in patients with stable angina and a positive exercise test. On the ECG, left ventricular hypertrophy was predictive, and on echocardiogram, increased left ventricular dimensions were predictive of adverse events. When combined with time to ischaemia on exercise testing in a simple clinically applicable table these factors could be used to predict of 2 year probability of events for an individual patient.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angina_Pectoris_MeSH S_complications_MeSH Angina_Pectoris_complications_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Angina__Unstable_MeSH S_complications_MeSH Angina__Unstable_complications_MeSH S_diagnosis_MeSH Angina__Unstable_diagnosis_MeSH M_Death__Sudden__Cardiac_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_Echocardiography_MeSH S_methods_MeSH Echocardiography_methods_MeSH M_Electrocardiography_MeSH S_methods_MeSH Electrocardiography_methods_MeSH M_Exercise_Test_MeSH S_methods_MeSH Exercise_Test_methods_MeSH M_Exercise_Tolerance_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH M_Predictive_Value_of_Tests_MeSH M_Prognosis_MeSH M_Ventricular_Dysfunction__Left_MeSH S_diagnosis_MeSH Ventricular_Dysfunction__Left_diagnosis_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH 
****** 12643888
----K 6
----T Bisoprolol dose-response relationship in patients with congestive heart failure: a subgroup analysis in the cardiac insufficiency bisoprolol study(CIBIS II).
----A AIMS: Whether all patients with congestive heart failure (CHF) need to reach the target dose of beta-blocker to obtain a benefit in terms of survival remains uncertain. METHODS AND RESULTS: We classified by tertile the 2647 patients enrolled in CIBIS II according to the last tolerated dose: low dose (LD: 1.25, 2.5 or 3.75mg/day, n=434), moderate dose (MD: 5 or 7.5mg/day, n=328) and high dose (HD: 10mg/day, n=565) of bisoprolol or placebo (LD=234, MD=278 and HD=808). In both groups, patients tolerating only low doses were significantly older with more severe New York Heart Association (NYHA) functional class and higher frequency of co-morbidities. Treatment withdrawal was associated with a significant increase of mortality in the bisoprolol group (relative hazard (RH)=2.13, 95% confidence interval (CI)=1.43-3.17, p=0.0002). After adjustment, all-cause mortality was significantly reduced in the bisoprolol group compared to placebo regardless of the dose level considered: LD (RH=0.66, 95% CI=0.48-0.92), MD (RH=0.33, 95% CI=0.21-0.51) or HD (RH=0.59, 95% CI=0.40-0.89). CONCLUSIONS: Bisoprolol reduces mortality in CHF patients at all tolerated dose levels and its withdrawal increases the risk of mortality. Efforts should be made to maintain bisoprolol therapy based on the individual patient's tolerability.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH M_Death__Sudden__Cardiac_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Treatment_Refusal_MeSH 
****** 12648985
----K 5
----T Prevention of variceal rebleeding.
----A CONTEXT: Variceal bleeding is the most frequent severe complication of portal hypertension and a leading cause of death and liver transplantation in patients with cirrhosis. Patients surviving a variceal bleed are at high risk of rebleeding (over 60% at 1 year). Portacaval shunts and transjugular intrahepatic portasystemic shunts (TIPS) are effective for prevention of rebleeding but carry a high risk of hepatic encephalopathy. Endoscopic techniques include band ligation (EBL) and injection sclerotherapy (EIS). Drug approaches are based on non-selective beta blocker with or without isosorbide-5-mononitrate (ISMN). STARTING POINT: David Patch and colleagues (Gastroenterology 2002; 123: 1013-19) randomised 102 patients surviving a variceal bleeding to EBL or drug therapy with propranolol with the addition of ISMN if target reductions in portal pressure (evaluated by the hepatic venous pressure-gradient [HVPG]) were not achieved at 3 months. Overall, results of drug therapy were similar to those of EBL (44% vs 54% rebleeding at 1 year). There were no differences in survival or non-bleeding complications. Christophe Bureau and colleagues (Hepatology 2002; 36: 1361-66) treated 34 patients with cirrhosis and portal hypertension with propranolol and measured HVPG after a median of 4 days. Target HVPG reductions were achieved in 13 "responders". ISMN was added in the 21 "non-responders" and HVPG measured again: seven more patients achieved target HPVG reduction. Re-bleeding rates were lower in responders than in non-responders (10% vs 64%). Both studies suggest that drug therapy can be improved by adding ISMN to b blockers in those patients with an insufficient decrease in HVPG. WHERE NEXT? Long-term drug therapy is emerging as effective treatment for the prevention of variceal rebleeding. The role of HVPG monitoring as a guide to identifying patients requiring further treatment needs to be further evaluated. Trials to determine the best treatment for patients who do not respond to drug therapies are also required.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_mortality_MeSH Esophageal_and_Gastric_Varices_mortality_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH P_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_mortality_MeSH Hemorrhage_mortality_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_complications_MeSH Hypertension__Portal_complications_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Sclerotherapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12652105
----K 5
----T Antihypertensive medication and quality of life--silent treatment of a silent killer?
----A Hypertension is one of the major killers in the modern world and one of the great ironies of the disease is that it has little or no immediate effect on affected individuals' quality of life (QOL). This makes treatment very difficult, as most medications will affect QOL negatively, either through side effects or through the change in life-style associated with chronic drug regimens. This review describes some of the conceptual background for QOL measurements and looks at the effects on QOL of different antihypertensive treatments available today. The latest addition to the range of antihypertensive drugs, angiotensin II-receptor blockers, may be a significant step forward in treatment, as their ease of dosing and excellent tolerability minimise negative effects on patients while their possible benefits on factors such as sexual function may even improve QOL in hypertensive patients.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_psychology_MeSH Hypertension_psychology_MeSH P_Quality_of_Life_MeSH M_Randomized_Controlled_Trials_MeSH M_Sex_Disorders_MeSH S_chemically_induced_MeSH Sex_Disorders_chemically_induced_MeSH 
****** 12652116
----K 5
----T Beta-blockers and diabetes: the bad guys come good.
----A Type 2 diabetes is becoming very common and is closely linked to physical inactivity and obesity. It is associated with clustering of coronary risk factors and 60-80% of cases have hypertension. The first therapeutic action is appropriate adjustment of life style. Anti-hypertensive therapies such as diuretics, ACE inhibitors and calcium antagonists have been effective in reducing cardiovascular events in type 2 diabetes, though calcium antagonists may be less effective than older therapies and ACE-inhibitors in reducing the risk of heart attacks and heart failure (but possibly more effective in stroke reduction). Beta-blockers (BBs) have a poor image as a potential therapy due to apparent adverse effects on surrogate end-points such as insulin-resistance. However large, controlled trials have shown BBs to be highly effective in reducing the risk of cardiovascular events and death in post myocardial infarction patients with diabetes. The UKPDS study in type 2 diabetics with hypertension showed first-line beta-blockade to be at least as effective as ACE-inhibition in preventing all primary macrovascular and microvascular end-points. The active ingredient appears to be beta-1 blockade, acting not only to lower blood pressure but also to prevent sudden death and cardiovascular damage stemming from chronic beta-1 stimulation associated with raised noradrenaline activity. By contrast, in the LIFE study atenolol was less effective than the angiotensin receptor antagonist losartan in reducing cardiovascular events and all-cause mortality in mainly elderly hypertensives with diabetes. Thus the best beta-blocker results in reducing hard cardiovascular end-points occur in hypertension studies (including the UKPDS study) involving younger/middle aged (say less than 60-65 years) patients, with relatively high sympathetic activity, relatively compliant/elastic arteries (narrow pulse-pressure) and normally functioning beta-1 receptors. In elderly hypertensive patients beta-blockers may be given as second-line therapy on the back of a low-dose diuretic (but possibly as first line agent in elderly hypertensives with prior myocardial infarction). Thus inappropriate attention to surrogate end-points can lead to faulty prescribing habits. Beta-blockers, currently severely underprescribed, should be considered as a first line therapeutic option for all diabetics with ischaemic heart disease or younger/middle aged diabetics with hypertension (but co-prescribed with low dose diuretic therapy in the elderly). The active ingredient for cardiovascular protection appears to be beta-1 blockade; optimal efficacy in lowering blood pressure and safety e.g. reducing risk of bronchoconstriction, is achieved by choosing an agent with high beta-1 selectivity.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Disease_drug_therapy_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_diagnosis_MeSH Diabetes_Mellitus__Type_II_diagnosis_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH 
****** 12655281
----K 5
----T Efficacy and tolerability of trimetazidine in stable angina: a meta-analysis of randomized, double-blind, controlled trials.
----A OBJECTIVE: The objective of this meta-analysis was to evaluate the efficacy and tolerance of the metabolic agent trimetazidine (TMZ), both in monotherapy and in combination with other antianginal agents, in the treatment of stable angina pectoris. A search of literature published between 1985 and 2001 was performed on computerized databases (MEDLINE and EMBASE). METHODS: Only double-blind, randomized, controlled trials were included in this meta-analysis. Patients had to be treated for at least 2 weeks. Four parameters were selected, one clinical parameter (number of weekly angina attacks) and three ergometric parameters (time to 1 mm ST-segment depression, total work and exercise duration at peak exercise). They were evaluated at baseline and at the end of the treatment period.The quality of the trials was assessed on specific methodological criteria. Standard statistical methods, pooled odds ratio and 95% confidence intervals for subjective symptoms and pooled z and P for objective symptoms, were used. RESULTS: Twelve clinical studies meeting our criteria were analyzed. Results showed that TMZ significantly reduced the number of weekly angina attacks in coronary patients and improved time to 1 mm segment depression and total work at peak exercise, while exercise duration at peak exercise showed a trend toward improvement (P = 0.09). CONCLUSION: This meta-analysis confirms the efficacy of TMZ in the treatment of stable angina, compared with placebo or conventional antianginal agent, as well as in monotherapy or in combination with conventional antianginal agents. TMZ is well tolerated in monotherapy as well as in combination.
----P Clinical_Trial Journal_Article Meta-Analysis Randomized_Controlled_Trial Review Review__Tutorial 
----M M_Aged_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nitroglycerin_MeSH S_therapeutic_use_MeSH Nitroglycerin_therapeutic_use_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH M_Trimetazidine_MeSH S_adverse_effects_MeSH Trimetazidine_adverse_effects_MeSH S_therapeutic_use_MeSH Trimetazidine_therapeutic_use_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12658255
----K 5
----T Droperidol, QT prolongation, and sudden death: what is the evidence?
----A STUDY OBJECTIVE: Droperidol is a butyrophenone commonly used as an antiemetic and antipsychotic in the United States since US Food and Drug Administration (FDA) approval in 1970. Its labeling has recently been revised, with a black box warning for cases of QT prolongation leading to torsades de pointes and death. A black box warning is applied when serious adverse drug reactions are uncovered for medications. We sought to examine the evidence of a causal association suggested by the black box warning to aid clinicians in their risk-benefit analyses regarding further use of droperidol. METHODS: A literature search was undertaken to determine the evidence regarding the association between droperidol and QT prolongation or torsades de pointes. The evidence was then evaluated by using evidence-based medicine principles. In addition, a review of the FDA regulatory process is presented. RESULTS: Three clinical studies, 1 published abstract, and 7 case reports were reviewed. Available postmarketing surveillance data (MedWatch reports) were also reviewed. Applying the criteria of evidence-based medicine and Hill's criteria, the evidence is not convincing for a causal relationship between therapeutic droperidol administration and life-threatening cardiac events. CONCLUSION: The recent black box warning appears to have originated from postmarketing surveillance data rather than data reported in the peer-reviewed medical literature. Ongoing monitoring of drug safety and more definitive study appear appropriate.
----P Journal_Article Review Review__Tutorial 
----M M_Adverse_Drug_Reaction_Reporting_Systems_MeSH M_Antiemetics_MeSH S_adverse_effects_MeSH Antiemetics_adverse_effects_MeSH M_Antipsychotic_Agents_MeSH S_adverse_effects_MeSH Antipsychotic_Agents_adverse_effects_MeSH M_Causality_MeSH M_Death__Sudden__Cardiac_MeSH S_epidemiology_MeSH Death__Sudden__Cardiac_epidemiology_MeSH S_etiology_MeSH Death__Sudden__Cardiac_etiology_MeSH M_Droperidol_MeSH S_adverse_effects_MeSH Droperidol_adverse_effects_MeSH M_Drug_Approval_MeSH S_organization_&_administration_MeSH Drug_Approval_organization_&_administration_MeSH M_Drug_Labeling_MeSH M_Drug_Monitoring_MeSH M_Electrocardiography_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Long_QT_Syndrome_MeSH S_chemically_induced_MeSH Long_QT_Syndrome_chemically_induced_MeSH S_diagnosis_MeSH Long_QT_Syndrome_diagnosis_MeSH S_epidemiology_MeSH Long_QT_Syndrome_epidemiology_MeSH M_Product_Surveillance__Postmarketing_MeSH M_Research_Design_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Safety_MeSH M_Torsades_de_Pointes_MeSH S_chemically_induced_MeSH Torsades_de_Pointes_chemically_induced_MeSH S_diagnosis_MeSH Torsades_de_Pointes_diagnosis_MeSH S_epidemiology_MeSH Torsades_de_Pointes_epidemiology_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_United_States_Food_and_Drug_Administration_MeSH 
****** 12656712
----K 5
----T Sumatriptan in migraine with unilateral cranial autonomic symptoms: an open study.
----A OBJECTIVE: To investigate the response to sumatriptan in migraineurs with unilateral cranial autonomic symptoms such as lacrimation, eye redness, eyelid edema, nasal congestion, and rhinorrhea. BACKGROUND: Given the potential large-scale recruitment of peripheral neurovascular 5-HT1B/1D receptors consequent to the activation of the trigeminal autonomic reflex in such patients, the presence of unilateral cranial autonomic symptoms may predict a positive response to sumatriptan. METHODS: Seventy-two consecutive migraineurs with unilateral cranial autonomic symptoms were given sumatriptan 50-mg tablets to treat 1 migraine attack and were asked to record their clinical response to the drug at different time points. End points were pain-relief and pain-free response at 1 and 2 hours. RESULTS: Pain relief was reported by 47 patients (65.3%) at 1 hour and by 59 (81.9%) at 2 hours. Pain-free response was reported by 22 patients (30.6%) at 1 hour and by 44 (61.1%) at 2 hours. Responsiveness to sumatriptan did not correlate with the type or number of unilateral cranial autonomic symptoms, demographic characteristics, prophylactic treatments, use of contraceptives, or concomitant tension-type headache. CONCLUSIONS: Migraineurs with unilateral cranial autonomic symptoms seem to respond to sumatriptan better than other migraineurs. The presence of unilateral cranial autonomic symptoms may predict a positive response to the triptans.
----P Clinical_Trial Journal_Article 
----M M_Adult_MeSH M_Autonomic_Nervous_System_MeSH S_physiopathology_MeSH Autonomic_Nervous_System_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH M_Reflex_MeSH S_drug_effects_MeSH Reflex_drug_effects_MeSH S_physiology_MeSH Reflex_physiology_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Trigeminal_Nerve_MeSH S_drug_effects_MeSH Trigeminal_Nerve_drug_effects_MeSH S_physiopathology_MeSH Trigeminal_Nerve_physiopathology_MeSH 
****** 12661775
----K 5
----T Focus on paroxetine.
----A This review of paroxetine is based on Medline and PsycLit searches and a manual search of the available research literature. It aims to cover the pharmacology of this frequently prescribed SSRI antidepressant in terms of its indications, efficacy and adverse effects. Overall, paroxetine is a well-tolerated and safe first-line SSRI antidepressant with anxiolytic qualities. It has been found useful in depression, anxiety and other conditions such as obsessive compulsive disorder and post-traumatic stress disorder. The antidepressant has some advantages over earlier tricyclic medication in terms of a lack of cardiovascular side-effects and relative safety in overdose. Cessation of use, however, is associated with withdrawal or discontinuation symptoms and patients should be counselled as to how these might be avoided. A 3- or 4-week graded withdrawal regimen, perhaps with concomitant fluoxetine to cover serotonergic discontinuation symptoms, may be advisable.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antidepressive_Agents__Second-Generation_MeSH S_administration_&_dosage_MeSH Antidepressive_Agents__Second-Generation_administration_&_dosage_MeSH S_adverse_effects_MeSH Antidepressive_Agents__Second-Generation_adverse_effects_MeSH S_pharmacokinetics_MeSH Antidepressive_Agents__Second-Generation_pharmacokinetics_MeSH S_therapeutic_use_MeSH Antidepressive_Agents__Second-Generation_therapeutic_use_MeSH M_Anxiety_Disorders_MeSH S_drug_therapy_MeSH Anxiety_Disorders_drug_therapy_MeSH M_Depression_MeSH S_drug_therapy_MeSH Depression_drug_therapy_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Paroxetine_MeSH S_administration_&_dosage_MeSH Paroxetine_administration_&_dosage_MeSH S_adverse_effects_MeSH Paroxetine_adverse_effects_MeSH S_pharmacokinetics_MeSH Paroxetine_pharmacokinetics_MeSH S_therapeutic_use_MeSH Paroxetine_therapeutic_use_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_administration_&_dosage_MeSH Serotonin_Uptake_Inhibitors_administration_&_dosage_MeSH S_adverse_effects_MeSH Serotonin_Uptake_Inhibitors_adverse_effects_MeSH S_pharmacokinetics_MeSH Serotonin_Uptake_Inhibitors_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Stress_Disorders__Post-Traumatic_MeSH S_drug_therapy_MeSH Stress_Disorders__Post-Traumatic_drug_therapy_MeSH M_Substance_Withdrawal_Syndrome_MeSH M_Treatment_Outcome_MeSH 
****** 12661910
----K 5
----T Guidelines for treatment of hypertension in the elderly--2002 revised version.
----A 
----P Consensus_Development_Conference Journal_Article Review 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Geriatrics_MeSH S_standards_MeSH Geriatrics_standards_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Practice_Guidelines_MeSH 
****** 12667031
----K 5
----T The evidence base for tight blood pressure control in the management of type 2 diabetes mellitus.
----A 
----P Guideline Journal_Article Practice_Guideline Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12667032
----K 5
----T Treatment of hypertension in type 2 diabetes mellitus: blood pressure goals, choice of agents, and setting priorities in diabetes care.
----A BACKGROUND: Hypertension in patients with type 2 diabetes mellitus is a prevalent condition that leads to substantial morbidity and mortality. PURPOSE: To evaluate the goals and optimal agents for treatment of hypertension in type 2 diabetes. DATA SOURCES: Review of the medical literature STUDY SELECTION: Randomized trials that evaluated the pharmacologic treatment of hypertension in patients with diabetes and reported microvascular and macrovascular outcomes. DATA EXTRACTION: Studies were identified by using the Cochrane Library, MEDLINE, meta-analyses, review articles, and expert recommendation. The searches of the Cochrane Library and MEDLINE were performed in May 2000 and updated in April 2002. Data were abstracted to standardized forms by a single reviewer and were confirmed by a second reviewer. DATA SYNTHESIS: Treatment of hypertension in type 2 diabetes provides dramatic benefit. Target diastolic blood pressures of less than 80 mm Hg appear optimal; systolic targets have not been as rigorously evaluated, but targets of 135 mm Hg or less are reasonable. Studies that compare drug classes do not suggest obviously superior agents. However, it is reasonable to conclude that thiazide diuretics, angiotensin-II receptor blockers, and perhaps angiotensin-converting enzyme (ACE) inhibitors may be the preferred first-line agents for treatment of hypertension in diabetes. beta-Blockers and calcium-channel blockers are more effective than placebo, but they may not be as effective as diuretics, angiotensin-II receptor blockers, or ACE inhibitors; however, study results are inconsistent in this regard. CONCLUSIONS: Treatment of hypertension in type 2 diabetes, with blood pressure goals of 135/80 mm Hg, provides dramatic benefits. Thiazide diuretics, angiotensin II receptor blockers, and ACE inhibitors may be the best first-line treatments, although other agents are usually necessary and goals may not be achieved even with three or four agents. Aggressive blood pressure control may be the most important factor in preventing adverse outcomes in patients with type 2 diabetes.
----P Journal_Article Meta-Analysis Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH 
****** 12668487
----K 5
----T Beta-blockers in chronic heart failure.
----A 
----P Case_Reports Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Bradycardia_MeSH S_complications_MeSH Bradycardia_complications_MeSH M_Chronic_Disease_MeSH M_Demography_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Hypotension_MeSH S_complications_MeSH Hypotension_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH 
****** 12667107
----K 5
----T New developments in migraine prophylaxis.
----A Migraine is a common neurological disorder that afflicts > or = 12% of the adult US population. Severe, frequent and disabling attacks require effective prophylaxis. Traditional preventive drugs such as beta-blockers, antidepressants and calcium antagonists, despite their documented efficacy, fail to offer relief for a significant proportion of migraine sufferers. Multiple threads of research over the last 15 years have led to the concept that migraine is generated from a hyperexcitable brain. This opens new perspectives in terms of preventive options, especially regarding the anticonvulsants agents. Additionally, different groups of substances, some of which nominated as non-orthodox agents, have been recently subjected to clinical trials and found to be effective. The aim of this review is to present and discuss the new options for migraine prevention.
----P Journal_Article Review Review__Tutorial 
----M M_Acupuncture_MeSH M_Adult_MeSH P_Anticonvulsants_MeSH S_adverse_effects_MeSH Anticonvulsants_adverse_effects_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH P_Expert_Testimony_MeSH M_Human_MeSH M_Migraine_MeSH S_epidemiology_MeSH Migraine_epidemiology_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 12667111
----K 5
----T Chronic daily headaches in children.
----A Chronic daily headache (CDH) or highly frequent headaches are being recognised as an increasing problem. In adults it is estimated that up to 4% of the population has CDH, however, this number appears to be lower in children. The actual prevalence of CDH in children, however, has not been determined. The simplest definition of CDH is > 15 headache days per month. In the international headache society (IHS) criteria, only chronic tension-type headaches and chronic cluster headaches are recognised as CDH. Criteria for CDH have been suggested for adults that mirror the IHS criteria. In children, the majority of CDH appear to be migraine related. The next revision of the IHS criteria has been proposed to include chronic migraine as one of the CDH. Evaluation of CDH needs to include a complete history and physical examination to identify any possibility of the headache representing secondary headaches. Treatment and management involves a multi-tiered approach, which includes abortive therapy when the headache becomes more severe. With the precaution of avoiding overuse of analgesic medication, prophylactic therapy is used to help reduce the characteristics of the headache as well as the frequency and mild behavioural therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_administration_&_dosage_MeSH Anti-Inflammatory_Agents__Non-Steroidal_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Child_MeSH P_Expert_Testimony_MeSH P_Headache_Disorders_MeSH S_classification_MeSH Headache_Disorders_classification_MeSH S_drug_therapy_MeSH Headache_Disorders_drug_therapy_MeSH S_epidemiology_MeSH Headache_Disorders_epidemiology_MeSH M_Human_MeSH 
****** 12669941
----K 5
----T Left ventricular systolic dysfunction and nonischemic cardiomyopathy.
----A Heart failure is a devastating chronic and progressive cardiac disorder affecting millions of Americans annually. Identifying the cause and initiating treatment early is the key to attempting to slow the progression of the condition. Recommended therapy is treatment with angiotensin-converting enzyme (ACE) inhibitors, diuretics, digoxin, beta blockers, and in patients with symptomatic class III and IV heart failure, the addition of aldactone.
----P Journal_Article Review Review__Tutorial 
----M P_Cardiomyopathy__Congestive_MeSH S_physiopathology_MeSH Cardiomyopathy__Congestive_physiopathology_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH P_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Medical_History_Taking_MeSH M_Risk_Factors_MeSH P_Ventricular_Dysfunction__Left_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12669942
----K 5
----T Left ventricular systolic dysfunction and ischemic cardiomyopathy.
----A Coronary artery disease is the primary risk factor for left ventricular systolic dysfunction and the most common cause of heart failure. Heart failure is the prevailing diagnosis for hospital admissions in the United States for people over 65 years of age. It has a great impact on the health care delivery system as a whole for both inpatient and outpatient treatment. A comprehensive understanding of this disease state is paramount for health care providers. This article describes the epidemiology, risk factors, pathophysiology, and current treatment modalities for left ventricular systolic dysfunction related to heart disease.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_complications_MeSH Coronary_Disease_complications_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Human_MeSH M_Risk_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12669947
----K 5
----T Sudden cardiac death: implantable cardioverter defibrillators and pharmacological treatments.
----A Sudden cardiac death (SCD) is the leading cause of death in advanced heart failure and cardiomyopathy patients, regardless of the underlying causes of cardiomyopathy. Ventricular tachycardia and ventricular fibrillation are the causes of SCD. This article examines pharmacological interventions and mostly, the role of implantable cardioverter defibrllators in preventing SCD in heart failure patients. The indications for various methods of treatment of SCD are discussed in this article.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH P_Defibrillators__Implantable_MeSH M_Heart_Failure__Congestive_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH 
****** 12671336
----K 5
----T Immunomodulating therapy: new treatment modality in congestive heart failure.
----A Accumulating evidence indicates that inflammatory cytokines play a pathogenic role in congestive heart failure (CHF) by influencing heart contractility, inducing hypertrophy, and promoting apoptosis or fibrosis, contributing to the continuous myocardial remodeling process. Traditional cardiovascular drugs seem to have little influence on the overall cytokine network, and immunomodulatory therapy has emerged as a possible new treatment modality in CHF. Several animal studies have suggested that modulation of inflammatory cytokines may improve cardiac performance. The authors have recently demonstrated that intravenous immunoglobulin enhances the left ventricular ejection fraction in CHF patients, and that this is significantly correlated with anti-inflammatory effects of such therapy. While intravenous immunoglobulin is not necessarily the drug of choice, this study suggests a potential role for immunomodulatory therapy in CHF in addition to optimal cardiovascular treatment regimens. Further research will more precisely identify the most important actors in the immunopathogenesis of CHF and contribute to the development of more specific immunomodulating agents for this disorder.
----P Journal_Article Review Review__Tutorial 
----M M_Adjuvants__Immunologic_MeSH S_therapeutic_use_MeSH Adjuvants__Immunologic_therapeutic_use_MeSH M_Cytokines_MeSH S_diagnostic_use_MeSH Cytokines_diagnostic_use_MeSH S_physiology_MeSH Cytokines_physiology_MeSH S_therapeutic_use_MeSH Cytokines_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_immunology_MeSH Heart_Failure__Congestive_immunology_MeSH M_Human_MeSH M_Inflammation_Mediators_MeSH S_diagnostic_use_MeSH Inflammation_Mediators_diagnostic_use_MeSH S_immunology_MeSH Inflammation_Mediators_immunology_MeSH S_therapeutic_use_MeSH Inflammation_Mediators_therapeutic_use_MeSH 
****** 12671333
----K 5
----T Scleroderma renal crisis.
----A Abrupt onset of severe uncontrolled hypertension and rapidly progressive oliguric renal failure characterizes scleroderma renal crisis. The etiology is unclear, but very high renin levels are present. While scleroderma is more common in women and whites, there is no difference in the prevalence of scleroderma renal crisis by gender. However, there appears to be a higher prevalence of scleroderma renal crisis among African Americans than whites. Survival was dismal prior to the introduction of the vigorous treatment of hypertension and use of converting-enzyme inhibitors. However, most data on the benefit of these medications are derived from uncontrolled and unblinded studies. Prospective, randomized controlled trials are needed to assess the role of angiotensin receptor blockers. Prevention trials could define the role of various drugs in decreasing the rate of scleroderma renal crisis.
----P Case_Reports Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Disease_Progression_MeSH M_Female_MeSH M_Human_MeSH M_Kidney_Diseases_MeSH S_etiology_MeSH Kidney_Diseases_etiology_MeSH M_Kidney_Failure_MeSH S_etiology_MeSH Kidney_Failure_etiology_MeSH M_Scleroderma__Systemic_MeSH S_complications_MeSH Scleroderma__Systemic_complications_MeSH S_diagnosis_MeSH Scleroderma__Systemic_diagnosis_MeSH 
****** 12674472
----K 5
----T AAFP/ACP-ASIM release guidelines on the management and prevention of migraines.
----A 
----P Guideline Journal_Article Practice_Guideline 
----M M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Patient_Education_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH 
****** 12673778
----K 5
----T Treatment of diabetic nephropathy in its early stages.
----A Diabetic nephropathy is one of the most frequent causes of end-stage renal disease (ESRD), and, in recent years, the number of diabetic patients entering renal replacement therapy has dramatically increased. The magnitude of the problem has led to numerous efforts to identify preventive and therapeutic strategies. In normoalbuminuric patients, optimal glycemic control (HbA(1c) lower than 7.5%) plays a fundamental role in the primary prevention of ESRD [weighted mean relative risk reduction (RRR) approximately 37% for metabolic control versus trivial renoprotection for intensive anti-hypertensive therapy or ACE-inhibitors (ACE-I)]. In the microalbuminuric stage, strict glycemic control probably reduces the incidence of overt nephropathy (weighted mean RRR approximately 50%), while blood pressure levels below 130/80 mmHg are recommended according to the average blood pressure levels obtained in various studies. In normotensive patients, ACE-I markedly reduce the development of overt nephropathy almost regardless of blood pressure levels; in hypertensive patients, ACE-I are less clearly active (weighted mean RRR approximately 23% versus other drugs), whereas angiotensin-receptor blockers (ARB) appear strikingly renoprotective. Once overt proteinuria appears, it is uncertain whether glycemic control affects the progression of nephropathy. In type 1 diabetes, various anti-hypertensive treatments, mainly ACE-I, are effective in slowing down the progression of nephropathy; in type 2 diabetes, two recent studies demonstrate that ARB are superior to conventional therapy or calcium channel blockers (CCB). In clinical practice, pharmacological tools are not always used to the best benefit of the patients. Therefore, clinicians and patients need to be educated regarding the renoprotection of drugs inhibiting the renin-angiotensin system (RAS) and the overwhelming importance of achieving target blood pressure.
----P Journal_Article Review Review_Literature 
----M M_Diabetic_Nephropathies_MeSH S_epidemiology_MeSH Diabetic_Nephropathies_epidemiology_MeSH S_therapy_MeSH Diabetic_Nephropathies_therapy_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_epidemiology_MeSH Hypertension__Renal_epidemiology_MeSH S_therapy_MeSH Hypertension__Renal_therapy_MeSH M_Renal_Replacement_Therapy_MeSH M_Risk_Factors_MeSH 
****** 12673376
----K 5
----T Long term effects of propranolol on portal pressure in cirrhotic patients.
----A Bleeding from varices is a very serious complication in cirrhotic patients, with a mean mortality rate around 30 %. If the portal vein pressure is decreased by pharmacological therapy the varices will not bleed and progressively decrease in size. The portal hypertension in cirrhotic patients develops as a consequence of two mechanisms: the increase of portal inflow and the increase of intrahepatic resistance. The aim of our study was to find out if propranolol can prevent the bleeding from esophageal varices and if it acts by reducing the portal inflow due to splanchnic vasodilatation. The study was initiated in 53 patients with portal hypertension, of whom 14 were withdrawn because of adverse effects of propranolol. Abdominal ultrasonography and Doppler of portal vein system were performed in all subjects. The ultrasonographic parameters were measured before and after a 3-year treatment with propranolol. The patients also underwent endoscopy for evaluation of esophageal varices; the endoscopy was repeated at the end-point of treatment. We noted that propranolol reduced the portal blood inflow and the size of esophageal varices, and that the incidence of hemorrhages by variceal rupture was very low in these patients.
----P Clinical_Trial Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_prevention_&_control_MeSH Esophageal_and_Gastric_Varices_prevention_&_control_MeSH M_Female_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_prevention_&_control_MeSH Gastrointestinal_Hemorrhage_prevention_&_control_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Prospective_Studies_MeSH 
****** 12675696
----K 5
----T Arterial hypertension and ischaemic stroke.
----A OBJECTIVES : Arterial hypertension is, besides age, the number one risk factor for ischaemic stroke. Patients with arterial hypertension frequently present with additional coexisting vascular risk factors interacting in a complex way. MATERIAL AND METHODS : This paper reviews the benefit of antihypertensive treatment, as well as different treatment options of arterial hypertension and their side-effects. RESULTS : Patients with definite arterial hypertension, but also patients with so-called normal or high-normal blood pressure are at increased risk to develop stroke and other cardiovascular complications. Vascular remodelling of small and large vessels provoked by arterial hypertension is the initial step in the development of atherosclerosis and lipohyalinosis. Vascular remodelling can be improved or even normalized by antihypertensive treatment with angiotensin-converting-enzyme inhibitors and angiotensin-I-receptor antagonists showing the most convincing effects. Angiotensin-converting-enzyme inhibitors and angiotensin-I-receptor antagonists have the lowest rate of side-effects, however, economic restraints hinder their general application. Statins are needed to treat dyslipidaemia. They also lower blood pressure and have a synergistic effect with the above two antihypertensive components in lowering blood pressure. In hypertensive patients, risk of stroke and other cardiovascular complications is determined by the blood pressure level and the presence or absence of target organ damage and the interaction with other risk factors, such as cigarette smoking, dyslipidaemia, and diabetes. These high-risk patients should be treated even more aggressively than usual. CONCLUSIONS : In the vast majority of patients and healthy individuals, target blood pressure should be as high as or below 120/80 mmHg to minimize the occurrence of stroke and other cardiovascular complications.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Brain_Infarction_MeSH S_etiology_MeSH Brain_Infarction_etiology_MeSH S_prevention_&_control_MeSH Brain_Infarction_prevention_&_control_MeSH M_Brain_Ischemia_MeSH S_complications_MeSH Brain_Ischemia_complications_MeSH S_etiology_MeSH Brain_Ischemia_etiology_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Risk_Factors_MeSH 
****** 12678218
----K 5
----T The ALLHAT Trial. Diuretics are still the preferred initial drugs for high blood pressure.
----A The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) compared four antihypertensive agents in patients 55 years and older: chlorthalidone, doxazosin, amlodipine, and lisinopril. The doxazosin arm was terminated early because of an excess of congestive heart failure. Chlorthalidone was at least equivalent to amlodipine and lisinopril in all of the outcomes measured, and was better in some, notably heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_Determination_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Doxazosin_MeSH S_therapeutic_use_MeSH Doxazosin_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Lisinopril_MeSH S_therapeutic_use_MeSH Lisinopril_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Probability_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH 
****** 12679750
----K 5
----T Heart failure with preserved systolic function after myocardial infarction: a growing burden?
----A The number of patients with coexisting chronic kidney disease (CKD) and cardiovascular disease is growing rapidly. Treatment of these patients is challenging, primarily because of a lack of pharmacokinetic and clinical trial data associated with these combined disease entities. In this report, we discuss the cardiovascular disease risk associated with CKD and review the use of anticoagulation for acute cardiovascular disease in patients with CKD. We evaluate the potential role of direct thrombin inhibitors in patients with renal disease who have acute coronary syndromes, with particular focus on the clinical efficacy of bivalirudin. We conclude that direct thrombin inhibitors, including bivalirudin and argatroban, may be promising alternatives to heparin in patients who have renal insufficiency and are therefore at an increased risk for bleeding. In the treatment of patients with advanced renal insufficiency and cardiovascular disease, however, these agents should be used with dose modification to account for altered excretion.
----P Comment Editorial 
----M M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_pathology_MeSH Myocardial_Infarction_pathology_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_therapy_MeSH Myocardial_Infarction_therapy_MeSH M_Sex_Factors_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Ventricular_Function__Left_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 12678691
----K 5
----T Classic histamine H1 receptor antagonists: a critical review of their metabolic and pharmacokinetic fate from a bird's eye view.
----A The so-called "classic" histamine H(1) receptor antagonists are highly lipophilic compounds associated with significant biotransformation and tissue distribution. They are categorized according to their chemical structure into ethanolamines, alkylamines, ethylenediamines, piperazines, phenothiazines and piperidines, all of which have characteristic metabolic fates. The former four categories undergo primarily cytochrome P450-mediated oxidative N-desalkylations and deamination whereas the aromatic rings of the latter two undergo P450-mediated oxidative hydroxylation and/or epoxide formation. The common tertiary amino group is susceptible to oxidative metabolism by flavin containing monooxygenases forming N-oxides, and the alicyclic tertiary amines produce small amounts (up to 7%) of N-glucuronides in humans. Species, sex and racial differences in the metabolism and pharmacokinetics of antihistamines are known. Specific P450-isozymes implicated in the metabolism were identified in a few cases, such as CYP2D6 that contributes to the metabolism of promethazine, diphenhydramine and chlorpheniramine. Low circulating plasma concentrations of antihistamines are in part explained by significant first-pass effect and tissue distribution. Antihistaminic effects last up to 6 hours though some compounds exhibit a longer duration of action due to circulating active metabolites. Importantly, diphenhydramine inhibited CYP2D6 leading to a clinically significant drug-drug interaction with metoprolol. Other classic antihistamines were shown to be potent in vitro inhibitors of CYP2D6 and CYP3A4. The prescription-free access to most classic antihistamines can easily lead to their co-administration with other drugs metabolized by the same enzyme system thereby leading to drug accumulation and adverse effects. In depth knowledge of the metabolic pathways of classic antihistamines and the enzymes involved is crucial to prevent the high incidence of drug interactions in humans, which are predictable based on pre-clinical data but unexpected when such data is unavailable.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Cytochrome_P-450_Enzyme_System_MeSH S_metabolism_MeSH Cytochrome_P-450_Enzyme_System_metabolism_MeSH M_Drug_Interactions_MeSH M_Ethanolamines_MeSH S_chemistry_MeSH Ethanolamines_chemistry_MeSH S_metabolism_MeSH Ethanolamines_metabolism_MeSH M_Ethylenediamines_MeSH S_chemistry_MeSH Ethylenediamines_chemistry_MeSH S_metabolism_MeSH Ethylenediamines_metabolism_MeSH M_Glucuronosyltransferase_MeSH S_metabolism_MeSH Glucuronosyltransferase_metabolism_MeSH M_Histamine_H1_Antagonists_MeSH S_chemistry_MeSH Histamine_H1_Antagonists_chemistry_MeSH S_metabolism_MeSH Histamine_H1_Antagonists_metabolism_MeSH S_pharmacokinetics_MeSH Histamine_H1_Antagonists_pharmacokinetics_MeSH M_Human_MeSH M_Oxygenases_MeSH S_metabolism_MeSH Oxygenases_metabolism_MeSH M_Phenothiazines_MeSH S_chemistry_MeSH Phenothiazines_chemistry_MeSH S_metabolism_MeSH Phenothiazines_metabolism_MeSH M_Piperazines_MeSH S_chemistry_MeSH Piperazines_chemistry_MeSH S_metabolism_MeSH Piperazines_metabolism_MeSH M_Piperidines_MeSH S_chemistry_MeSH Piperidines_chemistry_MeSH S_metabolism_MeSH Piperidines_metabolism_MeSH M_Pyridines_MeSH S_chemistry_MeSH Pyridines_chemistry_MeSH S_metabolism_MeSH Pyridines_metabolism_MeSH M_Structure-Activity_Relationship_MeSH 
****** 12679216
----K 5
----T Hypertension, angiotensin II, aldosterone, and race.
----A 
----P Comment Editorial 
----M P_African_Continental_Ancestry_Group_MeSH M_Aldosterone_MeSH S_blood_MeSH Aldosterone_blood_MeSH M_Aldosterone_Antagonists_MeSH S_adverse_effects_MeSH Aldosterone_Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH P_European_Continental_Ancestry_Group_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH S_drug_effects_MeSH Renin_drug_effects_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Spironolactone_MeSH S_adverse_effects_MeSH Spironolactone_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Spironolactone_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12680475
----K 5
----T Expanding role of beta-blockade in the management of chronic heart failure.
----A Although recent advances have been made in the treatment of heart failure, this disease continues to result in significant morbidity and mortality. Among the negative effects associated with progression of heart failure are decline in myocardial reserve, decreased exercise tolerance, decreased contractile function, and altered cardiac gene expression. Guidelines recommend neurohormonal antagonists for treatment and stress the importance of angiotensin-converting enzyme inhibition and beta-blockade in reversing the cardiac remodeling process. beta-Blockade slows or reverses the adverse effects resulting from chronic adrenergic stimulation. Traditionally, beta-blockers were reserved for mild-to-moderate heart failure, based on evidence from large, randomized clinical trials showing their positive effects on myocardial function and clinical outcomes. More recently, clinical data reveal that the agents can be expanded to patients with severe heart failure and those with left ventricular systolic dysfunction after myocardial infarction. Individual beta-blocking agents vary in their pharmacology and dosing requirements. These variations may influence treatment decisions and affect clinical measurements of left ventricular function and ventricular remodeling.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Chronic_Disease_MeSH M_Disease_Management_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12683600
----K 5
----T Cardiac complications after noncardiac thoracic surgery: an evidence-based current review.
----A Despite advances in perioperative management, thoracic surgery remains a high-risk procedure for many patients. A systematic review of cardiac complications after thoracic surgery is presented. Most reviews about noncardiac thoracic surgery discuss postoperative analgesic regimens and pulmonary complications. In the present review, we also discuss atrial fibrillation as the most frequently encountered cardiac side effect. An evidence-based approach to other complications, such as myocardial ischemia, pulmonary edema, embolism, and shunt, is described. Furthermore, we offer recommendations for daily practice.
----P Journal_Article Review Review_Literature 
----M M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH M_Cardiac_Output__Low_MeSH S_etiology_MeSH Cardiac_Output__Low_etiology_MeSH M_Heart_Diseases_MeSH S_etiology_MeSH Heart_Diseases_etiology_MeSH M_Human_MeSH M_Myocardial_Ischemia_MeSH M_Postoperative_Complications_MeSH M_Pulmonary_Embolism_MeSH S_etiology_MeSH Pulmonary_Embolism_etiology_MeSH P_Thoracic_Surgical_Procedures_MeSH 
****** 12684599
----K 5
----T Prevention of heart failure: effective strategies to combat the growing epidemic.
----A In light of the increasing prevalence, morbidity, and mortality of heart failure, effective preventative strategies are urgently needed. Risk factors for heart failure include coronary artery disease and other atherosclerotic vascular diseases, hypertension, diabetes, renal insufficiency, obesity, and family history of cardiomyopathy. Essential strategies for prevention of heart failure are modification of risk factors for heart failure development; comprehensive hypertension, atherosclerosis, and diabetes treatment; and detection and treatment of asymptomatic left ventricular dysfunction. The B-type natriuretic peptide assay may aid in identifying asymptomatic left ventricular dysfunction in patients with risk factors for heart failure. In patients with hypertension, atherosclerosis, and/or diabetes, angiotensin-converting enzyme inhibitor, beta-blocker, aspirin, and statin therapy can prevent progression to symptomatic heart failure. Avoidance of calcium channel-blockers as first-line antihypertensive therapy can also reduce the risk of heart failure. There remain substantial opportunities to improve implementation of therapies proven to prevent heart failure in the large number of patients at risk.
----P Journal_Article Review Review__Tutorial 
----M M_Diabetic_Angiopathies_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Health_Behavior_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Kidney_MeSH S_physiopathology_MeSH Kidney_physiopathology_MeSH M_Patient_Compliance_MeSH M_Risk_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12684601
----K 5
----T Fatal case of delayed repolarization due to cocaine abuse and global ischemia.
----A When a previously healthy, middle-aged patient presents with apparent seizures, what should alert the physician to the possibility of underlying cardiac disease? This report describes a case of long QT syndrome, initially presenting as seizures, which expressed itself at an atypically advanced age as a result of cocaine use, global myocardial ischemia, and ventricular tachycardia.
----P Case_Reports Journal_Article 
----M M_Cocaine-Related_Disorders_MeSH S_physiopathology_MeSH Cocaine-Related_Disorders_physiopathology_MeSH M_Electrocardiography_MeSH M_Fatal_Outcome_MeSH M_Heart_Conduction_System_MeSH S_physiopathology_MeSH Heart_Conduction_System_physiopathology_MeSH M_Human_MeSH M_Long_QT_Syndrome_MeSH S_etiology_MeSH Long_QT_Syndrome_etiology_MeSH S_physiopathology_MeSH Long_QT_Syndrome_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Ischemia_MeSH S_physiopathology_MeSH Myocardial_Ischemia_physiopathology_MeSH M_Torsades_de_Pointes_MeSH S_physiopathology_MeSH Torsades_de_Pointes_physiopathology_MeSH 
****** 12691286
----K 4
----T Effects of therapeutic beta blockade on myocardial function and cardiac remodelling in congenital cardiac disease.
----A BACKGROUND: Cardiac remodelling is now recognised as an important aspect of cardiovascular disease progression and is, therefore, emerging as a therapeutic target in cardiac failure due to different etiologies. Little is known about the influence of different therapies for cardiac failure on the remodelling seen in infants with congenital cardiac disease. METHODS: During follow-up of a prospective and randomized trial, we investigated therapeutic effects on neurohormonal activation, ventricular function, and myocardial gene expression. We compared the data from 8 infants with severe congestive heart failure due to left-to-right shunts, who received digoxin and diuretics alone, to 9 infants who received additional treatment with propranolol. RESULTS: In these infants, beta-adrenergic blockade significantly reduced highly elevated levels of renin, from 284 +/- 319 microU/ml compared to 1061 +/- 769 microU/ml. Systolic ventricular function was normal in both groups, but diastolic ventricular function was improved in those receiving propranolol, indicated by significantly lower left atrial pressures, lower end-diastolic pressures, and less pronounced ventricular hypertrophy, the latter estimated by lower ratios of myocardial wall to ventricular cavity areas on average of 42%. Further hemodynamic parameters showed no significant differences between the groups, except for the lower heart rate in infants treated with propranolol. In those treated with digoxin and diuretics, there was a significant downregulation of beta2-receptor and angiotensin-2 receptor genes, and up-regulation of endothelin A receptor and connective tissue growth factor genes, that were partially prevented by additional treatment with propranolol. CONCLUSIONS: Beta-blockade is a new therapeutic approach for congestive heart failure in infants with congenital cardiac disease, producing with significant benefits on neurohormonal activation, diastolic ventricular function, and cardiac remodelling.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Digoxin_MeSH S_administration_&_dosage_MeSH Digoxin_administration_&_dosage_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Defects__Congenital_MeSH S_complications_MeSH Heart_Defects__Congenital_complications_MeSH S_diagnosis_MeSH Heart_Defects__Congenital_diagnosis_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Heart_Function_Tests_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Infant_MeSH M_Male_MeSH M_Probability_MeSH M_Prognosis_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Prospective_Studies_MeSH M_Reference_Values_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Statistics__Nonparametric_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 12690915
----K 5
----T Current perspectives. Heart failure woman: does she make any difference?
----A Significant differences between sexes may influence the prevalence, incidence and severity of the heart failure syndrome. These differences may also interfere with treatment and management. In this review sex differences and similarities have been analyzed focusing on epidemiology, drug therapy and psychological implications. Pathophysiological differences but also a selection bias are evident; such differences bear an influence on clinical management. Gender differences exist even in the health-related quality of life, depression and coping ability. No studies have been specifically designed to investigate gender differences and the exclusion of elderly persons (mainly women) from large trials may compromise the quality of their care.
----P Journal_Article Review Review__Tutorial 
----M M_Age_Distribution_MeSH M_Age_of_Onset_MeSH M_Aged_MeSH M_Confidence_Intervals_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Italy_MeSH S_epidemiology_MeSH Italy_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Odds_Ratio_MeSH M_Prevalence_MeSH M_Probability_MeSH M_Severity_of_Illness_Index_MeSH M_Sex_Factors_MeSH M_Survival_Rate_MeSH 
****** 12693729
----K 5
----T Beta-blockers for heart failure: why, which, when, and where.
----A Beta-blockers are a highly effective treatment for patients with all grades of heart failure secondary to LV systolic dysfunction. Beta-blockers are best deployed as a form of tertiary prevention in heart failure but have a very limited role for the treatment of a heart failure crisis. Physicians and patients need to understand the time course of the effects of beta-blocker therapy. The initial effects are often neutral or adverse, though the benefits, at least of carvedilol, may be apparent within days in patients with severe heart failure. Benefits accumulate gradually over a period of weeks to months. Some patience, perseverance, and education are required in order to allow patients to reap the full benefits of beta-blocker therapy for this malignant disease. Initiation of treatment early in the course of the disease maximizes the effectiveness and acceptance of therapy. Trials are under way to determine whether the benefits of beta-blockers extend to patients over 80 years of age and to those with preserved LV systolic function. It is likely that important differences exist between beta-blockers in terms of their clinical benefit, though whether differences exist between the agents that have been reported to be effective so far awaits the outcome of a large clinical trial. It is unclear whether the target doses of beta-blockers currently recommended are optimal.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_contraindications_MeSH Adrenergic_beta-Antagonists_contraindications_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Age_Factors_MeSH M_Cardiovascular_Agents_MeSH S_administration_&_dosage_MeSH Cardiovascular_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Cardiovascular_Agents_adverse_effects_MeSH S_contraindications_MeSH Cardiovascular_Agents_contraindications_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Drug_Administration_Schedule_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function_MeSH S_drug_effects_MeSH Ventricular_Function_drug_effects_MeSH 
****** 12693740
----K 5
----T Pharmacogenomics of congestive heart failure.
----A Information on the probable efficacy and safety of drugs for individualized patients should change both the economics and the management of congestive heart failure. Rapidly profiling patients should enhance the ability to develop "designer" drugs for those with similar disease phenotypes. Pharmacogenomics also may resurrect promising drugs that did not show benefit when previously added to standard therapy. The promise of pharmacogenomics has to be tempered, however, by a sensitivity to concerns regarding the potential misuse of genomic information, including loss of confidentiality for the patient, as well as possible stigmatization of groups. Such difficult genoethical issues must be addressed in order to reap the full benefits of this evolving and exciting field.
----P Journal_Article Review Review__Tutorial 
----M M_Aldosterone_Synthase_MeSH S_genetics_MeSH Aldosterone_Synthase_genetics_MeSH M_Cardiovascular_Agents_MeSH S_pharmacokinetics_MeSH Cardiovascular_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_genetics_MeSH Heart_Failure__Congestive_genetics_MeSH M_Human_MeSH P_Pharmacogenetics_MeSH P_Polymorphism_(Genetics)_MeSH M_Receptors__Adrenergic_MeSH S_genetics_MeSH Receptors__Adrenergic_genetics_MeSH M_Receptors__Bradykinin_MeSH S_genetics_MeSH Receptors__Bradykinin_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH 
****** 12695723
----K 5
----T Congestive heart failure in patients with chronic kidney disease and on dialysis.
----A CHF is highly prevalent in ESRD and is a leading cause of death in such patients. Hypertension, renal anemia, and comorbid conditions such as coronary artery disease are particularly important risk factors for CHF in ESRD. Dialysis hypotension may be a marker of poor prognosis in such persons. Recent studies suggest that lipid peroxidation and L-carnitine deficiency may contribute to CHF in some patients with ESRD. All forms of renal replacement therapy are capable of ameliorating symptoms of CHF, but their effect on cardiovascular mortality has not been firmly established. Drug therapy, particularly angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers, is under-used in patients with ESRD and CHF. Heart/kidney transplantation may be a viable option for some patients with advanced CHF and ESRD.
----P Journal_Article Review Review__Tutorial 
----M M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Kidney_Failure__Chronic_MeSH S_complications_MeSH Kidney_Failure__Chronic_complications_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH M_Kidney_Transplantation_MeSH P_Renal_Dialysis_MeSH M_Risk_Factors_MeSH 
****** 12695725
----K 5
----T Hypertension after kidney transplantation: impact, pathogenesis and therapy.
----A Hypertension (HTN) contributes to the high incidence of cardiovascular disease mortality as well as chronic allograft nephropathy (CAN) and late graft failure in renal transplant recipients. The mechanisms are complex and may involve pathogenic factors attributable to the host, allograft, and immunosuppressive drugs. Calcium channel blockers should be used to ameliorate the nephrotoxicity of calcineurin inhibitors in the early years after transplantation. Angiotensin-converting enzyme inhibitors and angiotensin-2 type-1 receptor blockers are safe and effective, have antiproteinuric effects, slow the progression of CAN, and may provide survival benefits. Diuretics and/or beta-adrenergic receptor blockers are frequently added in combination regimen. Appropriate adjustment of the immunosuppressive drugs should also be considered for the long-term care of kidney recipients with HTN.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH P_Graft_Rejection_MeSH M_Graft_Survival_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Immunosuppressive_Agents_MeSH S_therapeutic_use_MeSH Immunosuppressive_Agents_therapeutic_use_MeSH P_Kidney_Transplantation_MeSH S_mortality_MeSH Kidney_Transplantation_mortality_MeSH M_Risk_Factors_MeSH 
****** 12695727
----K 5
----T Diagnosis and therapy of coronary artery disease in renal failure, end-stage renal disease, and renal transplant populations.
----A Even though cardiovascular disease is the leading cause of death in patients with CRF and end-stage renal disease (ESRD), ill-conceived notions have led to therapeutic nihilism as the predominant strategy in the management of cardiovascular disease in these populations. The recent data clearly support the application of proven interventions in the general population, such as angiotensin-converting enzyme inhibitors and statins to patients with CRF and ESRD. The advances in coronary stents and intracoronary irradiation have decreased the restenosis rates in renal failure patients. Coronary artery bypass with internal mammary graft might be the procedure of choice for coronary revascularization in these patients. The role of screening for asymptomatic coronary disease is established as a pretransplant procedure, but it is unclear whether this will be applicable to all patients with ESRD. Future studies need to focus on unraveling the mechanisms by which uremia leads to increased cardiovascular events to design optimal therapies targeted toward these mechanisms and improve cardiovascular outcomes.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_MeSH S_metabolism_MeSH Calcium_metabolism_MeSH M_Coronary_Arteriosclerosis_MeSH S_diagnosis_MeSH Coronary_Arteriosclerosis_diagnosis_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH M_Homocysteine_MeSH S_metabolism_MeSH Homocysteine_metabolism_MeSH M_Human_MeSH M_Inflammation_MeSH S_metabolism_MeSH Inflammation_metabolism_MeSH M_Kidney_Failure_MeSH S_physiopathology_MeSH Kidney_Failure_physiopathology_MeSH M_Kidney_Failure__Chronic_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH S_surgery_MeSH Kidney_Failure__Chronic_surgery_MeSH P_Kidney_Transplantation_MeSH M_Lipids_MeSH S_metabolism_MeSH Lipids_metabolism_MeSH M_Myocardial_Revascularization_MeSH M_Nutrition_MeSH M_Oxidative_Stress_MeSH M_Parathyroid_Hormone_MeSH S_metabolism_MeSH Parathyroid_Hormone_metabolism_MeSH M_Risk_Factors_MeSH M_Vitamin_D_MeSH S_metabolism_MeSH Vitamin_D_metabolism_MeSH 
****** 12695241
----K 4
----T The effect of latanoprost, brimonidine, and a fixed combination of timolol and dorzolamide on circadian intraocular pressure in patients with glaucoma or ocular hypertension.
----A OBJECTIVE: To compare the circadian intraocular pressure (IOP) reductions induced by latanoprost, brimonidine tartrate, and a fixed combination of timolol maleate and dorzolamide hydrochloride in patients with primary open-angle glaucoma (POAG) or ocular hypertension (OHT). METHODS: In this crossover study, 10 patients with POAG and 10 with OHT were treated with latanoprost once a day, brimonidine twice a day, and a fixed combination of timolol and dorzolamide twice a day for 1 month. Four 24-hour tonometric curves were obtained for each patient. Intraocular pressure (IOP) was measured at 3, 6, and 9 AM, and at noon and at 3, 6, and 9 PM, and at midnight, using a handheld electronic tonometer with the patient in supine and sitting positions and a Goldmann applanation tonometer with the patient sitting at the slitlamp. MAIN OUTCOME MEASURE: Reduction of circadian IOP. RESULTS: All the drugs significantly reduced IOP compared with the baseline at all times, except for brimonidine at midnight, 3 AM, and 6 AM. Latanoprost was more effective than brimonidine in lowering IOP at 3 and 6 AM and at 3 PM (P=.03), and the combination of timolol and dorzolamide was more effective than brimonidine at 3 and 9 AM (P=.04) and at 3 and 6 PM (P =.05) and more effective than latanoprost at 9 AM (P=.05). CONCLUSION: Latanoprost and the fixed combination of timolol and dorzolamide led to similar circadian reductions in IOP, whereas brimonidine was less effective, particularly during the night.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Posture_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Tonometry__Ocular_MeSH 
****** 12697002
----K 5
----T The triptan formulations : how to match patients and products.
----A The 5-HT(1B/1D) receptor agonists (the 'triptans') are migraine-specific agents that have revolutionised the treatment of migraine. They are usually the drugs of choice to treat a migraine attack in progress. Different triptans are available in various strengths and formulations, including oral tablets, orally disintegrating tablets, nasal sprays and subcutaneous injections. In Europe, sumatriptan is also available as a suppository. Specific differences among the triptans exist, as evidenced by different pharmacological profiles including half-life, time to peak plasma concentrations, peak plasma concentrations, area under the concentration-time curve, metabolism and drug-drug interaction profiles. How or whether these differences translate to clinical efficacy and tolerability advantages for one agent over another is not well differentiated. However, delivery systems may play an important role in onset of action. Given that the clinical distinctions among these agents are subtle, identification of the most appropriate triptan for an individual patient requires consideration of the specific characteristics of the patient and knowledge of patient preference, an accurate history of the efficacy of previous acute-care medications and individual features of the drug being considered. The selection of an acute antimigraine drug also depends upon the stratification of the patient's migraine attack by peak intensity, time to peak intensity, level of associated symptoms such as nausea and vomiting, time to associated symptoms, comorbid diseases and concomitant treatments that might cause drug-drug interactions. Individual patient response to the triptans seems to be idiosyncratic and possibly genetically determined. Therefore, a set of specific questions can be used to determine whether a currently used triptan is optimally effective, whether the dose needs to be increased or whether another triptan should be tried. The clinician has in his/her armamentarium an ever-expanding variety of triptans, available in multiple formulations and dosages, which have good safety and tolerability profiles. Continued clinical use will yield familiarity with the various triptans, and it should become possible for the interested physician to match individual patient needs with the specific characteristics of a triptan to optimise therapeutic benefit. Use of the methods outlined in this review in choosing a triptan for an individual patient is probably more likely to lead to migraine relief than making an educated guess as to which triptan is most appropriate.
----P Journal_Article Review Review__Tutorial 
----M M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Routes_MeSH M_Drug_Delivery_Systems_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Prescriptions__Drug_MeSH M_Serotonin_Agonists_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Sumatriptan_MeSH S_analogs_&_derivatives_MeSH Sumatriptan_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Sumatriptan_pharmacokinetics_MeSH S_therapeutic_use_MeSH Sumatriptan_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12699397
----K 5
----T Pulse pressure: an important tool in cardiovascular pharmacology and therapeutics.
----A Epidemiological studies in the past decade have stressed the importance of pulse pressure (PP) as an independent risk factor for cardiovascular morbidity and mortality. We briefly review the epidemiological evidence and discuss the pathophysiological mechanisms which involve arterial stiffness and wave reflections in older patients. We discuss the therapeutic consequences of targeting PP rather than systolic (S) or diastolic (D) blood pressure (BP) when using antihypertensive agents. With this line of evidence it is important, first, to determine what minimal PP level indicates cardiovascular risk and, second, to note that an increasing number of clinical studies indicate that PP is poorly sensitive to placebo, while SBP and DBP are conversely highly sensitive. Finally, on the basis of large-scale intervention trials, PP seems to be an appropriate tool for studies of clinical pharmacology and therapeutics in the fields of hypertension, congestive heart failure and other cardiovascular diseases.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Biological_Markers_MeSH P_Blood_Pressure_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_physiopathology_MeSH Cardiovascular_Diseases_physiopathology_MeSH M_Epidemiologic_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Pulse_MeSH 
****** 12701984
----K 3
----T Initial findings of the AASK: African Americans with hypertensive kidney disease benefit from an ACE inhibitor.
----A Experts have long thought that African Americans were less responsive to ACE inhibitors than other racial or ethnic groups. The African American Study of Kidney Disease and Hypertension (AASK) provides the first evidence of a beneficial effect of ACE inhibition on renal function in African American patients, in addition to excellent blood pressure control.
----P Journal_Article 
----M P_African_Americans_MeSH M_Amlodipine_MeSH S_therapeutic_use_MeSH Amlodipine_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Renal_MeSH S_drug_therapy_MeSH Hypertension__Renal_drug_therapy_MeSH S_ethnology_MeSH Hypertension__Renal_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ramipril_MeSH S_therapeutic_use_MeSH Ramipril_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12701988
----K 5
----T Preventing kidney failure: primary care physicians must intervene earlier.
----A Mild chronic kidney disease often goes unnoticed until a substantial loss of renal function has occurred. Given the increasing incidence of chronic kidney disease, primary care physicians play a critical role in the early evaluation and intervention of patients at risk. This article discusses the key steps, with emphasis on patients with mild disease due to diabetes or hypertension.
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH M_Blood_Pressure_MeSH M_Creatinine_MeSH S_urine_MeSH Creatinine_urine_MeSH M_Glomerular_Filtration_Rate_MeSH M_Human_MeSH M_Kidney_Failure__Chronic_MeSH S_classification_MeSH Kidney_Failure__Chronic_classification_MeSH S_diagnosis_MeSH Kidney_Failure__Chronic_diagnosis_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH S_prevention_&_control_MeSH Kidney_Failure__Chronic_prevention_&_control_MeSH M_Proteinuria_MeSH S_etiology_MeSH Proteinuria_etiology_MeSH 
****** 12702626
----K 5
----T Cardiovascular disease, hypertension, and lipids.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH P_Diabetic_Angiopathies_MeSH S_diagnosis_MeSH Diabetic_Angiopathies_diagnosis_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_diagnosis_MeSH Hyperlipidemia_diagnosis_MeSH S_etiology_MeSH Hyperlipidemia_etiology_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12703677
----K 5
----T Pathophysiology and management of neurocardiogenic syncope.
----A OBJECTIVE: To discuss the physiologic mechanisms underlying neurocardiogenic syncope in the context of several different management strategies. PATHOPHYSIOLOGY: Neurocardiogenic syncope or the "common faint" is variously called neurally mediated hypotension, vasovagal syncope, or vasodepressor syncope. It is the most common type of syncope. The pathophysiology of neurocardiogenic syncope is complex and not completely elucidated. Individuals susceptible to neurocardiogenic syncope are unable to maintain the adaptive neurocardiovascular responses to upright posture for prolonged periods. These patients tend to have a modest reduction in central blood volume, which is aggravated by upright posture. It is often noted in individuals receiving sympathetic blocking agents and vasodilator drugs for hypertension, elderly patients receiving tranquilizers, patients with anemia, and individuals with tran- sient reductions in blood volume such as those that occur after a brisk diuresis or blood donation. The classic syncopal episode often is preceded by a constellation of prodromal symptoms several seconds before the event that may include nausea, headache, diaphoresis, dizziness, chest pain, palpitations, dyspnea, and paresthesia. MANAGEMENT: Head-up tilt testing has become the diagnostic study of choice for the identification of patients with neurocardiogenic syncope. Therapeutic options include general measures such as volume expansion; pharmacologic approaches such as beta-adrenergic receptor blockade, anticholinergic agents, selective serotonin reuptake inhibitors, methylxanthines, and alpha agonists; and invasive methods such as placement of a dual-chamber cardiac pacemaker.
----P Journal_Article 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Arrhythmia_MeSH S_complications_MeSH Arrhythmia_complications_MeSH M_Cardiac_Pacing__Artificial_MeSH M_Cardiovascular_Abnormalities_MeSH S_complications_MeSH Cardiovascular_Abnormalities_complications_MeSH M_Cholinergic_Antagonists_MeSH S_therapeutic_use_MeSH Cholinergic_Antagonists_therapeutic_use_MeSH M_Education__Medical__Continuing_MeSH M_Head-Down_Tilt_MeSH M_Human_MeSH M_Managed_Care_Programs_MeSH M_Mineralocorticoids_MeSH S_therapeutic_use_MeSH Mineralocorticoids_therapeutic_use_MeSH M_Prognosis_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Syncope__Vasovagal_MeSH S_drug_therapy_MeSH Syncope__Vasovagal_drug_therapy_MeSH S_etiology_MeSH Syncope__Vasovagal_etiology_MeSH S_physiopathology_MeSH Syncope__Vasovagal_physiopathology_MeSH S_therapy_MeSH Syncope__Vasovagal_therapy_MeSH M_United_States_MeSH M_Xanthines_MeSH S_therapeutic_use_MeSH Xanthines_therapeutic_use_MeSH 
****** 12704478
----K 5
----T The 2002/3 Canadian Cardiovascular Society consensus guideline update for the diagnosis and management of heart failure.
----A 
----P Consensus_Development_Conference Guideline Journal_Article Practice_Guideline Review 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atrial_Natriuretic_Factor_MeSH S_blood_MeSH Atrial_Natriuretic_Factor_blood_MeSH M_Canada_MeSH M_Cardiology_MeSH M_Defibrillators__Implantable_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Natriuretic_Peptide__Brain_MeSH M_Societies__Medical_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12708620
----K 5
----T Partial fatty acid oxidation (pFOX) inhibition: a new therapy for chronic stable angina.
----A During myocardial ischemia, fatty acids are the principal source of energy, increasing myocardial oxygen consumption and making a decrease in coronary blood flow less well tolerated. Increasing glucose oxidation during myocardial ischemia may improve cardiac efficiency. The pFOX inhibitors have the potential to accomplish this. In 2003, I think we can look forward to learning more about this class of compounds called pFOX inhibitors. Perhaps they will provide us alternative therapies in our patients who have persistent chronic stable angina pectoris despite aggressive medical therapy and/or revascularization. It seems to methat this is an increasing problem, and it is particularly common in older patients who want to remain active, but whose chronic stable angina interferes with that lifestyle.
----P Editorial 
----M M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Energy_Metabolism_MeSH M_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Enzyme_Inhibitors_therapeutic_use_MeSH M_Fatty_Acids_MeSH S_metabolism_MeSH Fatty_Acids_metabolism_MeSH M_Human_MeSH M_Myocardial_Contraction_MeSH M_Oxidation-Reduction_MeSH S_drug_effects_MeSH Oxidation-Reduction_drug_effects_MeSH M_Piperazines_MeSH S_therapeutic_use_MeSH Piperazines_therapeutic_use_MeSH 
****** 12708950
----K I
----T Extended-release metoprolol succinate in chronic heart failure.
----A OBJECTIVE: To review the pharmacology, pharmacokinetics, efficacy, and tolerability of extended-release (ER) metoprolol succinate and its role in the management of chronic heart failure. DATA SOURCES: A MEDLINE search of English-language literature (1990-October 2002) was conducted using congestive heart failure and metoprolol CR/XL or metoprolol CR/ZOK as search terms to identify pertinent studies. STUDY SELECTION/DATA EXTRACTION: All of the articles identified from the data sources were evaluated, with priority given to randomized, double-blind, placebo-controlled studies. DATA SYNTHESIS: ER metoprolol succinate is a controlled-release tablet designed to produce even and consistent beta(1)-blockade throughout the 24-hour dosing interval, with less fluctuation in metoprolol plasma concentrations compared with immediate-release metoprolol. Three randomized, double-blind, placebo-controlled trials have evaluated the efficacy of ER metoprolol succinate in the treatment of patients with chronic heart failure. The MERIT-HF (Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure) study, the largest of these trials and the largest randomized mortality trial with beta-blockers in heart failure to date, demonstrated that ER metoprolol succinate reduced the relative risk of all-cause mortality by 34% versus placebo. Furthermore, the relative risk of the combined endpoint of mortality plus all-cause hospitalizations was reduced by 19% and sudden death was reduced by 41%. The benefits of therapy were evident in various patient subgroups, including elderly patients and those with diabetes mellitus. ER metoprolol succinate was generally well tolerated, with a similar proportion of patients discontinuing therapy due to adverse events relative to placebo (9.8% and 11.7%, respectively). CONCLUSIONS: ER metoprolol succinate therapy provides substantial mortality and morbidity benefits in patients with New York Heart Association class II and III heart failure who are stabilized on angiotensin-converting enzyme inhibitors and diuretics. ER metoprolol succinate is administered once daily, is well tolerated, and provides consistent beta(1)-blockade over the 24-hour dosing interval.
----P Journal_Article Review Review__Tutorial 
----M M_Delayed-Action_Preparations_MeSH S_adverse_effects_MeSH Delayed-Action_Preparations_adverse_effects_MeSH S_pharmacokinetics_MeSH Delayed-Action_Preparations_pharmacokinetics_MeSH S_pharmacology_MeSH Delayed-Action_Preparations_pharmacology_MeSH S_therapeutic_use_MeSH Delayed-Action_Preparations_therapeutic_use_MeSH M_Drug_Interactions_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_pharmacokinetics_MeSH Metoprolol_pharmacokinetics_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12709465
----K 3
----T Principal results of the Controlled Onset Verapamil Investigation of Cardiovascular End Points (CONVINCE) trial.
----A CONTEXT: Hypertensive patients are often given a calcium antagonist to reduce cardiovascular disease risk, but the benefit compared with other drug classes is controversial. OBJECTIVE: To determine whether initial therapy with controlled-onset extended-release (COER) verapamil is equivalent to a physician's choice of atenolol or hydrochlorothiazide in preventing cardiovascular disease. DESIGN, SETTING, AND PARTICIPANTS: Double-blind, randomized clinical trial conducted at 661 centers in 15 countries. A total of 16 602 participants diagnosed as having hypertension and who had 1 or more additional risk factors for cardiovascular disease were enrolled between September 1996 and December 1998 and followed up until December 31, 2000. After a mean of 3 years of follow-up, the sponsor closed the study before unblinding the results. INTERVENTION: Initially, 8241 participants received 180 mg of COER verapamil and 8361 received either 50 mg of atenolol or 12.5 mg of hydrochlorothiazide. Other drugs (eg, diuretic, beta-blocker, or an angiotensin-converting enzyme inhibitor) could be added in specified sequence if needed. MAIN OUTCOME MEASURES: First occurrence of stroke, myocardial infarction, or cardiovascular disease-related death. RESULTS: Systolic and diastolic blood pressure were reduced by 13.6 mm Hg and 7.8 mm Hg for participants assigned to the COER verapamil group and by 13.5 and 7.1 mm Hg for partcipants assigned to the atenolol or hydrochlorothiazide group. There were 364 primary cardiovascular disease-related events that occurred in the COER verapamil group vs 365 in atenolol or hydrochlorothiazide group (hazard ratio [HR], 1.02; 95% confidence interval [CI], 0.88-1.18; P =.77). For fatal or nonfatal stroke, the HR was 1.15 (95% CI, 0.90-1.48); for fatal or nonfatal myocardial infarction, 0.82 (95% CI, 0.65-1.03); and for cardiovascular disease-related death, 1.09 (95% CI, 0.87-1.37). The HR was 1.05 (95% CI, 0.95-1.16) for any prespecified cardiovascular disease-related event and 1.08 (95% CI, 0.93-1.26) for all-cause mortality. Nonstroke hemorrhage was more common with participants in the COER-verapamil group (n = 118) compared with the atenolol or hydrochlorothiazide group (n = 79) (HR, 1.54 [95% CI, 1.16-2.04]; P =.003). More cardiovascular disease-related events occurred between 6 AM and noon in both the COER verapamil (99/277) and atenolol or hydrochlorothiazide (88/274) groups; HR, 1.15 (95% CI, 0.86-1.53). CONCLUSIONS: The CONVINCE trial did not demonstrate equivalence of a COER verapamil-based antihypertensive regimen compared with a regimen beginning with a diuretic or beta-blocker. When considered in the context of other trials of calcium antagonists, these data indicate that the effectiveness of calcium-channel therapy in reducing cardiovascular disease is similar but not better than diuretic or beta-blocker treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cerebrovascular_Accident_MeSH S_mortality_MeSH Cerebrovascular_Accident_mortality_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Delayed-Action_Preparations_MeSH M_Diabetes_Mellitus_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Risk_Factors_MeSH M_Smoking_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12710862
----K 5
----T Prevention and treatment of diabetic nephropathy in older patients.
----A Renal disease in older diabetic patients is costly in terms of morbidity, mortality and expenditure. Therefore, prevention and treatment of diabetic nephropathy has become a prominent goal in the treatment of patients with diabetes mellitus. Preventive treatment should begin no later than at the stage of microalbuminuria, and regular screening for microalbuminuria is recommended for all patients with diabetes, irrespective of age. Improved metabolic control has been demonstrated to lower urinary albumin excretion. Target glycosylated haemoglobin levels should be below 7%, or 1% above the upper limit of normal of non-diabetic subjects. The use of an intensified treatment regimen is recommended. Insulin therapy has no adverse effects on renal indexes. To preserve renal function in older diabetic patients, blood pressure should be kept at or below 130/80 mm Hg. Treatment with ACE inhibitors or angiotensin II receptor antagonists (angiotensin II receptor blockers; ARBs) is superior to other pharmacological therapy, and should be initiated as first-line treatment. Most of the calcium channel antagonists have been found to increase or to have no effect on microalbuminuria despite blood pressure reduction. Moreover, there is substantial controversy as to whether they may be associated with increased cardiovascular morbidity. Non-dihydropyridine derivatives and calcium channel antagonists, such as nitrendipine, may be nephroprotective and have favourable effects on patients outcomes. A renoprotective action of diuretics may be confined to indapamide. Although beta-adrenoreceptor blockers are effective antihypertensive agents, they may not adequately preserve kidney function in older diabetic patients. However, as add-on treatment to ACE inhibitors or ARBs, they are particularly beneficial in nephropathic patients at risk of cardiovascular disease or with arrhythmias, in whom they may prove life-saving.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Albuminuria_MeSH S_prevention_&_control_MeSH Albuminuria_prevention_&_control_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Blood_Glucose_MeSH S_metabolism_MeSH Blood_Glucose_metabolism_MeSH M_Clinical_Trials_MeSH M_Diabetic_Nephropathies_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH S_prevention_&_control_MeSH Diabetic_Nephropathies_prevention_&_control_MeSH S_therapy_MeSH Diabetic_Nephropathies_therapy_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Obesity_MeSH S_therapy_MeSH Obesity_therapy_MeSH 
****** 12713106
----K 5
----T Childhood glaucoma.
----A The childhood glaucomas represent of variety of glaucoma subtypes that can cause serious and permanent visual damage. Early detection and treatment of infantile glaucoma is essential to preserve vision. The clinical signs and symptoms of infantile glaucoma are recognizable by nonophthalmologists but may be confused with other common clinical entities. Surgical and occasionally medical interventions can control raised intraocular pressure and thus prevent permanent glaucoma damage to the eye. Amblyopia is a common reason for permanent visual loss in this disease and needs to be treated aggressively as well.
----P Journal_Article Review Review__Tutorial 
----M M_Child_MeSH M_Diagnosis__Differential_MeSH P_Glaucoma_MeSH S_diagnosis_MeSH Glaucoma_diagnosis_MeSH S_physiopathology_MeSH Glaucoma_physiopathology_MeSH S_therapy_MeSH Glaucoma_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Optic_Nerve_Diseases_MeSH S_etiology_MeSH Optic_Nerve_Diseases_etiology_MeSH M_Trabeculectomy_MeSH 
****** 12714146
----K 5
----T Meta-analysis of corticosteroid treatment in acute myocardial infarction.
----A Acute and chronic inflammation play a central role in the pathophysiology of atherosclerosis. Corticosteroids are the gold standard anti-inflammatory agent and may have a role in treating acute myocardial infarction. However, concern exists regarding the potential for impaired wound healing and wall thinning. The MEDLINE and PreMEDLINE databases were searched for articles from 1966 through May 2002. A total of 186 articles and 16 English-language publications were identified. A meta-analysis of mortality in controlled trials was performed. Sensitivity analyses and 2 tests for publication bias were used to test the robustness of the results. Sixteen studies involving 3,793 patients were reviewed. Most studies were small (<100 patients) and revealed conflicting efficacy using surrogate outcome measures, such as infarct size. No clear association with myocardial rupture was observed. Meta-analysis of 11 controlled trials (2,646 patients) revealed a 26% decrease in mortality with corticosteroids (odds ratio 0.74, 95% confidence interval [CI] 0.59 to 0.94; p = 0.015). Sensitivity analyses limited to large studies and randomized controlled trials revealed odds ratios of 0.76 (95% CI 0.53 to 1.09) and 0.95 (95% CI 0.72 to 1.26), respectively. Two tests revealed no evidence for publication bias. Thus, the review of available clinical studies demonstrated no harm and a possible mortality benefit of corticosteroids in acute myocardial infarction.
----P Journal_Article Meta-Analysis 
----M M_Adrenal_Cortex_Hormones_MeSH S_therapeutic_use_MeSH Adrenal_Cortex_Hormones_therapeutic_use_MeSH M_Anti-Inflammatory_Agents_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Female_MeSH M_Heart_Rupture__Post-Infarction_MeSH M_Human_MeSH M_Male_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Odds_Ratio_MeSH M_Proportional_Hazards_Models_MeSH M_Publication_Bias_MeSH M_Randomized_Controlled_Trials_MeSH M_Steroids_MeSH 
****** 12714402
----K 3
----T Unoprostone as adjunctive therapy to timolol: a double masked randomised study versus brimonidine and dorzolamide.
----A AIMS: To compare the safety and efficacy of unoprostone, brimonidine, and dorzolamide as adjunctive therapy to timolol in patients with primary open angle glaucoma or ocular hypertension. METHODS: This was a randomised, double masked, parallel group, multicentre (14) study. After using timolol maleate 0.5% monotherapy twice a day for 2 weeks, patients (n = 146) with an early morning intraocular pressure (IOP) between 22 and 28 mm Hg, inclusively, received unoprostone isopropyl 0.15% (n = 50), brimonidine tartrate 0.2% (n = 48), or dorzolamide hydrochloride 2.0% (n = 48) twice daily as adjunctive therapy to timolol maleate 0.5% for another 12 weeks. Safety was based on comprehensive ophthalmic examinations, adverse events, and vital signs. Efficacy was based on mean change from baseline in the 8 hour diurnal IOP at week 12. Baseline was defined as values obtained after 2 weeks of timolol monotherapy. RESULTS: Each drug was safe and well tolerated. Burning/stinging was the most common treatment emergent adverse event. No clinically relevant changes from baseline were observed for any ophthalmic examination or vital signs. At week 12, each adjunctive therapy produced statistically significant (p<0.001) reductions from timolol treated baseline in the mean 8 hour diurnal IOP (-2.7 mm Hg, unoprostone; -2.8 mm Hg, brimonidine; -3.1 mm Hg, dorzolamide). The extent of IOP reduction did not differ significantly between unoprostone and either brimonidine (p = 0.154) or dorzolamide (p = 0.101). CONCLUSION: Unoprostone was safe and well tolerated and provided a clinically and statistically significant additional reduction in IOP when added to stable monotherapy with timolol. Furthermore, unoprostone was not significantly different from brimonidine and dorzolamide as adjunctive therapy to timolol.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Chemotherapy__Adjuvant_MeSH S_methods_MeSH Chemotherapy__Adjuvant_methods_MeSH M_Dinoprost_MeSH S_adverse_effects_MeSH Dinoprost_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Dinoprost_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Dinoprost_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Quinoxalines_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Sulfonamides_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 12713682
----K 5
----T Cardiovascular effects of selective serotonin reuptake inhibitors and other novel antidepressants.
----A This paper reviews the current knowledge of cardiovascular effects of the most commonly used novel antidepressants and their possible interactions with cardiovascular medications. The literature was reviewed through Medline 1980-2001. Materials were located by using terms such as SSRIs, individual names of novel antidepressants matched with terms like cardiovascular effects, cardiovascular diseases, cardiovascular risk factors, etc. Drug compendiums from 1998-2001 and some psychopharmacology texts were also used. The article focuses on the cardiovascular effects of the newer antidepressants, their use in patients with cardiovascular disease, and interactions with various commonly used cardiovascular drugs.
----P Journal_Article Review Review__Tutorial 
----M M_Antidepressive_Agents_MeSH S_pharmacology_MeSH Antidepressive_Agents_pharmacology_MeSH M_Cardiovascular_System_MeSH S_drug_effects_MeSH Cardiovascular_System_drug_effects_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_pharmacology_MeSH Serotonin_Uptake_Inhibitors_pharmacology_MeSH 
****** 12714973
----K 5
----T Shifting trends in the pharmacologic treatment of hypertension in a Nigerian tertiary hospital: a real-world evaluation of the efficacy, safety, rationality and pharmaco-economics of old and newer antihypertensive drugs.
----A The current prescription patterns for essential hypertension and the efficacy, safety, tolerability and cost-effectiveness of the newer antihypertensive drugs were evaluated in Nigerian patients. The findings were compared with that of a previous study conducted in the same tertiary hospital 10 years earlier. A cross-sectional evaluation of blood pressure (BP) control in a hypertension clinic was undertaken among 150 Nigerian patients aged 61 +/- 12 years (55% females), with a duration of treatment on a particular drug class or combination of 9 +/- 3 months. The initial blood pressure was 176 +/- 20/108 +/- 11 mmHg and 22% of the patient had concurrent diabetes mellitus. Thiazide diuretics (D) alone or in combination remained the most commonly prescribed drugs in 56% of all patients. There were significant increases in the prescriptions of calcium channel blockers (CCBs) (51%), P < 0.0001, and ACE-inhibitors (ACEIs) (24%), P < 0.0001, but a slight reduction in the use of methyldopa, and fixed drug combinations (P < 0.01) compared to the previous study. The fall in systolic blood pressure on D (r = 0.65, P < 0.001) or CCB (r = 0.48, P < 0.02) was significantly correlated with the initial systolic blood pressure, but not age. More patients achieved normotension BP < 140/90 mmHg on CCB monotherapy (71%), than D monotherapy (56%). Combination therapy with ACEIs + D or methyldopa+thiazides normalized BP in 63 and 68%, respectively. Pulse pressure, a surrogate marker for cardiovascular complications and mortality in essential hypertension, was significantly reduced (P < 0.01) equally by all treatments, with 95% confidence intervals ranging from -28 to -1 mmHg. However, hypertensive-diabetic (HT-DM) patients (n = 33) exhibited no significant change in pulse pressure in response to treatment. Adverse drug reactions that occurred in 11% were impotence or postural dizziness with D, headache and pitting oedema with CCB, and dry cough with ACEI. Pharmaco-economic comparison of the drug classes revealed that for every US dollar (dollar) spent per month, the percentage of treated patients attaining normotension was 18.6 for D, 4.73 for CCB, 3.5 for ACEI + D and 13.6 for methyldopa + thiazides. A combination of ACEI + CCB or D was the preferred treatment for hypertensive-diabetic Nigerians, but only 24% attained a BP < 130/85 mmHg. These results demonstrate a shift in trend to a more rational and efficacious treatment of hypertension over a 10 year period. This may be associated, at least in part, with the intensive and continuous education of the prescribers in rational drug use and the introduction of a hospital formulary. Methyldopa is still a highly efficacious and cost-effective drug in this population. Black HT-DM Africans still constitute a subgroup who not only require more and costlier antihypertensive drugs, but whose BP control is suboptimal, and exhibit a poor therapeutic response to other risk factors (pulse pressure) that constitute a continuing risk for cardiovascular mortality.
----P Evaluation_Studies Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_economics_MeSH Antihypertensive_Agents_economics_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Comorbidity_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH S_economics_MeSH Cost-Benefit_Analysis_economics_MeSH M_Cross-Sectional_Studies_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH S_physiology_MeSH Diastole_physiology_MeSH M_Diuretics__Thiazide_MeSH S_economics_MeSH Diuretics__Thiazide_economics_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Echocardiography_MeSH M_Economics__Pharmaceutical_MeSH S_trends_MeSH Economics__Pharmaceutical_trends_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Hospitals__University_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nigeria_MeSH S_epidemiology_MeSH Nigeria_epidemiology_MeSH M_Predictive_Value_of_Tests_MeSH M_Risk_Factors_MeSH M_Severity_of_Illness_Index_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH S_physiology_MeSH Systole_physiology_MeSH M_Treatment_Outcome_MeSH 
****** 12715904
----K 5
----T Congenital long QT syndrome: 50 years of electrophysiological research from cell to bedside.
----A Congenital long QT syndrome (LQTS) is a group of ion channel disorders of ventricular myocytes due to genetic mutations. The main symptoms of LQTS are pre-syncopal or syncopal attacks and cardiac arrest. Anti-adrenergic therapy with beta-blockers has been the mainstay of treatment. Left cardiac sympathectomy has also been used as an alternative in those in whom beta-blockers failed. ICDs are highly effective in preventing mortality and should be the first choice of therapy for those with cardiac arrest as the first symptom or those with LQT3 genotype not responding to anti-adrenergic therapy alone. Research on new therapeutic options, specifically those targeting at defective genes or mutant ion channels, may provide more effective treatment for this rare but potentially fatal electrophysiological disorder.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Cardiac_Pacing__Artificial_MeSH M_Defibrillators__Implantable_MeSH M_Electrocardiography_MeSH M_Electrophysiologic_Techniques__Cardiac_MeSH M_Heart_Conduction_System_MeSH S_drug_effects_MeSH Heart_Conduction_System_drug_effects_MeSH M_Human_MeSH M_Long_QT_Syndrome_MeSH S_congenital_MeSH Long_QT_Syndrome_congenital_MeSH S_drug_therapy_MeSH Long_QT_Syndrome_drug_therapy_MeSH S_physiopathology_MeSH Long_QT_Syndrome_physiopathology_MeSH S_therapy_MeSH Long_QT_Syndrome_therapy_MeSH 
****** 12716219
----K 5
----T Neurocardiogenic syncope in children : current concepts in diagnosis and management.
----A A wide variety of pharmacologic agents are currently used for the prevention of recurrent neurocardiogenic syncope in children and adolescents. Significant advances in the understanding of this syncopal disorder have occurred in the past decade, and the list of medications recommended has changed, reflecting the evolving understanding of the pathophysiology and development of agents with enhanced efficacy and fewer adverse effects. Clinicians have few randomized controlled trials available to guide their decisions about treating neurocardiogenic syncope, and even fewer when it comes to medications targeting the pediatric population. At the present time, beta-adrenergic receptor blockers, fludrocortisone, and also specific serotonin reuptake inhibitors and midodrine, appear to be favored treatment options. Ideally, specific therapy would be tailored to specific pathophysiologic mechanisms. Unfortunately, at present, specific treatments based on those abnormalities have not been identified.
----P Journal_Article Review Review__Tutorial 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Inflammatory_Agents_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents_therapeutic_use_MeSH M_Child_MeSH M_Fludrocortisone_MeSH S_therapeutic_use_MeSH Fludrocortisone_therapeutic_use_MeSH M_Human_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH P_Syncope__Vasovagal_MeSH S_diagnosis_MeSH Syncope__Vasovagal_diagnosis_MeSH S_drug_therapy_MeSH Syncope__Vasovagal_drug_therapy_MeSH S_etiology_MeSH Syncope__Vasovagal_etiology_MeSH 
****** 12723015
----K I
----T Adjunctive sympathoplegic therapy to ACE inhibition in Blacks with congestive heart failure: a comparison of alpha-1 with beta-1 blockade on exercise tolerance and cardiac sympathovagal reflex activity.
----A OBJECTIVES: Congestive heart failure (CHF) is characterized by an initial compensatory, but subsequently deleterious, activation of both the renin-angiotensin (RAS) and the sympathetic nervous system (SNS). Incomplete suppression of the SNS may contribute to the residual mortality during optimal ACE inhibitor therapy in CHF. Carvedilol, a mixed alpha and beta-blocker with antioxidant properties, and other pure beta-adrenoceptor blockers reduce morbidity and mortality in Caucasians with CHF. However, beta-blocker monotherapy is of poor efficacy in Blacks with essential hypertension or in the treatment of glaucoma. The efficacy of beta-blockers in the treatment of African Americans with congestive heart failure is a controversial issue with conflicting findings. The aims of the present study were to examine and compare the cardiovascular, autonomic, and clinical effects of additional alpha-1, or beta-1 blockade in ACE-inhibitor treated Black patients with moderate to severe CHF. METHODS: Twenty-eight Nigerian patients with chronic CHF stabilized on digoxin and diuretics, were randomized to 3 groups of similar demographics according to a single blind, parallel group design. The patients were aged 53 +/- 6 years, and comprised 14 men and 14 women, with a mean cardiothoracic ratio of 0.66 +/- 0.03, and ejection fraction of 0.38 +/- 0.10, 60% hypertensive etiology. Group 1 patients received 5 mg enalapril alone, group 2 received 5 mg enalapril + 1 mg prazosin, and group 3 received 5 mg enalapril + 50 mg atenolol. All medication was taken daily for 4 weeks. Blood pressure, heart rate, pressure rate product, 6-minute walk test, NYHA class, and cardiac autonomic reflexes were measured at baseline and again at 2 and 4 weeks of treatment. Two-way repeated measures ANOVA, and a one-way ANOVA were used in data analysis. RESULTS: The 3 treatments caused significant (P<.001 ANOVA) and similar improvements for the NYHA class (-1.0 to -1.6), and increased the 6-minute distance covered (+130 m to +205 m). Although no treatment differences were observed, a trend suggesting a greater improvement with enalapril + atenolol became apparent. By the fourth week, the sympathoplegic treatments, enalapril + atenolol, and enalapril + prazosin, caused significant reductions in the pressure rate product (-3726 +/- 1885 mm Hg x beats/min; -3498 +/- 396 mm Hg beats/min, respectively), (compared to enalapril alone (-1349 +/- 894 mm Hg x beats/min) (P<.001 ANOVA). During the Valsalva maneuver, the phase IV bradycardia were significantly greater after treatment with enalapril + atenolol (944 +/- 66 msec) or with enalapril + prazosin (825 +/- 48 msec), compared to enalapril alone (760 +/- 45 msec) (P<.001 ANOVA). The phase II Valsalva tachycardia were similar between treatments. The respiratory sinus arrhythmia ratio increased significantly (P<.005 ANOVA) and equally on all treatments. However, the pressor and chronotropic responses to forearm isometric handgrip increased significantly on the enalapril + prazosin combination (P<.02), compared to the other treatments. CONCLUSIONS: Our findings demonstrated not only the safety of providing additional therapy with alpha-1 or beta-1 receptor blockade concurrent with ACE inhibition in Blacks with CHF, but also the resultant improvement in exercise tolerance and NYHA class. Compared to using ACE inhibition alone, the combined therapies caused a marked reduction in the pressure rate product, an index of myocardial oxygen consumption, and a greater enhancement of cardiac parasympathetic activity. Selective beta-1 blockade caused a greater enhancement of central baroreceptor vagal activity compared to alpha-1 blockade. Conversely, the pressor and chronotropic abnormalities during forearm isometric handgrip in CHF, were normalized by alpha-1, but not beta-1, blockade. Thus, the combined reflex cardiac vagal augmentation following selective beta-1 blockade, and the hemodynamic effects of alpha-1 antagonism with concurrent ACE inhibition, may be of major therapeutic and prognostic benefit in Blacks with non-ischemic (hypertensive) CHF stabilized on digoxin and diuretics.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_African_Continental_Ancestry_Group_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nigeria_MeSH S_ethnology_MeSH Nigeria_ethnology_MeSH M_Prazosin_MeSH S_therapeutic_use_MeSH Prazosin_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Respiration_MeSH S_drug_effects_MeSH Respiration_drug_effects_MeSH M_Single-Blind_Method_MeSH 
****** 12723027
----K 5
----T For the patient. New treatments for heart failure in Black people. Adjunctive sympathoplegic therapy to ACE inhibition in Blacks with congestive heart failure: a comparison of alpha-1 with beta-1 blockade on exercise tolerance and cardiac sympathovagal reflex activity.
----A 
----P Comment Journal_Article Patient_Education_Handout 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_African_Continental_Ancestry_Group_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ethnology_MeSH Hypertension_ethnology_MeSH M_Nigeria_MeSH S_epidemiology_MeSH Nigeria_epidemiology_MeSH M_Prazosin_MeSH S_therapeutic_use_MeSH Prazosin_therapeutic_use_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH 
****** 12720497
----K 5
----T Implications of the LIFE trial.
----A The recent Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study was conducted in patients with essential hypertension with electrocardiogram evidence of left ventricular hypertrophy. This showed that losartan compared to atenolol resulted in a significant reduction in the primary endpoint of cardiovascular morbidity and mortality, as well as a greater reduction in electrocardiographically-defined left ventricular hypertrophy. Importantly, this was despite a mean blood pressure reduction which was similar in both groups. Furthermore, the atenolol arm was associated with higher incidence of newly diagnosed diabetics. The LIFE study has firmly confirmed a place for losartan (and other angiotensin receptor blockers) in the management of hypertension. Losartan has also been shown to be effective in diabetics and in patients with atrial fibrillation, as well as in left ventricular hypertrophy regression. This trial also raises the possibility that beta-blockers should perhaps not be used as first-line monotherapy.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12720498
----K 5
----T What are the best first-line antihypertensives: answers and more questions from the ALLHAT study.
----A The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is considered the largest trial of antihypertensive therapy conducted to date. It compared the cardiovascular effects of three more recently developed classes of antihypertensive agents to those of a diuretic in an attempt to identify which of these drugs should be the recommended first-line agent for the treatment of hypertension. In this report the paper is discussed with the significance and the clinical implications of the results contrasted with existing evidence in hypertension research. Additionally, further questions raised by the ALLHAT study are explored with ongoing studies, and future directions with which to answer these emerging new questions are outlined.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12723726
----K 5
----T Endothelial dysfunction and cardiovascular disease: the promise of blocking the renin-angiotensin system.
----A As a crucial regulator of vascular function the endothelium balances a complex range of actions. Accordingly, damage to the endothelium often precedes the development of clinically manifest vascular disease. This review surveys our current understanding of risk factors involved in causing endothelial damage and the effects of lifestyle changes and pharmacotherapy on the endothelium. Our developing understanding of the intricacies of endothelial function and the effects of risk factors may aid in optimising cardiovascular prevention as well as therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetic_Angiopathies_MeSH S_complications_MeSH Diabetic_Angiopathies_complications_MeSH P_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiology_MeSH Endothelium__Vascular_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Lipids_MeSH S_blood_MeSH Lipids_blood_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH S_therapeutic_use_MeSH Receptors__Angiotensin_therapeutic_use_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH M_Risk_Factors_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH S_physiology_MeSH Vasodilation_physiology_MeSH 
****** 12724485
----K 5
----T Management of drug and alcohol withdrawal.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH P_Alcoholism_MeSH M_Ambulatory_Care_MeSH M_Anti-Anxiety_Agents_MeSH S_therapeutic_use_MeSH Anti-Anxiety_Agents_therapeutic_use_MeSH M_Anticonvulsants_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Benzodiazepines_MeSH S_therapeutic_use_MeSH Benzodiazepines_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Narcotic_Antagonists_MeSH S_therapeutic_use_MeSH Narcotic_Antagonists_therapeutic_use_MeSH M_Narcotics_MeSH S_therapeutic_use_MeSH Narcotics_therapeutic_use_MeSH M_Physician's_Role_MeSH M_Substance_Withdrawal_Syndrome_MeSH S_drug_therapy_MeSH Substance_Withdrawal_Syndrome_drug_therapy_MeSH P_Substance-Related_Disorders_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12729241
----K 5
----T What to do if an initial antidepressant fails?
----A OBJECTIVE: To provide family physicians with practical ways of managing depressed patients responding insufficiently to initial antidepressant treatment. QUALITY OF EVIDENCE: A search of MEDLINE and relevant bibliographies showed most studies could be categorized as level III evidence. Few well controlled studies (eg, level I evidence) specify treatment of next choice in rigorously defined treatment-refractory depression (TRD). MAIN MESSAGE: Failure to achieve and sustain full symptom remission affects relatively few treated depressed patients. Most chronically depressed people are not absolutely resistant but are relatively resistant to treatment; they fail to achieve the goals of treatment because of improper diagnosis or insufficient treatment application. The literature on TRD has largely focused on medication strategies; fewer studies investigated psychosocial approaches. The best established augmentation strategies are lithium salts and triidothyronine (T3). Combination antidepressants have become clinical psychiatrists' preferred treatment, despite limited evidence. Electroconvulsive therapy (ECT) remains a feasible option for TRD, but response rates are poor among people with TRD. High relapse rates after ECT remain a serious and common clinical dilemma. CONCLUSION: Family physicians should familiarize themselves with some new strategies to modify inadequate response to initial antidepressant treatment.
----P Journal_Article Review Review__Tutorial 
----M M_Algorithms_MeSH M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Depressive_Disorder_MeSH S_diagnosis_MeSH Depressive_Disorder_diagnosis_MeSH S_drug_therapy_MeSH Depressive_Disorder_drug_therapy_MeSH S_therapy_MeSH Depressive_Disorder_therapy_MeSH M_Diagnosis__Differential_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Recurrence_MeSH P_Treatment_Failure_MeSH 
****** 12731424
----K 1
----T [Reduction of cardiovascular events with lorsartan? The LIFE Study]
----A 
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cerebral_Infarction_MeSH S_mortality_MeSH Cerebral_Infarction_mortality_MeSH S_prevention_&_control_MeSH Cerebral_Infarction_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Survival_Rate_MeSH M_Treatment_Outcome_MeSH 
****** 12695290
----K 4
----T Defibrillator Versus beta-Blockers for Unexplained Death in Thailand (DEBUT): a randomized clinical trial.
----A BACKGROUND: Sudden Unexplained Death Syndrome (SUDS) is the leading cause of death in young, healthy, Southeast Asian men. The role of an implantable cardioverter defibrillator (ICD) for mortality reduction in these patients remains unclear. METHODS AND RESULTS: The Defibrillator Versus beta-Blockers for Unexplained Death in Thailand (DEBUT) study is a randomized, clinical trial conducted in 2 phases (pilot study followed by the main trial) to compare the annual all-cause mortality rates among SUDS patients treated with beta-blockers versus that among those treated with an ICD. A total of 86 patients who were SUDS survivors and probable SUDS survivors were randomized to receive an ICD or propranolol (20 patients were in the pilot study and 66 were in the main trial). The primary end point was death from all causes. The secondary end point was recurrent ventricular tachycardia/ventricular fibrillation (VF) or cardiac arrest. During the 3-year follow-up period of the main trial, there were 4 deaths; all occurred in the beta-blocker group (P=0.02). Seven subjects in the ICD arm had recurrent VF, and all were effectively treated by the ICD. On the basis of the main trial results, the Data Safety Monitoring Board stopped the study. In total (both from the Pilot study and the main trial), there were 7 deaths (18%) in the beta-blocker group and no deaths in the ICD group, but there were a total of 12 ICD patients receiving ICD discharges due to recurrent VF. CONCLUSIONS: ICD treatment provides full protection from death related to primary VF in a SUDS population and is superior to beta-blockade treatment.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Arrhythmia_MeSH S_diagnosis_MeSH Arrhythmia_diagnosis_MeSH S_epidemiology_MeSH Arrhythmia_epidemiology_MeSH M_Comparative_Study_MeSH M_Death__Sudden_MeSH S_prevention_&_control_MeSH Death__Sudden_prevention_&_control_MeSH P_Defibrillators__Implantable_MeSH S_adverse_effects_MeSH Defibrillators__Implantable_adverse_effects_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH M_Syndrome_MeSH M_Thailand_MeSH S_epidemiology_MeSH Thailand_epidemiology_MeSH M_Ventricular_Fibrillation_MeSH S_epidemiology_MeSH Ventricular_Fibrillation_epidemiology_MeSH 
****** 12732798
----K 5
----T LIFE and ARBITER.
----A 
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Carotid_Artery_Diseases_MeSH S_drug_therapy_MeSH Carotid_Artery_Diseases_drug_therapy_MeSH M_Heptanoic_Acids_MeSH S_therapeutic_use_MeSH Heptanoic_Acids_therapeutic_use_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_drug_effects_MeSH Lipoproteins__LDL_Cholesterol_drug_effects_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Pravastatin_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH M_Pyrroles_MeSH S_therapeutic_use_MeSH Pyrroles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12732448
----K 5
----T A missense mutation in the CASQ2 gene is associated with autosomal-recessive catecholamine-induced polymorphic ventricular tachycardia.
----A Catecholamine-induced polymorphic ventricular tachycardia (CPVT), a rare disease that occurs in subjects without obvious organic heart disease, is characterized by episodes of syncope, seizures, or sudden death in response to physiologic or emotional stress. This report reviews evidence that a missense mutation in the CASQ2 gene is associated with autosomal-recessive CPVT.
----P Journal_Article Review Review__Tutorial 
----M M_Calsequestrin_MeSH S_genetics_MeSH Calsequestrin_genetics_MeSH M_Catecholamines_MeSH S_genetics_MeSH Catecholamines_genetics_MeSH M_Genes__Recessive_MeSH S_genetics_MeSH Genes__Recessive_genetics_MeSH M_Genetic_Predisposition_to_Disease_MeSH S_genetics_MeSH Genetic_Predisposition_to_Disease_genetics_MeSH M_Human_MeSH M_Mutation__Missense_MeSH S_genetics_MeSH Mutation__Missense_genetics_MeSH M_Polymorphism_(Genetics)_MeSH S_genetics_MeSH Polymorphism_(Genetics)_genetics_MeSH M_Tachycardia__Ventricular_MeSH S_genetics_MeSH Tachycardia__Ventricular_genetics_MeSH S_therapy_MeSH Tachycardia__Ventricular_therapy_MeSH 
****** 12735115
----K 5
----T Asthma in the elderly.
----A Asthma is common in the elderly population and the differences between younger and older asthmatics should be appreciated (Table 2). Asthma is frequently overlooked in the geriatric population. Objective measures of pulmonary function can aid in a prompt diagnosis and lead to effective treatment and improved quality of life. Because smoking is an important risk factor for asthma-like symptoms of wheezing, cough, and sputum production, asthma is frequently confused with COPD. When airflow obstruction is found, attempts to demonstrate reversibility can uncover an asthmatic component to the disease. In patients who have asthma symptoms and no airflow obstruction, methacholine testing is helpful. When a normal methacholine challenge is present, a diagnosis of asthma can be excluded and the physician can pursue other diagnostic considerations such as heart failure, chronic aspiration syndrome, pulmonary embolic disease, and carcinoma of the lung. The onset of wheezing, shortness of breath, and cough in an elderly patient is likely to cause concern. Although the adage "all that wheezes is not asthma" is true at any age, it is especially true in the elderly. Diagnosis based on objective measures is essential.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Anti-Inflammatory_Agents_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents_therapeutic_use_MeSH M_Asthma_MeSH S_diagnosis_MeSH Asthma_diagnosis_MeSH S_drug_therapy_MeSH Asthma_drug_therapy_MeSH S_epidemiology_MeSH Asthma_epidemiology_MeSH S_physiopathology_MeSH Asthma_physiopathology_MeSH M_Bronchial_Hyperreactivity_MeSH S_physiopathology_MeSH Bronchial_Hyperreactivity_physiopathology_MeSH M_Bronchodilator_Agents_MeSH S_therapeutic_use_MeSH Bronchodilator_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypersensitivity_MeSH S_epidemiology_MeSH Hypersensitivity_epidemiology_MeSH M_Incidence_MeSH M_Prognosis_MeSH M_Respiratory_Function_Tests_MeSH M_Steroids_MeSH M_Treatment_Outcome_MeSH 
****** 12735229
----K 5
----T Targeting sources of superoxide and increasing nitric oxide bioavailability in hypertension.
----A Overproduction of oxygen free radicals, which is mainly mediated by superoxide, occurs in human hypertension and a wide variety of animal models. There are several important enzymatic sources of superoxide production, including NADPH oxidase, xanthine oxidase and uncoupled nitric oxide synthase. Superoxide levels are also controlled through endogenous antioxidant systems and superoxide dismutase is the primary antioxidant in the vascular system. Strategies have therefore focused on combating hypertension and vascular disease through the inhibition of superoxide-generating enzymes, and scavenging superoxide. While results from animal studies are promising, no consensus has been reached on identifying a drug target for the reliable and effective treatment of oxidative stress in hypertension.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antioxidants_MeSH S_metabolism_MeSH Antioxidants_metabolism_MeSH M_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Enzyme_Inhibitors_therapeutic_use_MeSH M_Free_Radical_Scavengers_MeSH S_pharmacology_MeSH Free_Radical_Scavengers_pharmacology_MeSH S_therapeutic_use_MeSH Free_Radical_Scavengers_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Nitric_Oxide_MeSH S_metabolism_MeSH Nitric_Oxide_metabolism_MeSH M_Oxidative_Stress_MeSH M_Superoxide_Dismutase_MeSH S_biosynthesis_MeSH Superoxide_Dismutase_biosynthesis_MeSH S_metabolism_MeSH Superoxide_Dismutase_metabolism_MeSH 
****** 12735785
----K 5
----T Benefits and risks of pharmacological treatments for essential tremor.
----A Essential tremor can cause significant functional disability in some patients. The arms are the most common body part affected and cause the most functional disability. The treatment of essential tremor includes medications, surgical options and other forms of therapy. Presently there is no cure for essential tremor nor are there any medications that can slow the progression of tremor. Treatment for essential tremor is recommended if the tremor causes functional disability. If the tremor is disabling only during periods of stress and anxiety, propranolol and benzodiazepines can be used during those periods when the tremor causes functional disability. The currently available medications can improve tremor in approximately 50% of the patients. If the tremor is disabling, treatment should be initiated with either primidone or propranolol. If either primidone or propranolol do not provide adequate control of the tremor, then the medications can be used in combination. If patients experience adverse effects with propranolol, occasionally other beta-adrenoceptor antagonists (such as atenolol or metoprolol) can be used. If primidone and propranolol do not provide adequate control of tremor, occasionally the use of benzodiazepines (such as clonazepam) can provide benefit. Other medications that may be helpful include gabapentin or topiramate. If a patient has disabling head or voice tremor, botulinum toxin injections into the muscles may provide relief from the tremor. Botulinum toxin in the hand muscles for hand tremor can result in bothersome hand weakness and is not widely used. There are other medications that have been tried in essential tremor and have questionable efficacy. These drugs include carbonic anhydrase inhibitors (e.g. methazolamide), phenobarbital, calcium channel antagonists (e.g. nimodipine), isoniazid, clonidine, clozapine and mirtazapine. If the patient still has disabling tremor after medication trials, surgical options are usually considered. Surgical options include thalamotomy and deep brain stimulation of the thalamus. These surgical options provide adequate tremor control in approximately 90% of the patients. Surgical morbidity and mortality for these procedures is low. Deep brain stimulation and thalamotomy have been shown to have comparable efficacy but fewer complications have been reported with deep brain stimulation. In patients undergoing bilateral procedures deep brain stimulation of the thalamus is the procedure of choice to avoid adverse effects seen with bilateral ablative procedures. The use of medication and/or surgery can provide adequate tremor control in the majority of the patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_Agonists_MeSH S_pharmacology_MeSH Adrenergic_Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_Agonists_therapeutic_use_MeSH M_Anticonvulsants_MeSH S_pharmacology_MeSH Anticonvulsants_pharmacology_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Electric_Stimulation_Therapy_MeSH M_Essential_Tremor_MeSH S_drug_therapy_MeSH Essential_Tremor_drug_therapy_MeSH S_physiopathology_MeSH Essential_Tremor_physiopathology_MeSH S_surgery_MeSH Essential_Tremor_surgery_MeSH M_Human_MeSH M_Neuromuscular_Agents_MeSH S_pharmacology_MeSH Neuromuscular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Neuromuscular_Agents_therapeutic_use_MeSH M_Primidone_MeSH S_pharmacology_MeSH Primidone_pharmacology_MeSH S_therapeutic_use_MeSH Primidone_therapeutic_use_MeSH M_Risk_Assessment_MeSH 
****** 12736284
----K 5
----T Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 14-2003. A 73-year-old woman with pneumonia and progressive respiratory failure.
----A 
----P Case_Reports Clinical_Conference Journal_Article 
----M M_Aged_MeSH M_Biopsy_MeSH M_Bronchiolitis_Obliterans_Organizing_Pneumonia_MeSH S_complications_MeSH Bronchiolitis_Obliterans_Organizing_Pneumonia_complications_MeSH S_pathology_MeSH Bronchiolitis_Obliterans_Organizing_Pneumonia_pathology_MeSH S_radiography_MeSH Bronchiolitis_Obliterans_Organizing_Pneumonia_radiography_MeSH M_Diagnosis__Differential_MeSH M_Female_MeSH M_Human_MeSH M_Legionnaires'_Disease_MeSH S_diagnosis_MeSH Legionnaires'_Disease_diagnosis_MeSH M_Lung_MeSH S_pathology_MeSH Lung_pathology_MeSH S_radiography_MeSH Lung_radiography_MeSH M_Pneumonia_MeSH S_diagnosis_MeSH Pneumonia_diagnosis_MeSH M_Respiratory_Distress_Syndrome__Adult_MeSH S_etiology_MeSH Respiratory_Distress_Syndrome__Adult_etiology_MeSH S_pathology_MeSH Respiratory_Distress_Syndrome__Adult_pathology_MeSH S_radiography_MeSH Respiratory_Distress_Syndrome__Adult_radiography_MeSH M_Respiratory_Insufficiency_MeSH S_etiology_MeSH Respiratory_Insufficiency_etiology_MeSH 
****** 12737504
----K 3
----T Effects of betaxolol and flunarizine on visual fields and intraocular pressure in patients with migraine.
----A Fifty-one patients with migraine were divided into four groups to investigate the effects of topical betaxolol and systemic calcium channel blocker flunarizine on visual fields (VF) and intraocular pressure (IOP). The first group (Group 0) was followed with no medications, topical betaxolol (bid) was precribed to the second group (Group B), oral flunarizine (10 mg daily) was prescribed to the third group (Group F), and the last group (Group BF) was assigned for combined betaxolol and flunarizine treatment. After a mean follow-up time of 4.2 +/- 1.2 months (3-6 months), IOP measurements and VF tests were repeated. Group B and Group BF were found to be statistically different from the other groups in terms of IOP reduction and VF improvement according to mean deviation and corrected pattern standard deviation indices in the second examinations. On the other hand, Group F and Group BF differed from the other two groups considering the improvement in migrainous complaints. VF findings which are probably influenced by perfusion problems due to vasospastic mechanisms in migraineurs, improved following topical betaxolol treatment. However, systemic use of flunarizine--a calcium channel blocker--did not seem to be effective on visual fields although it had beneficial effects on migraine.
----P Journal_Article 
----M M_Adolescent_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Betaxolol_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Flunarizine_MeSH S_therapeutic_use_MeSH Flunarizine_therapeutic_use_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Visual_Fields_MeSH S_drug_effects_MeSH Visual_Fields_drug_effects_MeSH 
****** 12738555
----K 4
----T Influence of topical betaxolol and timolol on visual field in Japanese open-angle glaucoma patients.
----A PURPOSE: To assess the effects of topical betaxolol and timolol on the visual field in Japanese open-angle glaucoma (OAG) patients. METHODS: This study was a multicenter, 2-year, prospective, randomized and double-masked study. Tests using the Humphrey 30-2 perimeter program were conducted every 6 months and the data of 95 patients were analyzed using regression analysis. Estimated regression coefficients for mean deviation (MD), corrected pattern standard deviation (CPSD), and total deviation (TD) values clustered into 15 sectors were obtained for each treatment group. RESULTS: Estimated slopes (dB/year) for MD and CPSD showed no significant difference from zero in either group. However, in the betaxolol group, estimated slopes (dB/year) for two adjacent sectors in the inferior arcuate area were significantly positive (P =.0135,.0116) while in the timolol group, no significant difference from zero was seen in any of the sectors. IOP changes from baseline in the timolol group were greater than in the betaxolol group, although no statistical significance was seen at any of the examination times. CONCLUSION: MD and CPSD showed no significant change in either group. In the betaxolol group, however, a significant trend in improvement of visual field performance was seen in the inferior arcuate subfield. Timolol reduced IOP more effectively than betaxolol in OAG patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Betaxolol_MeSH S_administration_&_dosage_MeSH Betaxolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Betaxolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_ethnology_MeSH Glaucoma__Open-Angle_ethnology_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH S_physiology_MeSH Intraocular_Pressure_physiology_MeSH M_Japan_MeSH S_epidemiology_MeSH Japan_epidemiology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Visual_Fields_MeSH S_drug_effects_MeSH Visual_Fields_drug_effects_MeSH S_physiology_MeSH Visual_Fields_physiology_MeSH 
****** 12740551
----K 5
----T Atheroprotective effects of long-acting dihydropyridine-type calcium channel blockers: evidence from clinical trials and basic scientific research.
----A Atherosclerosis is a systemic disease that can ultimately lead to ischaemia and infarction in the heart, brain and peripheral vasculature. According to the "response to injury" hypothesis, endothelial dysfunction is the early event that allows penetration of lipids and inflammatory cells into the arterial wall, contributing to the development of the atherosclerotic lesion. Endothelial dysfunction is causally related to a variety of risk factors for atherosclerosis, including hyperlipidaemia and hypertension. Agents that restore endothelial function and NO bioavailability have beneficial anti-atherogenic activities and can improve cardiovascular outcomes; this has been observed with angiotensin-converting enzyme (ACE) inhibitors, statins and certain dihydropyridine-type calcium channel blockers (CCBs). In the Prospective Randomised Evaluation of the Vascular Effects of Norvasc Trial (PREVENT), the CCB amlodipine provided significant clinical benefits compared with placebo, including a marked reduction in cardiovascular morbidity and a reduction in the progression of carotid atherosclerosis. As these beneficial effects of amlodipine have not been observed with other dihydropyridine-type CCBs, it has been proposed that this agent has distinct anti-atherosclerotic properties related to its strong lipophilicity and membrane location. Experimental support for this hypothesis has been obtained from various in vitro and in vivo models of atherosclerosis. These findings support a broader therapeutic role for third-generation dihydropyridine-type CCBs in the treatment of atherosclerosis.
----P Journal_Article Review Review__Tutorial 
----M M_Arteriosclerosis_MeSH S_prevention_&_control_MeSH Arteriosclerosis_prevention_&_control_MeSH M_Calcium_Channel_Blockers_MeSH S_administration_&_dosage_MeSH Calcium_Channel_Blockers_administration_&_dosage_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Delayed-Action_Preparations_MeSH S_therapeutic_use_MeSH Delayed-Action_Preparations_therapeutic_use_MeSH M_Dihydropyridines_MeSH S_administration_&_dosage_MeSH Dihydropyridines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Dihydropyridines_therapeutic_use_MeSH M_Human_MeSH M_In_Vitro_MeSH M_Models__Cardiovascular_MeSH P_Randomized_Controlled_Trials_MeSH M_Time_Factors_MeSH 
****** 12740552
----K 5
----T Clinical trials: Evidence and unanswered questions--hypertension.
----A Since the pioneering publications of the Hypertension Detection and Follow-up Program (HDFP) and the Multiple Risk Factor Intervention Trial (MRFIT) in the late 1970s and early 1980s, it has become established that lowering blood pressure in high-risk patients is a highly effective form of primary prevention for stroke. Over the subsequent 25 years, over 30 large clinical trials have extended these initial observations to allow us to conclude that treatment of mild, moderate or severe hypertension, and isolated systolic hypertension in the elderly, all produce important absolute benefits. In addition, excellent specific evidence of benefit is now accumulating for certain groups of normotensive patients, including those with previous stroke, and those with established cardiovascular disease. Although the importance of vigorous antihypertensive therapy for the primary and secondary prevention of stroke is increasingly clear, a large number of unanswered questions remain. For example, while it is apparent that diuretics, beta-blockers, calcium channel blockers (CCBs) and angiotensin-converting enzyme (ACE) inhibitors are all effective antihypertensive agents, the question remains as to which drug, or combination of drugs, is best for which patients. The results of several ongoing comparative trials of different drug regimens, including the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), may elucidate this further.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH P_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH 
****** 12740554
----K 5
----T Blood pressure and lipid lowering in the prevention of stroke: a note to neurologists.
----A Stroke is the leading cause of adult disability and dependency in western society. Despite the determined efforts of basic science and clinical investigators, neuroprotective therapies for acute stroke have yet to be realised. Stroke prevention, therefore, remains the key route for reducing morbidity and mortality. Hypertension and hypercholesterolaemia are the most important modifiable risk factors for stroke. Several recent landmark studies have shown that lipid lowering with statins can reduce the risk of ischaemic stroke, as well as coronary heart disease. In addition, clinical trials evaluating the effects of blood pressure lowering have shown that antihypertensive agents such as angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers (CCBs) and angiotensin II receptor antagonists can reduce stroke risk. Accumulating evidence suggests certain antihypertensive agents such as CCBs might also prevent the formation and progression of carotid atheroma, independently of their blood-pressure-lowering effects. It follows that rigorous identification and targeting of high- risk or stroke-prone individuals for blood pressure and lipid-lowering interventions should be of practical importance to all physicians involved in the management of stroke.
----P Journal_Article Review Review__Tutorial 
----M M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH P_Cooperative_Behavior_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_therapy_MeSH Hyperlipidemia_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_therapy_MeSH Hypertension_therapy_MeSH P_Neurology_MeSH P_Physician's_Role_MeSH P_Physicians__Family_MeSH 
****** 12739989
----K 5
----T Current pharmacotherapy in the management of cirrhosis: focus on the hyperdynamic circulation.
----A Many major complications of hepatic cirrhosis relate to the development of a characteristic hyperdynamic circulatory state in these patients, irrespective of the underlying disease aetiology. Vasodilatation of the systemic and splanchnic circulations leads to a reduced total systemic vascular resistance, increased cardiac output and intense activation of neurohumoral vasoconstrictor systems including the sympathetic nervous system, renin-angiotensin system and vasopressin. Vasoconstriction of the renal and hepatic circulations contributes to the development of renal failure and portal hypertension, respectively. Current treatments that focus on amelioration of these circulatory derangements offer much promise, however, they are often limited by side effects in these patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Ascites_MeSH S_etiology_MeSH Ascites_etiology_MeSH S_physiopathology_MeSH Ascites_physiopathology_MeSH S_therapy_MeSH Ascites_therapy_MeSH M_Blood_Circulation_MeSH S_physiology_MeSH Blood_Circulation_physiology_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH P_Expert_Testimony_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Kidney_Failure_MeSH S_drug_therapy_MeSH Kidney_Failure_drug_therapy_MeSH S_physiopathology_MeSH Kidney_Failure_physiopathology_MeSH M_Liver_Circulation_MeSH S_drug_effects_MeSH Liver_Circulation_drug_effects_MeSH P_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_drug_therapy_MeSH Liver_Cirrhosis_drug_therapy_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Male_MeSH 
****** 12742278
----K I
----T Carvedilol increases two-year survivalin dialysis patients with dilated cardiomyopathy: a prospective, placebo-controlled trial.
----A OBJECTIVES: We sought to evaluate the effects of carvedilol on mortality and morbidity in dialysis patients with dilated cardiomyopathy. BACKGROUND: Several lines of evidence support the concept that therapy with beta-blocking agents reduces morbidity and mortality in patients with congestive heart failure (HF), but the demonstration of such a survival benefit in dialysis patients with dilated cardiomyopathy is still lacking. METHODS: A total of 114 dialysis patients with dilated cardiomyopathy were randomized to receive either carvedilol or placebo in addition to standard therapy. A first analysis was performed at one year and was followed by an additional follow-up period of 12 months. RESULTS: Two-year echocardiographic data revealed a significant attenuation of pathologic remodeling, with smaller cavity diameters and higher ejection fractions in the active treatment group than in the placebo group. At two years, 51.7% of the patients died in the carvedilol group, compared with 73.2% in the placebo group (p < 0.01). Furthermore, there were significantly fewer cardiovascular deaths (29.3%) and hospital admissions (34.5%) among patients receiving carvedilol than among those receiving a placebo (67.9% and 58.9%, respectively; p < 0.00001). The exploratory analyses revealed that fatal myocardial infarctions, fatal strokes, and hospital admissions for worsening HF were lower in the carvedilol group than in the placebo group. A reduction in sudden deaths and pump-failure deaths was also observed, though it did not reach statistical significance. CONCLUSIONS: Carvedilol reduced morbidity and mortality in dialysis patients with dilated cardiomyopathy. These data suggest the use of carvedilol in all dialysis patients with chronic HF.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiomyopathy__Congestive_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_etiology_MeSH Cardiomyopathy__Congestive_etiology_MeSH S_mortality_MeSH Cardiomyopathy__Congestive_mortality_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Kidney_Diseases_MeSH S_complications_MeSH Kidney_Diseases_complications_MeSH S_mortality_MeSH Kidney_Diseases_mortality_MeSH S_therapy_MeSH Kidney_Diseases_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Renal_Dialysis_MeSH S_mortality_MeSH Renal_Dialysis_mortality_MeSH M_Survival_Rate_MeSH M_Time_Factors_MeSH 
****** 12742290
----K 5
----T Anti-ischemic properties of calcium-channel blockers: lessons from cardiac surgery.
----A 
----P Comment Editorial 
----M M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiac_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiac_Surgical_Procedures_adverse_effects_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Myocardial_Ischemia_MeSH S_etiology_MeSH Myocardial_Ischemia_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Ischemia_prevention_&_control_MeSH P_Postoperative_Complications_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12742294
----K 5
----T Efficacy of angiotensin-converting enzyme inhibitors and beta-blockers in the management of left ventricular systolic dysfunction according to race, gender, and diabetic status: a meta-analysis of major clinical trials.
----A OBJECTIVES: This study sought to assess the effect of angiotensin-converting enzyme (ACE) inhibitors and beta-blockers on all-cause mortality in patients with left ventricular (LV) systolic dysfunction according to gender, race, and the presence of diabetes. BACKGROUND: Major randomized clinical trials have established that ACE inhibitors and beta-blockers have life-saving benefits in patients with LV systolic dysfunction. Most patients enrolled in these trials were Caucasian men. Whether an equal effect is achieved in women, non-Caucasians, and patients with major comorbidities has not been established. METHODS: The authors performed a meta-analysis of published and individual patient data from the 12 largest randomized clinical trials of ACE inhibitors and beta-blockers to produce random effects estimates of mortality for subgroups. RESULTS: Data support beneficial reductions in all-cause mortality for the use of beta-blockers in men and women, the use of ACE inhibitors and some beta-blockers in black and white patients, and the use of ACE inhibitors and beta-blockers in patients with or without diabetes. Women with symptomatic LV systolic dysfunction probably benefit from ACE inhibitors, but women with asymptomatic LV systolic dysfunction may not have reduced mortality when treated with ACE inhibitors (pooled relative risk = 0.96; 95% confidence interval: 0.75 to 1.22). The pooled estimate of three beta-blocker studies supports a beneficial effect in black patients with heart failure, but one study assessing bucindolol reported a nonsignificant increase in mortality. CONCLUSIONS: Angiotensin-converting enzyme inhibitors and beta-blockers provide life-saving benefits in most of the subpopulations assessed. Women with asymptomatic LV systolic dysfunction may not achieve a mortality benefit when treated with ACE inhibitors.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Continental_Population_Groups_MeSH S_genetics_MeSH Continental_Population_Groups_genetics_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH S_genetics_MeSH Diabetes_Mellitus_genetics_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Randomized_Controlled_Trials_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH P_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Survival_Rate_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_epidemiology_MeSH Ventricular_Dysfunction__Left_epidemiology_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH 
****** 12745200
----K 3
----T Antihypertensive therapy with verapamil SR plus trandolapril versus atenolol plus chlorthalidone on glycemic control.
----A BACKGROUND: There is evidence that diuretics and beta blockers impair glucose tolerance, whereas calcium channel blockers and angiotensin converting enzyme blockers lack this metabolic effect. We compared the effect of a combination therapy with a nondihydropyridine calcium channel blocker plus an angiotensin converting enzyme inhibitor and a beta blocker plus a diuretic on hemoglobin A(1c) (Hb A(1c)) in patients with type 2 diabetes and mild-to- moderate hypertension. METHODS: A total of 463 hypertensive outpatients with non-insulin treated type 2 diabetes on stable antidiabetic therapy for at least 3 months and with HbA(1c) between 6.5% and 10% were recruited. In a randomized, double blind trial patients were treated for 20 weeks with fixed combinations of verapamil sustained release (SR) plus trandolapril and of atenolol plus chlorthalidone following a 2-week placebo run-in period. The main outcome measures were HbA(1c), fasting plasma glucose, and fructosamine levels as well as systolic and diastolic blood pressure. RESULTS: HbA(1c) remained stable at 7.9% after administration of verapamil SR plus trandolapril and increased from 7.8% to 8.6% with atenolol plus chlorthalidone; the differences between treatment groups were significant at 4, 12, and 20 weeks of treatment and at last visit (P <.0001). Mean blood pressure fell from 169/96 to 150/85 and from 168/95 to 145/83 mm Hg after administration of verapamil SR plus trandolapril and atenolol plus chlorthalidone, respectively. Both combinations were well tolerated. CONCLUSIONS: HbA(1c) and other parameters of short- and long-term glycemic control were in a more favorable range after antihypertensive treatment with verapamil SR plus trandolapril as compared with atenolol plus chlorthalidone.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biological_Markers_MeSH S_blood_MeSH Biological_Markers_blood_MeSH M_Blood_Glucose_MeSH S_drug_effects_MeSH Blood_Glucose_drug_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_blood_MeSH Diabetes_Mellitus__Type_II_blood_MeSH S_drug_therapy_MeSH Diabetes_Mellitus__Type_II_drug_therapy_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Diuretics__Sulfamyl_MeSH S_therapeutic_use_MeSH Diuretics__Sulfamyl_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Fasting_MeSH S_blood_MeSH Fasting_blood_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Hemoglobin_A__Glycosylated_MeSH S_drug_effects_MeSH Hemoglobin_A__Glycosylated_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_blood_MeSH Hypertension_blood_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Patient_Compliance_MeSH M_Support__Non-U_S__Gov't_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12745204
----K 5
----T Relevance of the plasma renin hormonal control system that regulates blood pressure and sodium balance for correctly treating hypertension and for evaluating ALLHAT.
----A 
----P Editorial Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Myocardial_Infarction_MeSH S_metabolism_MeSH Myocardial_Infarction_metabolism_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_North_America_MeSH S_epidemiology_MeSH North_America_epidemiology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH M_Renin-Angiotensin_System_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Sodium_MeSH S_metabolism_MeSH Sodium_metabolism_MeSH 
****** 12745004
----K 5
----T Primary open-angle glaucoma in blacks: a review.
----A Glaucoma is one of the leading causes of blindness worldwide. Primary open-angle glaucoma (POAG) is the most prevalent form of glaucoma and has a particularly devastating impact in blacks. In the black American population, POAG prevalence is estimated to be six times as high in certain age groups compared to whites. POAG is more likely to result in irreversible blindness, appears approximately 10 years earlier and progresses more rapidly in blacks than in whites. Racial differences in optic disk parameters have been reported and show that blacks have larger optic disks than whites. This finding is robust and may account for the reported differences in other optic disk parameters. The existence of racial differences in intraocular pressure remains to be demonstrated, as conflicting findings are reported in the literature. Intraocular pressure may actually be underestimated in blacks, perhaps because they have thinner corneas. The prevalence of diabetes and hypertension is higher in blacks than in whites, and although no causal relationship has been established between POAG and each of these systemic diseases, some reports suggest that they often occur together, perhaps through an indirect relationship with intraocular pressure. Compounding the problem, there is evidence that blacks are less responsive to both drug and surgical treatment for POAG. Finally, they often have reduced accessibility to treatment and are less aware of the risks of having POAG. This article provides a comprehensive review of the current knowledge pertaining to POAG in blacks.
----P Journal_Article Review Review__Academic 
----M P_African_Continental_Ancestry_Group_MeSH M_Developing_Countries_MeSH M_Glaucoma__Open-Angle_MeSH S_diagnosis_MeSH Glaucoma__Open-Angle_diagnosis_MeSH S_ethnology_MeSH Glaucoma__Open-Angle_ethnology_MeSH S_etiology_MeSH Glaucoma__Open-Angle_etiology_MeSH S_therapy_MeSH Glaucoma__Open-Angle_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH M_Prevalence_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 12748215
----K 2
----T Different responses to dobutamine in the presence of carvedilol or metoprolol in patients with chronic heart failure.
----A OBJECTIVE: To determine whether patients with congestive heart failure on different beta adrenoreceptor blocking drugs have similar haemodynamic responses to dobutamine. DESIGN: Single centre, single blind, randomised, two period crossover study comparing carvedilol with metoprolol CR/XL. PATIENTS: Ten patients with stable chronic congestive heart failure (ejection fraction < 40%) on chronic treatment with metoprolol CR/XL. METHODS: Patients were treated with carvedilol or metoprolol CR/XL (target dose 50 mg twice daily and 200 mg once daily, respectively) for eight weeks. Stress echocardiography was undertaken at the end of each maintenance period, using dobutamine 5 and 15 microg/kg/min. RESULTS: No significant haemodynamic differences were seen at rest on the two treatments. There was a more pronounced increase in heart rate and cardiac output during dobutamine infusion when the patients were on metoprolol than when they were on carvedilol. Mean arterial pressure increased significantly when the patients were on carvedilol, and cardiac output increased during low dose dobutamine, without further change during high dose dobutamine. During the dobutamine infusion, there was no significant difference in ejection fraction between carvedilol and metoprolol treatment. CONCLUSIONS: Patients with congestive heart failure on a non-selective beta adrenoreceptor blocker or beta1 selective blocker responded differently to the inotropic drug dobutamine: the beta1 blockade caused by metoprolol could be counteracted by dobutamine, whereas with carvedilol a low dose of dobutamine increased cardiac output, and a higher dose of dobutamine caused a pressor effect. These findings may be clinically relevant when choosing an inotropic drug.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cardiotonic_Agents_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Chronic_Disease_MeSH M_Cross-Over_Studies_MeSH M_Dobutamine_MeSH S_therapeutic_use_MeSH Dobutamine_therapeutic_use_MeSH M_Dopamine_MeSH S_diagnostic_use_MeSH Dopamine_diagnostic_use_MeSH M_Echocardiography__Stress_MeSH S_methods_MeSH Echocardiography__Stress_methods_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_ultrasonography_MeSH Heart_Failure__Congestive_ultrasonography_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12748238
----K 8
----T A rational basis for selection among drugs of the same class.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Agonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_economics_MeSH Cardiovascular_Agents_economics_MeSH S_pharmacology_MeSH Cardiovascular_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH P_Decision_Making_MeSH M_Drug_Costs_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_pharmacology_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH 
****** 12748317
----K 5
----T Heart failure.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_classification_MeSH Heart_Failure__Congestive_classification_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Models__Cardiovascular_MeSH M_Pacemaker__Artificial_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Remodeling_MeSH 
****** 12749165
----K 5
----T Role of angiotensin-converting-enzyme inhibitors in stroke prevention.
----A 
----P Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12751655
----K 5
----T Open-angle glaucoma.
----A Glaucoma is the second most common cause of legal blindness in the United States. Open-angle glaucoma is an asymptomatic, progressive optic neuropathy characterized by enlarging optic disc cupping and visual field loss. Patients at increased risk for open-angle glaucoma include blacks older than 40 years, whites older than 65 years, and persons with a family history of glaucoma or a personal history of diabetes or severe myopia. Elevated intraocular pressure is a strong, modifiable risk factor for open-angle glaucoma, but it is not diagnostic. Some patients with glaucoma have normal intraocular pressure (i.e., normal-pressure glaucoma), and many patients with elevated intraocular pressure do not have glaucoma (i.e., glaucoma suspects). Routine measurement of intraocular pressure by primary care physicians to screen patients for glaucoma is not recommended. Open-angle glaucoma usually is discovered during an adult eye evaluation performed for other indications. Final diagnosis and treatment occur in collaboration with ophthalmologists and optometrists. Formal visual field testing (perimetry) is a mainstay of glaucoma diagnosis and management. Eye drops, commonly nonspecific beta-blocker or prostaglandin analog drops, generally are the first-line treatment to reduce intraocular pressure. Laser treatment and surgery usually are reserved for patients in whom medical treatment has failed. Without treatment, open-angle glaucoma can end in irreversible vision loss.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Blindness_MeSH S_etiology_MeSH Blindness_etiology_MeSH M_Glaucoma__Open-Angle_MeSH S_diagnosis_MeSH Glaucoma__Open-Angle_diagnosis_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_surgery_MeSH Glaucoma__Open-Angle_surgery_MeSH M_Human_MeSH M_Mass_Screening_MeSH M_Ophthalmic_Solutions_MeSH S_therapeutic_use_MeSH Ophthalmic_Solutions_therapeutic_use_MeSH 
****** 12751913
----K 5
----T The economics of screening and treatment in type 2 diabetes mellitus.
----A A systematic review of the literature was conducted to identify articles on the economics of type 2 diabetes mellitus. Articles were classified into two main categories: cost/burden-of-illness studies of type 2 diabetes and economic evaluations of type 2 diabetes interventions. This systematic review was supplemented by an overview of the findings relating to economic evaluations of associated diabetic complications. A number of conclusions emerge from this review, the most important of which is that intensive treatment of patients with type 2 diabetes appears to be relatively cost effective compared with more conservative strategies. This finding reflects the cost offsets that arise from the range and degree of complications attributable to diabetes. Primary prevention of type 2 diabetes also appears to be cost effective, particularly in high-risk groups. The evidence on screening for type 2 diabetes is less conclusive and further economic analysis is required.
----P Journal_Article Review Review__Academic 
----M M_Coronary_Disease_MeSH S_economics_MeSH Coronary_Disease_economics_MeSH S_etiology_MeSH Coronary_Disease_etiology_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_economics_MeSH Diabetes_Mellitus__Type_II_economics_MeSH S_therapy_MeSH Diabetes_Mellitus__Type_II_therapy_MeSH M_Diabetic_Foot_MeSH S_economics_MeSH Diabetic_Foot_economics_MeSH S_etiology_MeSH Diabetic_Foot_etiology_MeSH M_Diabetic_Nephropathies_MeSH S_economics_MeSH Diabetic_Nephropathies_economics_MeSH S_etiology_MeSH Diabetic_Nephropathies_etiology_MeSH M_Diabetic_Retinopathy_MeSH S_economics_MeSH Diabetic_Retinopathy_economics_MeSH S_etiology_MeSH Diabetic_Retinopathy_etiology_MeSH P_Health_Care_Costs_MeSH S_statistics_&_numerical_data_MeSH Health_Care_Costs_statistics_&_numerical_data_MeSH S_trends_MeSH Health_Care_Costs_trends_MeSH M_Human_MeSH M_Mass_Screening_MeSH S_economics_MeSH Mass_Screening_economics_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12751915
----K 5
----T The cost effectiveness of ACE inhibitors as first-line antihypertensive therapy.
----A BACKGROUND: Current hypertension guidelines differ in their recommendations for first-line antihypertensive therapy. OBJECTIVE: To evaluate the cost effectiveness of ACE inhibitor therapy as antihypertensive first-line therapy as compared with conventional antihypertensive therapy with beta-adrenoceptor antagonists or diuretics. STUDY DESIGN: Cost-effectiveness analysis based on data from randomised trials and observational studies comparing the effectiveness of ACE inhibitor and conventional antihypertensive therapy, we constructed a Markov model to compare four strategies in the management of uncomplicated hypertension: (i) prescribing ACE inhibitor therapy to all patients; (ii) prescribing conventional therapy to all patients; (iii) individualised antihypertensive therapy based on the presence or absence of left ventricular hypertrophy on electrocardiography (ECG); or (iv) individualised antihypertensive therapy based on the presence or absence of left ventricular hypertrophy on echocardiography. METHODS: Cost data were derived from the medical literature and focus groups, and utility values were derived from patients on antihypertensive monotherapy. All costs were calculated in 1999 Canadian dollars, but are reported in US dollars according to the 1999 purchasing power parity rate for medical and healthcare. The effectiveness of ACE inhibitor therapy in the presence of left ventricular hypertrophy was derived from observational studies. The time horizon was over a lifetime. PERSPECTIVE: Third-party payer. PATIENTS/PARTICIPANTS: A cohort of men aged 40 years without cardiovascular comorbidity requiring antihypertensive drug therapy. MAIN OUTCOME MEASURES AND RESULTS: In the baseline analysis, all four strategies resulted in expected discounted QALYs that differed from each other only at the third decimal point (i.e. less than 0.003). Given the uncertainties in the variable estimates and the small size of the differences, these differences are extremely small and unlikely to represent real differences. Even accepting the small gains as real, the resulting cost-effectiveness ratios are unattractively high: $US 200,000 per QALY gained for the echocardiography strategy (compared with ECG), and $US 700,000 for the "ACE inhibitor for all" strategy (compared with ECG). The incremental cost effectiveness of prescribing ACE inhibitor therapy to everybody was never less than $US 100,000/QALY in the sensitivity analysis. CONCLUSIONS: Prescribing ACE inhibitors as antihypertensive first-line therapy in patients without cardiovascular morbidity cannot be recommended at the present time unless the acquisition costs of ACE inhibitors become substantially more attractive.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_economics_MeSH Angiotensin-Converting_Enzyme_Inhibitors_economics_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Canada_MeSH S_epidemiology_MeSH Canada_epidemiology_MeSH M_Cohort_Studies_MeSH M_Comparative_Study_MeSH M_Cost-Benefit_Analysis_MeSH M_Diuretics_MeSH S_economics_MeSH Diuretics_economics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Drug_Utilization_MeSH S_economics_MeSH Drug_Utilization_economics_MeSH S_statistics_&_numerical_data_MeSH Drug_Utilization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_economics_MeSH Hypertrophy__Left_Ventricular_economics_MeSH M_Markov_Chains_MeSH M_Practice_Guidelines_MeSH M_Quality-Adjusted_Life_Years_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12748199
----K I
----T The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report.
----A "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guideline for hypertension prevention and management. The following are the key messages(1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP; (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg; individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension; (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease); (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.
----P Guideline Journal_Article Practice_Guideline 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Algorithms_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Blood_Pressure_Determination_MeSH M_Blood_Pressure_Monitors_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diagnostic_Tests__Routine_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Risk_Factors_MeSH M_Risk_Reduction_Behavior_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12762972
----K 4
----T Prevention of type 2 diabetes.
----A Diabetes is a major public health problem that is approaching epidemic proportions in our society and worldwide. Cardiovascular disease is the major cause of morbidity and mortality in people with diabetes. Control of cardiovascular disease risk factors is achieved only in a minority of patients. Given the magnitude of the problem and the seriousness of diabetes complications, prevention appears to be a logical approach to curb the rising prevalence of the disease. Interventions such as lifestyle modifications and the use of metformin and acarbose have been shown in randomized prospective trials to prevent diabetes in high-risk patients. Other interventions are currently being examined in large prospective studies. It is likely that one or a combination of these approaches will make diabetes prevention a reality in the near future.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH S_prevention_&_control_MeSH Diabetes_Mellitus__Type_II_prevention_&_control_MeSH S_psychology_MeSH Diabetes_Mellitus__Type_II_psychology_MeSH M_Diabetic_Angiopathies_MeSH S_epidemiology_MeSH Diabetic_Angiopathies_epidemiology_MeSH S_prevention_&_control_MeSH Diabetic_Angiopathies_prevention_&_control_MeSH M_Diabetic_Diet_MeSH P_Exercise_MeSH M_Glucose_Tolerance_Test_MeSH M_Human_MeSH M_Hypoglycemic_Agents_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Incidence_MeSH P_Life_Style_MeSH 
****** 12764397
----K 5
----T The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT): ALL predictable, and no big surprise out of a HAT?
----A 
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH P_Outcome_Assessment_(Health_Care)_MeSH M_Predictive_Value_of_Tests_MeSH 
****** 12764398
----K 5
----T ALLHAT: a saga of missed opportunities.
----A 
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Clinical_Protocols_MeSH M_Clinical_Trials_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH P_Outcome_Assessment_(Health_Care)_MeSH M_Predictive_Value_of_Tests_MeSH 
****** 12766755
----K 6
----T Relation of QT interval and QT dispersion to regression of echocardiographic and electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) study.
----A BACKGROUND: In hypertensive patients, both echocardiographic and electrocardiographic left ventricular hypertrophy (LVH) increase the risk of sudden death, possibly in part because of LVH-induced proarrhythmic repolarization changes. Experimentally, regression of LVH normalizes ventricular electrophysiology. METHODS: To assess the relation of regression of LVH to changes in electrocardiographic measures of ventricular repolarization, we studied 317 hypertensive (61.2% men, mean age 65 +/- 7 years) participants in the Losartan Intervention For Endpoint Reduction (LIFE) study with electrocardiographic evidence of LVH, at study baseline, and after 1 year of blood pressure-lowering treatment with losartan or atenolol and hydrochlorothiatzide as the first adjunct therapy if needed to reach target blood pressure of 140/90 mm Hg. As indexes of LVH, we used echocardiographically determined LV mass as well as the Sokolow-Lyon and Cornell voltages from the electrocardiogram. QT interval duration and QT dispersion from the 12-lead electrocardiogram were used as ventricular repolarization measures. RESULTS: By using tertiles of LV mass change and adjusting for the difference in treatment (losartan or atenolol), shortening of the rate-adjusted QT intervals as well as reduction in QT(apex) dispersion were observed in the tertile showing the greatest decrease in LV mass but not in the tertile without substantial changes in LV mass despite a significant reduction in blood pressure. Similar results were obtained with the use of Sokolow-Lyon and Cornell voltage change tertiles. CONCLUSIONS: In hypertensive patients with electrocardiographic evidence of LVH, regression of echocardiographically determined LV mass and electrocardiographic indexes of LVH may partially reverse the LVH-induced proarrhythmic repolarization changes. This may have a beneficial impact on the increased incidence of sudden death in these patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Echocardiography_MeSH P_Electrocardiography_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH S_ultrasonography_MeSH Hypertrophy__Left_Ventricular_ultrasonography_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Remission_Induction_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12767649
----K 3
----T The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial (AIRCRAFT).
----A OBJECTIVES: The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial was a multicenter trial of atrioventricular junction ablation and pacing (AVJAP) compared with pharmacologic ventricular rate control (medication [MED]) in patients with mild to moderately symptomatic permanent atrial fibrillation (AF). BACKGROUND: There have been very few prospective randomized trials, undertaken in highly symptomatic patients, comparing AVJAP with pharmacologic methods of ventricular rate control for patients with permanent AF. METHODS: There were 99 patients (70 men, mean age 68 +/- 8.6 years) at five centers. Forty-nine patients were randomized to AVJAP while 50 patients were randomized to pharmacologic control. The primary end point was cardiac function measured by echocardiography and exercise tolerance. The secondary end points were ventricular rate control, evaluated by 24-h ambulatory electrocardiographic monitoring, and quality of life. Data were collected at randomization and then at one month, six months, and 12 months post-randomization. RESULTS: At 12 months follow-up there was no significant difference in left ventricular ejection fraction (AVJAP: 54 +/- 17%; MED: 61 +/- 13% [p = ns]) or exercise duration on treadmill testing (AVJAP: 4.1 +/- 2 min; MED: 4.6 +/- 2 min [p = ns]); however, the peak ventricular rate was lower in the AVJAP group during exercise (112 +/- 17 beats/min vs. 153 +/- 36 beats/min, p < 0.05) and activities of daily life (117 +/- 16 beats/min vs. 152 +/- 37 beats/min, p < 0.05). The CAST quality-of-life questionnaire revealed that patients in the AVJAP group had fewer symptoms at six months (p = 0.003) and at 12 months (p = 0.004). The observed relative risk reduction in symptoms at 12 months was 18%. Global subjective semiquantitative measurement of quality of life using the "ladder of life" revealed that the AVJAP group reported a 6% better quality of life at six months (p = 0.011). CONCLUSIONS: In this trial, AVJAP for patients with mild to moderately symptomatic permanent AF did not worsen cardiac function during long-term follow-up, and quality of life was improved.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Activities_of_Daily_Living_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Atrioventricular_Node_MeSH S_surgery_MeSH Atrioventricular_Node_surgery_MeSH M_Catheter_Ablation_MeSH S_adverse_effects_MeSH Catheter_Ablation_adverse_effects_MeSH M_Comparative_Study_MeSH M_Echocardiography_MeSH M_Electrocardiography__Ambulatory_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Pacemaker__Artificial_MeSH S_adverse_effects_MeSH Pacemaker__Artificial_adverse_effects_MeSH M_Quality_of_Life_MeSH M_Stroke_Volume_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Function__Left_MeSH 
****** 12769666
----K 5
----T Pharmacokinetics of topical ocular drug delivery: potential uses for the treatment of diseases of the posterior segment and beyond.
----A In developing a drug delivery strategy, issues of absorption, distribution, metabolism, and elimination must be considered. The eye presents unique opportunities and challenges when it comes to the delivery of pharmaceuticals, and is most accessible to the application of topical medications. While absorption by this route is inefficient, there are few side effects. While it has been assumed that topically applied drugs penetrated into the intraocular environment through the cornea, this is currently being reassessed. More recent investigations have shown that the conjunctival route of entry plays an important role in the penetration of drugs into the anterior segment. Furthermore, topically applied drugs have been shown to have access to the sclera from the conjunctiva. As such, it is conceivable that such drugs could find their way to the posterior segment. Data suggest that the sclera is readily permeable to even large molecular weight compounds ( approximately 150 kD). The recent finding that topically applied nepafenac inhibited choroidal and retinal neovascularization by decreasing the production of VEGF, as well as our data showing that even a large molecular weight peptide like insulin can accumulate in the retina and optic nerve after topical application, supports the contention that topically applied drugs can not only reach the posterior segment, but that they can also be therapeutic. Finally, the implications of our findings that topically applied insulin also accumulates in the contralateral eye as well as in the central nervous system are discussed.
----P Journal_Article Review Review__Academic 
----M M_Absorption_MeSH M_Animals_MeSH M_Brain_MeSH S_metabolism_MeSH Brain_metabolism_MeSH M_Diffusion_MeSH M_Drug_Therapy_MeSH M_Eye_MeSH S_metabolism_MeSH Eye_metabolism_MeSH M_Eye_Diseases_MeSH S_drug_therapy_MeSH Eye_Diseases_drug_therapy_MeSH M_Human_MeSH M_Hypoglycemic_Agents_MeSH S_administration_&_dosage_MeSH Hypoglycemic_Agents_administration_&_dosage_MeSH S_cerebrospinal_fluid_MeSH Hypoglycemic_Agents_cerebrospinal_fluid_MeSH S_therapeutic_use_MeSH Hypoglycemic_Agents_therapeutic_use_MeSH M_Insulin_MeSH S_administration_&_dosage_MeSH Insulin_administration_&_dosage_MeSH S_cerebrospinal_fluid_MeSH Insulin_cerebrospinal_fluid_MeSH S_therapeutic_use_MeSH Insulin_therapeutic_use_MeSH M_Ophthalmic_Solutions_MeSH S_pharmacokinetics_MeSH Ophthalmic_Solutions_pharmacokinetics_MeSH M_Pharmaceutical_Preparations_MeSH S_administration_&_dosage_MeSH Pharmaceutical_Preparations_administration_&_dosage_MeSH 
****** 12772815
----K 4
----T Brimonidine Purite and bimatoprost compared with timolol and latanoprost in patients with glaucoma and ocular hypertension.
----A This 3-month multicenter, investigator-masked, parallel-group study compared brimonidine Purite and bimatoprost (brimP/bim) with timolol gel-forming solution and latanoprost (tim/latan) in 28 patients with open-angle glaucoma or ocular hypertension. IOP was measured at baseline and 2 hours after morning instillation at weeks 2, 4, and 12. The primary outcome measure was the mean IOP reduction from baseline. Secondary measures were the percentage of patients in each group who achieved specific low target pressures and the incidence of adverse events. Mean IOP at baseline was 24.8 mm Hg in each group. At follow-up visits, mean reductions from baseline ranged from 8.5 to 9.0 mm Hg with brimP/bim and from 7.5 to 7.7 mm Hg with tim/latan. More patients achieved low target pressures with brimP/bim. At week 12, 69.2% of brimP/bim patients and 27.3% of tim/latan patients had IOPs of 16 mm Hg or lower (P = .024). Both regimens were well tolerated, and adverse events were infrequent. The combination of brimonidine Purite and bimatoprost was well tolerated and at least as effective as Timoptic-XE and latanoprost in reducing IOP. More patients achieved low target IOPs with brimonidine Purite and bimatoprost than with Timoptic-XE and latanoprost. A larger study is needed to confirm these results.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Glaucoma__Open-Angle_MeSH S_diagnosis_MeSH Glaucoma__Open-Angle_diagnosis_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lipids_MeSH S_administration_&_dosage_MeSH Lipids_administration_&_dosage_MeSH S_adverse_effects_MeSH Lipids_adverse_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_diagnosis_MeSH Ocular_Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Probability_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH M_Reference_Values_MeSH M_Risk_Assessment_MeSH M_Sensitivity_and_Specificity_MeSH M_Severity_of_Illness_Index_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH M_Tonometry__Ocular_MeSH M_Treatment_Outcome_MeSH 
****** 12774001
----K 5
----T Nonselective beta-blockers plus nitrates in portal hypertension: an open question.
----A 
----P Comment Editorial Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH M_Nitrates_MeSH S_therapeutic_use_MeSH Nitrates_therapeutic_use_MeSH 
****** 12774003
----K 3
----T Propranolol plus placebo versus propranolol plus isosorbide-5-mononitrate in the prevention of a first variceal bleed: a double-blind RCT.
----A Nonselective beta-blockers are very effective in preventing first variceal bleeding in patients with cirrhosis. Treatment with isosorbide-5-mononitrate (IS-MN) plus propranolol achieves a greater reduction in portal pressure than propranolol alone. The present multicenter, prospective, double-blind, randomized, controlled trial evaluated whether combined drug therapy could be more effective than propranolol alone in preventing variceal bleeding. A total of 349 consecutive cirrhotic patients with gastroesophageal varices were randomized to receive propranolol + placebo (n = 174) or propranolol + IS-MN (n = 175). There were no significant differences in the 1- and 2-year actuarial probability of variceal bleeding between the 2 groups (propranolol + placebo, 8.3% and 10.6%; propranolol + IS-MN, 5% and 12.5%). The only independent predictor of variceal bleeding was a variceal size greater than 5 mm. However, among patients with varices greater than 5 mm (n = 196), there were no significant differences in the incidence of variceal bleeding between the 2 groups. Survival was also similar. Adverse effects were significantly more frequent in the propranolol + IS-MN group due to a greater incidence of headache. There were no significant differences in the incidence of new-onset or worsening ascites or in impairment of renal function. In conclusion, propranolol effectively prevents variceal bleeding. Adding IS-MN does not further decrease the low residual risk of bleeding in patients receiving propranolol. However, the long-term use of this combination drug therapy is safe and may be an alternative in clinical conditions associated with a greater risk of bleeding.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_drug_therapy_MeSH Esophageal_and_Gastric_Varices_drug_therapy_MeSH S_pathology_MeSH Esophageal_and_Gastric_Varices_pathology_MeSH M_Female_MeSH M_Hemorrhage_MeSH S_epidemiology_MeSH Hemorrhage_epidemiology_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH S_physiopathology_MeSH Hemorrhage_physiopathology_MeSH S_prevention_&_control_MeSH Hemorrhage_prevention_&_control_MeSH M_Human_MeSH M_Incidence_MeSH M_Isosorbide_Dinitrate_MeSH S_adverse_effects_MeSH Isosorbide_Dinitrate_adverse_effects_MeSH S_analogs_&_derivatives_MeSH Isosorbide_Dinitrate_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Isosorbide_Dinitrate_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Placebos_MeSH M_Propranolol_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Severity_of_Illness_Index_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Vasodilator_Agents_MeSH S_adverse_effects_MeSH Vasodilator_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12776018
----K 5
----T Paradoxical coronary embolism: a rare cause of acute myocardial infarction.
----A Since it was first described in 1877, paradoxical embolism has become widely accepted as an etiology of stroke and peripheral vascular thrombotic occlusion. Less common are paradoxical emboli to the coronary artery. On the basis of limited pathologic and clinical series, it appears that paradoxical coronary emboli account for 5%-10% of all paradoxical emboli. Paradoxical coronary emboli have been described in all age groups, from neonates to the elderly, reflecting a wide spectrum of cardiac structural abnormality and clinical circumstance. Strategies for management should focus on treatment of acute coronary occlusion as well as prevention of future emboli.
----P Case_Reports Journal_Article 
----M M_Anticoagulants_MeSH S_administration_&_dosage_MeSH Anticoagulants_administration_&_dosage_MeSH M_Chest_Pain_MeSH S_diagnosis_MeSH Chest_Pain_diagnosis_MeSH M_Coronary_Angiography_MeSH M_Echocardiography_MeSH M_Embolism__Paradoxical_MeSH S_complications_MeSH Embolism__Paradoxical_complications_MeSH S_diagnosis_MeSH Embolism__Paradoxical_diagnosis_MeSH S_drug_therapy_MeSH Embolism__Paradoxical_drug_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Catheterization_MeSH M_Heart_Function_Tests_MeSH M_Heparin_MeSH S_administration_&_dosage_MeSH Heparin_administration_&_dosage_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_diagnosis_MeSH Myocardial_Infarction_diagnosis_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Treatment_Outcome_MeSH 
****** 12780402
----K 4
----T Efficacy and safety of timolol maleate/latanoprost fixed combination versus timolol maleate and brimonidine given twice daily.
----A PURPOSE: To evaluate the efficacy and safety of the timolol maleate/latanoprost fixed combination (TLFC) given once each evening versus brimonidine and timolol solution given twice daily as concomitant therapy in primary open-angle glaucoma or ocular hypertension patients. METHODS: Qualified subjects were begun on timolol alone twice daily for 1 month and then randomized to either TLFC or brimonidine and timolol concomitant therapy for 6 weeks. Patients were then switched to the other treatment regimen. Intraocular pressures (IOPs) were measured every 2 hours between 08 : 00 and 20 : 00 hours at baseline and at the end of periods 1 and 2. RESULTS: This study found that in 32 subjects the IOP diurnal curve on timolol alone (20.9 +/- 2.8 mmHg) decreased to 17.9 +/- 3.2 mmHg when patients were treated with TLFC and to 19.0 +/- 2.4 mmHg when patients were treated with brimonidine and timolol (p = 0.02). Intraocular pressures at individual time-points were statistically similar between the groups at the 08 : 00 trough and 2 and 4 hours after dosing. However, beyond 4 hours after dosing, TLFC-treated subjects demonstrated a trend towards lower IOPs at each 2-hour time-point that was not statistically significant after a Bonferroni correction (p <or= 0.05). The incidence of both solicited and unsolicited side-effects was similar between groups. CONCLUSION: This study suggests that TLFC given in the evening reduces the mean daytime diurnal IOP more than brimonidine and timolol given concomitantly twice daily.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH M_Comparative_Study_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prostaglandins_F__Synthetic_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Quinoxalines_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Safety_MeSH M_Support__Non-U_S__Gov't_MeSH M_Timolol_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH 
****** 12783070
----K 5
----T Effects of ACE-inhibitors and beta-blockers on left ventricular remodeling in chronic heart failure.
----A In recent years, it has become increasingly recognised that a central feature of the disease progression associated with heart failure is the process of left ventricular remodeling. The remodeling process manifests as an increase in left ventricular volumes, leading to a rise in wall stress and a compensatory increase in myocardial mass. The left ventricle also gradually assumes a more spherical shape, resulting in functional mitral regurgitation leading to further haemodynamic overload, worsening myocardial function and an unfavourable clinical course. Accumulating clinical data support the hypothesis that the benefits in clinical outcome with ACE-inhibitors and beta-blockers may relate to modification of the remodeling process resulting in slowing of disease progression and preservation of contractile function. The general trend from a number of clinical studies indicates that whereas ACE-inhibitors seem to prevent progressive left ventricular dilatation, the third generation beta-blocker, carvedilol, may actually reverse the remodelling process by reducing left ventricular volumes and improving systolic function. Direct comparisons indicate that carvedilol has a similar safety and tolerability profile to ACE-inhibitors and thereby support the feasibility of administering this drug as first-line therapy in selected patients with mild to moderate chronic heart failure. Therefore, the decision to initiate treatment with carvedilol or an ACE-inhibitor might in future be tailored on an individual basis and followed thereafter by combination therapy at the earliest and safest opportunity. Finally, the possible development of treatment strategies addressing the cellular and molecular mechanisms responsible for the remodeling process and the recently published benefits of device therapies herald a combined, synergistic approach to the future management of heart failure.
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Drug_Therapy__Combination_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Randomized_Controlled_Trials_MeSH M_Survival_Rate_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 12783629
----K 5
----T ALLHAT: is the final answer in?
----A Blood pressure rises rapidly upon waking and may be responsible, in part, for the increased incidence of myocardial infarction and stroke during the morning hours. Current formulations and dosing of antihypertensive drugs do not provide maximum coverage during this vulnerable period. This study was performed to demonstrate that propranolol CR (Innopran XL), a novel chronotherapeutic formulation of propranolol designed for nighttime dosing, has appropriate pharmacokinetics to provide maximum cardioprotective effect in the morning. Pharmacokinetics of propranolol CR and sustained-release propranolol after single and multiple doses were determined in normal male volunteers in this open-label, 2-period crossover study. The drugs were dosed in the evening and serial blood samples were taken for determination of propranolol concentration the next 24 to 72 hours. After a single 160-mg dose of propranolol CR administered at 10 pm, absorption was delayed by about 4 hours, after which plasma concentration rose steadily, reaching a peak at about 10:00 am. In contrast, after dosing with sustained release propranolol, plasma levels of propranolol began to rise almost immediately, reaching a plateau between 4:00 am and 10:00 am. During multiple dosing, steady-state trough plasma concentrations were achieved after 2 days with either drug. After the final dose, the plasma profiles of both drugs were similar to those observed in the single-dose study. Bioavailability was similar for both formulations of propranolol. Propranolol CR exhibited appropriate pharmacokinetics for a chronotherapeutic approach to the treatment of hypertension.
----P Editorial 
----M M_African_Americans_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Chlorthalidone_MeSH S_therapeutic_use_MeSH Chlorthalidone_therapeutic_use_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Kidney_MeSH S_drug_effects_MeSH Kidney_drug_effects_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12783630
----K 6
----T Pharmacokinetics of propranolol after single and multiple dosing with sustained release propranolol or propranolol CR (innopran XL) , a new chronotherapeutic formulation.
----A Blood pressure rises rapidly upon waking and may be responsible, in part, for the increased incidence of myocardial infarction and stroke during the morning hours. Current formulations and dosing of antihypertensive drugs do not provide maximum coverage during this vulnerable period. This study was performed to demonstrate that propranolol CR (Innopran XL), a novel chronotherapeutic formulation of propranolol designed for nighttime dosing, has appropriate pharmacokinetics to provide maximum cardioprotective effect in the morning. Pharmacokinetics of propranolol CR and sustained-release propranolol after single and multiple doses were determined in normal male volunteers in this open-label, 2-period crossover study. The drugs were dosed in the evening and serial blood samples were taken for determination of propranolol concentration the next 24 to 72 hours. After a single 160-mg dose of propranolol CR administered at 10 pm, absorption was delayed by about 4 hours, after which plasma concentration rose steadily, reaching a peak at about 10:00 am. In contrast, after dosing with sustained release propranolol, plasma levels of propranolol began to rise almost immediately, reaching a plateau between 4:00 am and 10:00 am. During multiple dosing, steady-state trough plasma concentrations were achieved after 2 days with either drug. After the final dose, the plasma profiles of both drugs were similar to those observed in the single-dose study. Bioavailability was similar for both formulations of propranolol. Propranolol CR exhibited appropriate pharmacokinetics for a chronotherapeutic approach to the treatment of hypertension.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_1-Propanol_MeSH S_administration_&_dosage_MeSH 1-Propanol_administration_&_dosage_MeSH S_adverse_effects_MeSH 1-Propanol_adverse_effects_MeSH S_blood_MeSH 1-Propanol_blood_MeSH S_pharmacokinetics_MeSH 1-Propanol_pharmacokinetics_MeSH M_Adult_MeSH M_Analysis_of_Variance_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_blood_MeSH Antihypertensive_Agents_blood_MeSH S_pharmacokinetics_MeSH Antihypertensive_Agents_pharmacokinetics_MeSH M_Biological_Availability_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH P_Chronotherapy_MeSH M_Cross-Over_Studies_MeSH M_Delayed-Action_Preparations_MeSH S_administration_&_dosage_MeSH Delayed-Action_Preparations_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Delayed-Action_Preparations_pharmacokinetics_MeSH M_Dizziness_MeSH S_chemically_induced_MeSH Dizziness_chemically_induced_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Propanols_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Propranolol_adverse_effects_MeSH S_blood_MeSH Propranolol_blood_MeSH S_pharmacokinetics_MeSH Propranolol_pharmacokinetics_MeSH 
****** 12783633
----K 5
----T Cardiovascular manifestations of substance abuse part 1: cocaine.
----A Substance abuse with cocaine is associated with multiple cardiovascular conditions, including myocardial infarction, dissection, left ventricular hypertrophy, arrhythmias, sudden death, and cardiomyopathy. Cocaine has effects to potentiate the physiologic actions of catecholamines and has direct effects on voltage-dependent sodium ion channels related to local anesthetic properties. The effects of cocaine can be augmented with concomitant alcohol consumption. Acute myocardial ischemia caused by cocaine may be related to in situ thromboisis and/or coronary vasospasm. Treatment strategies for cocaine-induced myocardial infarction would include antiplatelet therapy, thrombolysis, and vasodilators (eg, nitrates, nifedipine). Beta-adrenergic blockers should not be used unless concomitant vasodilator therapy is given.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Cocaine_MeSH S_chemistry_MeSH Cocaine_chemistry_MeSH S_pharmacology_MeSH Cocaine_pharmacology_MeSH M_Cocaine-Related_Disorders_MeSH S_complications_MeSH Cocaine-Related_Disorders_complications_MeSH M_Dopamine_Uptake_Inhibitors_MeSH S_chemistry_MeSH Dopamine_Uptake_Inhibitors_chemistry_MeSH S_pharmacology_MeSH Dopamine_Uptake_Inhibitors_pharmacology_MeSH M_Heart_Conduction_System_MeSH S_drug_effects_MeSH Heart_Conduction_System_drug_effects_MeSH M_Heart_Diseases_MeSH S_chemically_induced_MeSH Heart_Diseases_chemically_induced_MeSH S_therapy_MeSH Heart_Diseases_therapy_MeSH M_Human_MeSH M_Molecular_Structure_MeSH M_Muscle__Smooth__Vascular_MeSH S_drug_effects_MeSH Muscle__Smooth__Vascular_drug_effects_MeSH M_Tachyphylaxis_MeSH M_Vasoconstrictor_Agents_MeSH S_chemistry_MeSH Vasoconstrictor_Agents_chemistry_MeSH S_pharmacology_MeSH Vasoconstrictor_Agents_pharmacology_MeSH 
****** 12783634
----K 5
----T Gender, ethnicity, and genes in cardiovascular disease. Part 2: implications for pharmacotherapy.
----A Women are underrepresented in clinical trials. Lower doses of beta-blockers are required for Southeast Asians. ACE and ARB's are teratogenic in the second trimester. Torsades de Pointes is more common in women related to a longer QT-interval. Lower dose OCPs decrease the risk of MI, stroke and thrombosis. HRTs are not effective for CAD prevention.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_ethnology_MeSH Cardiovascular_Diseases_ethnology_MeSH S_genetics_MeSH Cardiovascular_Diseases_genetics_MeSH M_Contraceptives__Oral__Hormonal_MeSH S_pharmacology_MeSH Contraceptives__Oral__Hormonal_pharmacology_MeSH M_Estrogen_Replacement_Therapy_MeSH M_Fibrinolytic_Agents_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH P_Sex_Characteristics_MeSH 
****** 12787690
----K 5
----T An appraisal of different cardiac risk reduction strategies in vascular surgery patients.
----A OBJECTIVES: to summarize existing evidence regarding the benefits and the risks of all available interventional and medical means aimed at cardiac risk reduction in patients undergoing vascular surgery. DESIGN: review of the literature. MATERIALS AND METHODS: a critical review of all studies examining the impact of various prophylactic cardiac maneuvers on perioperative outcome following vascular surgery was performed. Overall mortality, cardiac mortality and myocardial infarction rate were used as the outcome measures. RESULTS: coronary artery bypass grafting is associated with a 60% decrease in perioperative mortality in patients undergoing vascular surgery, but in most of the cases this decrease does not outweigh the combined risk of the cardiac and the subsequent noncardiac vascular procedure. Data supporting the cardioprotective effect of percutaneous transluminal angioplasty in the perioperative setting are insufficient. beta-blockade has been shown to decrease perioperative mortality and cardiac morbidity in both high-risk (strong evidence) and low-risk (weak evidence) patients. CONCLUSIONS: coronary revascularization is rarely indicated to simply get the patient through vascular surgery and should be reserved for patients who would need it irrespective of the scheduled vascular procedure. Among all available pharmacological agents, including beta-blockers, alpha-agonists, calcium channel blockers and nitrates, only beta-blockers have been proven to reduce the cardiac risk of vascular surgery.
----P Journal_Article Review Review__Tutorial 
----M M_Cardiac_Surgical_Procedures_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Evidence-Based_Medicine_MeSH M_Heart_Diseases_MeSH S_diagnosis_MeSH Heart_Diseases_diagnosis_MeSH S_psychology_MeSH Heart_Diseases_psychology_MeSH S_surgery_MeSH Heart_Diseases_surgery_MeSH M_Human_MeSH M_Risk_Factors_MeSH P_Risk_Reduction_Behavior_MeSH P_Vascular_Surgical_Procedures_MeSH 
****** 12719441
----K 2
----T Different effect of antihypertensive drugs on conduit artery endothelial function.
----A To compare the effect of antihypertensive drugs on endothelium-dependent vasodilation in the peripheral conduit arteries of patients with essential hypertension, in a prospective, randomized, parallel group study, endothelial function was assessed in 168 hypertensive patients before and after 6-month treatment with randomly assigned nifedipine GITS (30 to 60 mg, n=28), amlodipine (5 to 10 mg, n=28), atenolol (50 to 100 mg, n=29), nebivolol (5 to 10 mg, n=28), telmisartan (80 to 160 mg, n=29), and perindopril (2 to 4 mg, n=28). If necessary, hydrochlorothiazide (25 mg) was added to each compound. We evaluated brachial artery flow-mediated, endothelium-dependent dilation (high-resolution ultrasound) compared with endothelium-independent response to glyceryl trinitrate (25 microg/s). Brachial artery diameter was measured by automatic computerized analysis. Forty healthy subjects were evaluated as a control group. Oxidative stress production was evaluated by measuring plasma malondialdehyde and plasma lipoperoxides; plasma antioxidant capacity was assessed as ferric-reducing antioxidant power. Hypertensive patients showed a significantly (P<0.01) lower flow-mediated dilation (5.2+/-1.9%) as compared with healthy control subjects (7.1+/-2.6%). Response to glyceryl trinitrate was similar in control subjects and patients. At baseline, blood pressure, diameter, flow-mediated dilation, and response to glyceryl trinitrate were similar in the different treatment groups. All treatments similarly reduced blood pressure, but only perindopril increased flow mediated dilation (from 5.1+/-2 to 6.4+/-2.4%; P<0.01) without modifying the response to glyceryl trinitrate. Perindopril but also telmisartan nifedipine and amlodipine reduced oxidative stress and increased plasma antioxidant capacity. In patients with essential hypertension, ACE inhibitors appear to be the only compounds able to improve conduit artery endothelium-dependent vasodilation.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH S_cytology_MeSH Arteries_cytology_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Brachial_Artery_MeSH S_cytology_MeSH Brachial_Artery_cytology_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Endothelium__Vascular_MeSH S_drug_effects_MeSH Endothelium__Vascular_drug_effects_MeSH S_physiopathology_MeSH Endothelium__Vascular_physiopathology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Oxidative_Stress_MeSH M_Receptor__Angiotensin__Type_1_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Vasodilation_MeSH S_drug_effects_MeSH Vasodilation_drug_effects_MeSH 
****** 12738891
----K 5
----T Community-based thrombolytic therapy of acute ischemic stroke in Helsinki.
----A BACKGROUND AND PURPOSE: Thrombolysis with alteplase is used in acute ischemic stroke within 3 hours after symptom onset in many stroke centers, but experience remains limited in Europe. METHODS: Using eligibility and management criteria similar to those published by the American Heart Association, we treated 75 consecutive patients aged 21 to 83 years (mean age, 63.6 years; median Scandinavian Stroke Scale score, 32/58) with hemispheric infarction with alteplase in 1998-2001. Their neuroradiological findings (ischemic and hemorrhagic changes) and functional outcome at 3 months were evaluated. RESULTS: Sixty-one percent of the patients had recovered functional independence (Barthel Index 95 to 100) at the 3-month follow-up. On the modified Rankin Scale (mRS), 37% (28/75) of patients had no or minimal symptoms (mRS 0 to 1), while 17% (13/75) remained dependent (mRS 4 to 5) and 5% (4/75) died. Cerebral parenchymal hematomas occurred in 8% (6/75) and hemorrhagic transformation in 8% (6/75) of the patients. Low initial diastolic blood pressure and administration of intravenous antihypertensive medication were associated with unfavorable outcome (mRS 3 to 6). CONCLUSIONS: We conclude that our management protocol for thrombolytic therapy is safe. These rates of functional outcome, case fatality, and hemorrhagic cerebral events compare favorably with those of other published series of stroke thrombolysis with similar time windows and management guidelines. Associations between blood pressure and its treatment during thrombolysis with functional outcome deserve further analysis.
----P Clinical_Trial Journal_Article 
----M M_Academic_Medical_Centers_MeSH M_Acute_Disease_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Brain_Ischemia_MeSH S_complications_MeSH Brain_Ischemia_complications_MeSH S_diagnosis_MeSH Brain_Ischemia_diagnosis_MeSH S_drug_therapy_MeSH Brain_Ischemia_drug_therapy_MeSH M_Cerebral_Hemorrhage_MeSH S_chemically_induced_MeSH Cerebral_Hemorrhage_chemically_induced_MeSH M_Cerebrovascular_Accident_MeSH S_complications_MeSH Cerebrovascular_Accident_complications_MeSH S_diagnosis_MeSH Cerebrovascular_Accident_diagnosis_MeSH S_drug_therapy_MeSH Cerebrovascular_Accident_drug_therapy_MeSH M_Community_Health_Centers_MeSH M_Demography_MeSH M_Disability_Evaluation_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_adverse_effects_MeSH Fibrinolytic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Finland_MeSH M_Human_MeSH M_Labetalol_MeSH S_administration_&_dosage_MeSH Labetalol_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Recovery_of_Function_MeSH S_drug_effects_MeSH Recovery_of_Function_drug_effects_MeSH P_Thrombolytic_Therapy_MeSH S_adverse_effects_MeSH Thrombolytic_Therapy_adverse_effects_MeSH M_Tissue_Plasminogen_Activator_MeSH S_adverse_effects_MeSH Tissue_Plasminogen_Activator_adverse_effects_MeSH S_therapeutic_use_MeSH Tissue_Plasminogen_Activator_therapeutic_use_MeSH M_Tomography__X-Ray_Computed_MeSH M_Treatment_Outcome_MeSH 
****** 12793706
----K 5
----T Heart failure in the elderly.
----A Heart failure is common in the elderly population. Approximately 6 to 10 percent of the population 65 years or older have heart failure. Heart failure is the most common reason for hospitalization in elderly patients. Etiology of heart failure is often multifactorial in the elderly. The common causes of heart failure include ischemic heart disease, valvular heart disease, hypertensive heart disease, and cardiomyopathy. Exacerbation of heart failure in the elderly is often accompanied by precipitating factors which include arrhythmia, renal failure, anemia, infection, adverse effect of drugs and non-compliance with medication and/or diet. Diagnosis of heart failure may be difficult in the elderly because symptoms of heart failure are often atypical or even absent. Heart failure with preserved systolic function is common in the elderly because aging has a greater impact on diastolic function. It is important to recognize that very old patients with heart failure are underrepresented in clinical trials.
----P Journal_Article Review Review__Tutorial 
----M M_Aged_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Precipitating_Factors_MeSH 
****** 12796749
----K 5
----T Role of single photon emission computed tomography imaging in the evaluation of therapy for angina pectoris.
----A BACKGROUND: Endothelial injury plays a critical role in coronary artery disease (CAD), but the assessment of this injury has been problematical. Recently, it has been shown in vitro that endothelial cells (ECs) release endothelial microparticles (EMPs) on activation or apoptosis and that an assay of EMPs can provide useful information on EC status in patients with thrombotic disorders. This study is aimed at assessing possible correlations between EMPs, which are markers of endothelial injury, and clinical subgroups of patients with CAD. METHODS: A prospective, case-controlled study was conducted on 84 patients with CAD and 42 control subjects to investigate EMP profiles. Included were 64 patients with acute coronary syndromes ([ACS], 38 with myocardial infarction [MI] and 26 with unstable angina [UA]) and 20 patients with stable angina (SA). EMPs in platelet-poor plasma were measured flow cytometrically with combinations of fluorescent antibodies (anti-CD31, -51, -42), allowing distinction of EMPs from platelet microparticles (PMPs). Clinical subgroups of patients were correlated with EMP and PMP levels in blood. RESULTS: Two species of EMPs (CD31+ and CD51+) were evaluated. Both were significantly higher in patients with CAD than in control subjects. CD31+ EMP was higher in ACS than SA. Among patients with first MI, CD31+ EMP was higher in patients with MI than in patients with UA and was significantly higher than in patients with recurring MI. CD51+ EMP did not discriminate ACS from SA. A simultaneous assay of PMP showed correlation between EMPs and PMPs. However, PMPs did not discriminate patients with SA from control subjects. CONCLUSIONS: EMP assay appears promising for assessing EC injury in CAD.
----P Journal_Article Review Review_Literature 
----M M_Angina_Pectoris_MeSH S_radionuclide_imaging_MeSH Angina_Pectoris_radionuclide_imaging_MeSH S_therapy_MeSH Angina_Pectoris_therapy_MeSH M_Clinical_Trials_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH S_physiology_MeSH Coronary_Circulation_physiology_MeSH M_Coronary_Disease_MeSH M_Endothelial_Growth_Factors_MeSH S_therapeutic_use_MeSH Endothelial_Growth_Factors_therapeutic_use_MeSH M_Exercise_Test_MeSH M_Fibroblast_Growth_Factors_MeSH S_therapeutic_use_MeSH Fibroblast_Growth_Factors_therapeutic_use_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Intercellular_Signaling_Peptides_and_Proteins_MeSH S_therapeutic_use_MeSH Intercellular_Signaling_Peptides_and_Proteins_therapeutic_use_MeSH M_Laser_Surgery_MeSH S_methods_MeSH Laser_Surgery_methods_MeSH M_Lymphokines_MeSH S_therapeutic_use_MeSH Lymphokines_therapeutic_use_MeSH M_Myocardial_Revascularization_MeSH S_methods_MeSH Myocardial_Revascularization_methods_MeSH P_Tomography__Emission-Computed__Single-Photon_MeSH M_Vascular_Endothelial_Growth_Factor_A_MeSH M_Vascular_Endothelial_Growth_Factors_MeSH 
****** 12796754
----K 3
----T Differential effects of antihypertensive agents on electrocardiographic voltage: results from the Appropriate Blood Pressure Control in Diabetes (ABCD) trial.
----A BACKGROUND: Serial decline in electrocardiographic voltage in patients with increased left ventricular mass has been associated with a lower risk of cardiovascular events. METHODS: We studied 468 patients with diabetes mellitus and hypertension in the Appropriate Blood Pressure Control in Diabetes (ABCD) trial. Patients were randomized in a stratified design to receive initial treatment with either enalapril or nisoldipine and to either intensive or moderate treatment goals. We measured an electrocardiographic index for increased left ventricular mass, the adjusted Cornell voltage, serially by treatment group. The association between changes in electrocardiographic voltage and cardiovascular events was defined with Cox proportional hazards analysis. RESULTS: In 5 years of follow-up, the decline in adjusted Cornell voltage was significantly greater for patients treated with enalapril than for patients treated with nisoldipine (repeated measures analysis of variance P =.002). In the Cox proportional hazards model, treatment assignment (enalapril vs nisoldipine) was the strongest predictor of cardiovascular events, but the presence of coronary disease at baseline, the duration of diabetes mellitus, and change in voltage were also independent predictors of cardiovascular events. CONCLUSIONS: In the ABCD study, enalapril treatment was associated with a lower risk of myocardial infarction. The reduction in left ventricular mass as reflected by diminished electrocardiographic voltage may explain some, but not all, of the effect of enalapril in this study.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH S_physiopathology_MeSH Diabetes_Mellitus__Type_II_physiopathology_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Enalapril_MeSH S_therapeutic_use_MeSH Enalapril_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_physiopathology_MeSH Hypertrophy__Left_Ventricular_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Nisoldipine_MeSH S_therapeutic_use_MeSH Nisoldipine_therapeutic_use_MeSH M_Proportional_Hazards_Models_MeSH M_Prospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 12795654
----K 5
----T Angiotensin converting enzyme inhibitors and modulation of skeletal muscle insulin resistance.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_metabolism_MeSH Angiotensin-Converting_Enzyme_Inhibitors_metabolism_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH M_Bradykinin_MeSH S_physiology_MeSH Bradykinin_physiology_MeSH M_Glucose_MeSH S_metabolism_MeSH Glucose_metabolism_MeSH M_Human_MeSH M_Insulin_Resistance_MeSH S_physiology_MeSH Insulin_Resistance_physiology_MeSH M_Monosaccharide_Transport_Proteins_MeSH S_metabolism_MeSH Monosaccharide_Transport_Proteins_metabolism_MeSH M_Muscle__Skeletal_MeSH S_drug_effects_MeSH Muscle__Skeletal_drug_effects_MeSH M_Nitric_Oxide_MeSH S_physiology_MeSH Nitric_Oxide_physiology_MeSH M_Receptors__Angiotensin_MeSH S_physiology_MeSH Receptors__Angiotensin_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12800857
----K 5
----T Expert consensus document on management of cardiovascular diseases during pregnancy.
----A 
----P Guideline Journal_Article Practice_Guideline 
----M M_Coronary_Disease_MeSH S_therapy_MeSH Coronary_Disease_therapy_MeSH M_Delivery__Obstetric_MeSH M_Expert_Testimony_MeSH M_Female_MeSH M_Fetal_Monitoring_MeSH M_Human_MeSH M_Hypertension_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Maternal_Welfare_MeSH M_Myocardial_Diseases_MeSH S_therapy_MeSH Myocardial_Diseases_therapy_MeSH M_Practice_Guidelines_MeSH S_standards_MeSH Practice_Guidelines_standards_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH M_Prenatal_Care_MeSH S_methods_MeSH Prenatal_Care_methods_MeSH M_Risk_Factors_MeSH 
****** 12801622
----K 3
----T Effect of xuezhikang, a cholestin extract, on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease.
----A The effect of xuezhikang on postprandial triglyceride (TG) level was investigated in patients with coronary heart disease (CHD) after a high-fat meal (800 cal; 50 g fat). Fifty CHD patients were randomly divided into two groups to accept xuezhikang (xuezhikang group) 1200 mg/day (600 mg twice daily) or not (control group) on the base of routine therapy which included aspirin, metoprolol and fosinopril and nitrates during the whole 6 weeks following-up. Xuezhikang significantly reduced fasting serum total cholesterol (TC) (-20%), low-density lipoprotein cholesterol (LDL-C, -34%), TG (-32%) and apoB (-27%) levels, and raised fasting high-density lipoprotein cholesterol (HDL-C, 18%) and apoA-I (13%) levels (P<0.001). The postprandial serum TG levels at 2, 4 and 6 h decreased 32, 38 and 43%, respectively, in xuezhikang group (P<0.001). The TG area under the curve over the fasting TG level (TG-AUC) significantly decreased in CHD patients accepted xuezhikang with normal (less than 1.7 mmol/l) and elevated (1.74 to 2.92 mmol/l) fasting TG levels by 45 and 50%, respectively (P<0.001). Routine therapy had no significant effect on the fasting and postprandial lipid and apolipoprotein levels. The change of TG-AUC was significantly related to the changes of fasting TG, TC, LDL-C, and HDL-C levels after the treatment, which were related to the changes of fasting apoA-I and apoB levels significantly (P<0.001). Xuezhikang was shown to be beneficial in the treatment of reflecting postprandial triglyceridemia in CHD patients with normal and mildly elevated fasting TG levels.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Apolipoproteins_B_MeSH S_blood_MeSH Apolipoproteins_B_blood_MeSH M_Area_Under_Curve_MeSH M_Biological_Products_MeSH S_chemistry_MeSH Biological_Products_chemistry_MeSH S_isolation_&_purification_MeSH Biological_Products_isolation_&_purification_MeSH S_pharmacology_MeSH Biological_Products_pharmacology_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Coronary_Disease_MeSH S_blood_MeSH Coronary_Disease_blood_MeSH M_Dietary_Fats_MeSH S_administration_&_dosage_MeSH Dietary_Fats_administration_&_dosage_MeSH M_Dietary_Supplements_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Fasting_MeSH S_blood_MeSH Fasting_blood_MeSH M_Female_MeSH M_Human_MeSH M_Lipoproteins__HDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__HDL_Cholesterol_blood_MeSH M_Lipoproteins__LDL_Cholesterol_MeSH S_blood_MeSH Lipoproteins__LDL_Cholesterol_blood_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Postprandial_Period_MeSH M_Triglycerides_MeSH S_blood_MeSH Triglycerides_blood_MeSH 
****** 12803580
----K 5
----T Cardiac complications after elective major vascular surgery.
----A Cardiac complications are the major cause of perioperative and late mortality and morbidity in patients undergoing elective major vascular surgery. This review focuses on the pathophysiology of perioperative complications, risk assessment and risk reduction strategies, all related to cardiovascular disease. Patients without cardiac risk factors are considered to be at low risk and no additional evaluation for coronary artery disease is recommended; beta-adrenergic blockers may reduce perioperative cardiac events; patients with one or more risk factors represent an intermediate to high-risk population. beta-Adrenergic blockers should be prescribed to all patients and coronary revascularization should be reserved for patients who have a clearly defined need for revascularization independent of the need for vascular surgery.
----P Journal_Article Review Review__Tutorial 
----M M_Anesthesia_MeSH M_Echocardiography_MeSH M_Heart_Diseases_MeSH S_diagnosis_MeSH Heart_Diseases_diagnosis_MeSH S_drug_therapy_MeSH Heart_Diseases_drug_therapy_MeSH S_etiology_MeSH Heart_Diseases_etiology_MeSH S_mortality_MeSH Heart_Diseases_mortality_MeSH S_physiopathology_MeSH Heart_Diseases_physiopathology_MeSH M_Human_MeSH M_Myocardial_Revascularization_MeSH M_Postoperative_Complications_MeSH S_diagnosis_MeSH Postoperative_Complications_diagnosis_MeSH S_drug_therapy_MeSH Postoperative_Complications_drug_therapy_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH M_Risk_Assessment_MeSH P_Vascular_Surgical_Procedures_MeSH S_mortality_MeSH Vascular_Surgical_Procedures_mortality_MeSH 
****** 12806521
----K 5
----T The triptan formulations: a critical evaluation.
----A The migraine-specific triptans have revolutionized the treatment of migraine and are usually the drugs of choice to treat a migraine attack in progress. Different triptans are available in different strengths and formulations including oral tablets, orally disintegrating tablets, nasal sprays and subcutaneous injections. In Europe, sumatriptan is also available as a suppository. Specific differences among the triptans exist as evidenced by different pharmacological profiles including T1/2, Tmax, Cmax, AUC, metabolism, drug-drug interaction profiles, amongst other parameters. How or whether these differences translate to clinical efficacy and tolerability differences is not well differentiated. Clinical distinctions among these agents are subtle and proper choice of triptan requires attention to the specific characteristics of each individual patient, knowledge of patient preference, accurate history of the efficacy of previous acute care medications as well as individual features of the drug being considered. Delivery systems may play an important role in the onset of action of triptans. The selection of an acute antimigraine drug for a patient depends upon the stratification of the patient's migraine attack by peak intensity, time to peak intensity, level of associated symptoms such as nausea and vomiting, time to associated symptoms, comorbid diseases, and concomitant treatments that might cause drug-drug interactions. The clinician has in his armamentarium an ever-expanding variety of medications, available in multiple formulations and dosages, with good safety and tolerability profiles. Continued clinical use will yield familiarity with the various triptans, and it should become possible for the interested physician to match individual patient needs with the specific characteristics of a triptan to optimize therapeutic benefit.
----P Journal_Article Review Review__Tutorial 
----M M_Analgesics_MeSH S_pharmacology_MeSH Analgesics_pharmacology_MeSH S_therapeutic_use_MeSH Analgesics_therapeutic_use_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Serotonin_Agonists_MeSH S_pharmacology_MeSH Serotonin_Agonists_pharmacology_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH 
****** 12804664
----K 5
----T Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance.
----A Migraine is a disorder in which central nervous sytem dysfunction might play a pivotal role. Electroneurophysiology seems thus particularly suited to study its pathophysiology. We have extensively reviewed evoked potential and transcranial magnetic stimulation studies performed in migraineurs in order to identify their pathophysiologic significance. Publications available to us were completed by a Medline search. Retrieved and personal data were compared with respect to methodology and interpreted according to present knowledge on cortical information processing. Results are in part contradictory which appears to be method-, patient- and disease- related. Nonetheless, both evoked potential and transcranial magnetic stimulation studies demonstrate that the cerebral cortex, and possibly subcortical structures, are dysfunctioning interictally in both migraine with and without aura. These electrophysiologic abnormalities tend to normalise just before and during an attack and some of them seem to have a clear familial and predisposing character. Besides the studies of magnetophosphenes which have yielded contrasting results, chiefly because the method is not sufficiently reliable, most recent electrophysiologic investigations of cortical activities in migraine favour deficient habituation and decreased preactivation cortical excitability as the predominant interictal dysfunctions. We propose that the former is a consequence of the latter and that it could favour both interictal cognitive disturbances as well as a cerebral metabolic disequilibrium that may play a role in migraine pathogenesis. To summarize, electrophysiologic studies demonstrate in migraine between attacks a cortical, and possibly subcortical, dysfunction of which the hallmark is deficient habituation.
----P Journal_Article Review Review__Academic 
----M M_Brain_Mapping_MeSH M_Cerebral_Cortex_MeSH S_anatomy_&_histology_MeSH Cerebral_Cortex_anatomy_&_histology_MeSH S_physiopathology_MeSH Cerebral_Cortex_physiopathology_MeSH M_Electric_Stimulation_MeSH S_methods_MeSH Electric_Stimulation_methods_MeSH P_Evoked_Potentials_MeSH M_Human_MeSH P_Magnetics_MeSH M_Migraine_MeSH S_physiopathology_MeSH Migraine_physiopathology_MeSH 
****** 12804926
----K 3
----T The effect of a neuropeptide Y Y1 receptor antagonist in patients with angina pectoris.
----A AIMS: Neuropeptide Y (NPY) is a potent vasoconstrictor released during sympathetic activation that may be involved in myocardial ischaemia. We examined the effect of a Y1 receptor antagonist on haemodynamic and ischaemic responses to exercise in patients with coronary artery disease. METHODS AND RESULTS: Eighty-two evaluable male patients were included in a randomized, double blind, two-way crossover study with a low dose (6.7 microg/kg/min; n=59)and a high dose (13.3 microg/kg/min; n=23) of the Y1 receptor antagonist AR-H040922 given as infusions for 2h or placebo. Myocardial ischaemia during a symptom-limited exercise test was monitored by conventional ST-segment analysis and heart rate (HR)-adjusted ST changes including the ST/HR slope and ST/HR recovery. Administration of the high dose AR-H040922 attenuated systolic blood pressure by 6-11 mmHg (p<0.05) during and after exercise without affecting HR. None of the two doses of AR-H040922 influenced any of the ischaemic parameters or duration of exercise, however. The maximal increase in NPY was higher during AR-H040922 (p<0.05) compared with placebo. CONCLUSIONS: Selective NPY Y1 receptor blockade attenuates the increase in blood pressure during exercise indicating a role for endogenous NPY in blood pressure regulation. Despite this effect, the Y1 receptor antagonist did not influence exercise-induced ischaemic parameters in patients with coronary artery disease.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Amides_MeSH S_blood_MeSH Amides_blood_MeSH S_therapeutic_use_MeSH Amides_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Chronic_Disease_MeSH M_Cross-Over_Studies_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Exercise_Test_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Neuropeptide_Y_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Neuropeptide_Y_antagonists_&_inhibitors_MeSH S_blood_MeSH Receptors__Neuropeptide_Y_blood_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12808481
----K 5
----T Classes of antianginal compounds: old and new--therapeutic implications.
----A A relatively novel group of drugs that inhibit the funny current in the sinus node pacemaker cells, the so-called specific bradycardic agents, are likely to play a significant role in the management of a wide range of cardiovascular disorders, including the sinus tachyarrhythmias. This comprehensive review initially provides an insight into these agents, their historical background, and their mechanism of action. It then discusses the differential diagnosis of the sinus tachyarrhythmias (normal sinus tachycardia, inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome, and sinus node reentry tachycardia), elaborates on their pathophysiologic basis, and provides up-to-date evidence-based information on their optimum management. The specific bradycardic agents, by the very nature of their mode of action, may prove ideal therapies for the management of the sinus tachyarrhythmias, and this is explored at every stage.
----P Comment Editorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angina_Pectoris_MeSH S_drug_therapy_MeSH Angina_Pectoris_drug_therapy_MeSH S_physiopathology_MeSH Angina_Pectoris_physiopathology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Enzyme_Inhibitors_therapeutic_use_MeSH M_Human_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 12808482
----K 5
----T Sinus tachyarrhythmias and the specific bradycardic agents: a marriage made in heaven?
----A A relatively novel group of drugs that inhibit the funny current in the sinus node pacemaker cells, the so-called specific bradycardic agents, are likely to play a significant role in the management of a wide range of cardiovascular disorders, including the sinus tachyarrhythmias. This comprehensive review initially provides an insight into these agents, their historical background, and their mechanism of action. It then discusses the differential diagnosis of the sinus tachyarrhythmias (normal sinus tachycardia, inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome, and sinus node reentry tachycardia), elaborates on their pathophysiologic basis, and provides up-to-date evidence-based information on their optimum management. The specific bradycardic agents, by the very nature of their mode of action, may prove ideal therapies for the management of the sinus tachyarrhythmias, and this is explored at every stage.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Benzazepines_MeSH S_pharmacology_MeSH Benzazepines_pharmacology_MeSH S_therapeutic_use_MeSH Benzazepines_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clonidine_MeSH S_analogs_&_derivatives_MeSH Clonidine_analogs_&_derivatives_MeSH S_pharmacology_MeSH Clonidine_pharmacology_MeSH S_therapeutic_use_MeSH Clonidine_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diagnosis__Differential_MeSH M_Human_MeSH M_Phthalimides_MeSH S_pharmacology_MeSH Phthalimides_pharmacology_MeSH S_therapeutic_use_MeSH Phthalimides_therapeutic_use_MeSH M_Pyrimidines_MeSH S_pharmacology_MeSH Pyrimidines_pharmacology_MeSH S_therapeutic_use_MeSH Pyrimidines_therapeutic_use_MeSH M_Sinoatrial_Node_MeSH S_drug_effects_MeSH Sinoatrial_Node_drug_effects_MeSH S_physiopathology_MeSH Sinoatrial_Node_physiopathology_MeSH M_Tachycardia__Sinus_MeSH S_diagnosis_MeSH Tachycardia__Sinus_diagnosis_MeSH S_drug_therapy_MeSH Tachycardia__Sinus_drug_therapy_MeSH S_physiopathology_MeSH Tachycardia__Sinus_physiopathology_MeSH M_Vasodilator_Agents_MeSH S_pharmacology_MeSH Vasodilator_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Verapamil_MeSH S_analogs_&_derivatives_MeSH Verapamil_analogs_&_derivatives_MeSH S_pharmacology_MeSH Verapamil_pharmacology_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 12808484
----K 5
----T Vasopressor agents for cardiopulmonary resuscitation.
----A The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents produce systemic vasoconstriction. This increases aortic diastolic pressure, and consequently, coronary and cerebral perfusion pressures. The pharmacologic responses to the adrenergic agents are mediated by a group of receptors that are classified as alpha (alpha), including alpha1 and alpha2, and beta (beta), including beta1 and beta2. Epinephrine, which has each of these adrenergic actions, has been the preferred adrenergic agent for the management of cardiac arrest for almost 40 years. Its primary efficacy is due to its alpha-adrenergic vasopressor effects. This contrasts with its beta-adrenergic actions, which are inotropic, chronotropic, and vasodilator. Accordingly, beta-adrenergic actions prompt increases in myocardial oxygen consumption, ectopic ventricular arrhythmias, and transient hypoxemia due to pulmonary arteriovenous shunting. This may account for the failure to demonstrate that epinephrine improves ultimate outcomes in human victims of cardiac arrest. Major interest has more recently been focused on selective alpha-adrenergic agonists. Both alpha1-agonists and alpha2-agonists are peripheral vasopressors. However, rapid desensitization of alpha1-adrenergic receptors occurs during cardiopulmonary resuscitation. Moreover, alpha1-adrenergic receptors are present in the myocardium, and beta1-agonists, like beta-adrenergic agonists, increase myocardial oxygen consumption. If they cross the blood-brain barrier, alpha2-adrenoceptor agonists also have centrally acting vasodilator effects. In the absence of central nervous system access, alpha2-adrenergic agonists have selective peripheral vasoconstrictor effects. Under experimental conditions of cardiopulmonary resuscitation, selective alpha2-agonists, which do not gain entrance into the brain, produce only systemic vasoconstriction. Experimentally, these selective alpha2-agonists are as effective as epinephrine for initial cardiac resuscitation and have the additional advantage of minimizing myocardial oxygen consumption during the global myocardial ischemia of cardiac arrest. Accordingly, myocardial ischemic injury during cardiopulmonary resuscitation is minimized, and postresuscitation myocardial function is preserved with improved survival.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_alpha-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Agonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Agonists_therapeutic_use_MeSH M_Animals_MeSH M_Brain_Ischemia_MeSH S_complications_MeSH Brain_Ischemia_complications_MeSH S_drug_therapy_MeSH Brain_Ischemia_drug_therapy_MeSH S_therapy_MeSH Brain_Ischemia_therapy_MeSH P_Cardiopulmonary_Resuscitation_MeSH M_Epinephrine_MeSH S_therapeutic_use_MeSH Epinephrine_therapeutic_use_MeSH M_Heart_Arrest_MeSH S_complications_MeSH Heart_Arrest_complications_MeSH S_drug_therapy_MeSH Heart_Arrest_drug_therapy_MeSH S_therapy_MeSH Heart_Arrest_therapy_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Vasoconstrictor_Agents_MeSH S_therapeutic_use_MeSH Vasoconstrictor_Agents_therapeutic_use_MeSH M_Vasopressins_MeSH S_therapeutic_use_MeSH Vasopressins_therapeutic_use_MeSH 
****** 12808486
----K 3
----T The combination of nebivolol plus pravastatin is associated with a more beneficial metabolic profile compared to that of atenolol plus pravastatin in hypertensive patients with dyslipidemia: a pilot study.
----A Nebivolol, a selective beta1-lipophilic blocker, achieves blood pressure control by modulating nitric oxide release in addition to b-blockade. This dual mechanism of action could result in minimum interference with lipid metabolism compared to atenolol, a classic beta1-selective blocker. Hypertensive patients commonly exhibit lipid abnormalities and frequently require statins in combination with the anti-hypertensive therapy. We conducted this trial in order to clarify the effect on the metabolic profile of beta-blocker therapy with atenolol or nebivolol alone, or in conjunction with pravastatin. Thirty hypertensive hyperlipidemic men and women (total cholesterol >240 mg/dL [6.2 mmol/L], low-density lipoprotein cholesterol >190 mg/dL [4.9 mmol/L], triglycerides <500 mg/dL [5.6 mmol/L]) were separated in two groups. One group consisted of 15 subjects on atenolol therapy (50 mg daily), and the other group included 15 subjects on nebivolol therapy (5 mg daily). After 12 weeks of beta-blocker therapy, pravastatin (40 mg daily) was added in both groups for another 12 weeks. Atenolol significantly increased triglyceride levels by 19% (P=.05), while nebivolol showed a trend to increase high-density lipoprotein cholesterol by 8% (NS) and to decrease triglyceride levels by 5% (NS). Atenolol significantly increased lipoprotein(a) by 30% (P=.028). Fibrinogen levels were equally and not significantly decreased in both groups by 9% and 7%, respectively. Furthermore, atenolol and nebivolol decreased serum high-sensitivity C-reactive protein levels by 14% (P=.05) and 15% (P=.05), respectively. On the other hand, both atenolol and nebivolol showed a trend to increase homocysteine levels (NS) by 13% and 11%, respectively. Although uric acid levels remained the same, atenolol significantly increased the fractional excretion of uric acid by 33% (P=.03). Following nebivolol administration, glucose levels remained the same, while insulin levels were reduced by 10% and the HOMA index (fasting glucose levels multiplied by fasting insulin levels and divided by 22.5) was reduced by 20% (P=.05). There were no significant differences between the two patient groups in the measured parameters after the administration of beta-blockers, except for triglycerides (P<.05) and the HOMA index (P=.05). The addition of pravastatin to all patients (n=30) decreased total cholesterol by 21% (P<.001), low-density lipoprotein cholesterol by 28% (P<.001), apolipoprotein-B by 22% (P<.001), apolipoprotein-E by 15% (P=.014) and lipoprotein(a) levels by 12% (P=.023). Moreover, homocysteine levels and C-reactive protein were reduced by 17% (P=.05) and 43% (P=.05), respectively. We conclude that nebivolol seems to be a more appropriate therapy in hypertensive patients with hyperlipidemia and carbohydrate intolerance. Finally, the addition of pravastatin could further correct the well-established predictors of cardiovascular events.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Anticholesteremic_Agents_MeSH S_pharmacology_MeSH Anticholesteremic_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anticholesteremic_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Benzopyrans_MeSH S_pharmacology_MeSH Benzopyrans_pharmacology_MeSH S_therapeutic_use_MeSH Benzopyrans_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Drug_Therapy__Combination_MeSH M_Ethanolamines_MeSH S_pharmacology_MeSH Ethanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Ethanolamines_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hyperlipidemia_MeSH S_complications_MeSH Hyperlipidemia_complications_MeSH S_drug_therapy_MeSH Hyperlipidemia_drug_therapy_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Pilot_Projects_MeSH M_Pravastatin_MeSH S_pharmacology_MeSH Pravastatin_pharmacology_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH 
****** 12809965
----K 5
----T An analysis of cholesterol control and statin use in the Losartan Intervention for Endpoint Reduction in Hypertension Study.
----A BACKGROUND: There is general agreement that patients who have elevated lipid levels and/or risk factors for or existing cardiovascular disease should receive aggressive cholesterol-lowering therapy. However, it is not clear whether patients are receiving the recommended treatment. OBJECTIVE: This study evaluated cholesterol control and statin use in the setting of a large, long-term cardiovascular end point trial. METHODS: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study was conducted between 1995 and 2001 to compare the incidence of cardiovascular morbidity and mortality with losartan- or atenolol-based treatment in 9193 patients aged 55 to 80 years with hypertension and left ventricular hypertrophy. The mean (SD) duration of follow-up was 4.8 (0.9) years. Use of lipid-lowering therapy was at the discretion of the investigator. In the present study, analyses of baseline and end-of-study mean total cholesterol (TC) and high-density lipoprotein cholesterol levels and statin use were performed for the combined treatment groups. Based on generally accepted guidelines, achievement of a TC level <5.0 mmol/L (193.5 mg/dL) was used as the treatment target for the purpose of these analyses. The proportions of patients with TC levels above this cutoff were calculated at baseline and at the final visit. RESULTS: A total of 8653 patients had baseline and end-of-study cholesterol measurements and were included in this analysis. At baseline, 528 (6.1%) patients were receiving statins; TC levels were above the cutoff in 381 (72.2%) of these patients, who had a mean TC level of 6.07 mmol/L (234.7 mg/dL). Of 8125 (93.9%) patients who were not receiving statins at baseline, TC levels were above the cutoff in 6859 (84.4%), with a mean TC level of 6.37 mmol/L (246.4 mg/dL). At the end of the study, 1892 (21.9%) patients were receiving a statin; TC levels were above the cutoff in 1096 (57.9%) of these patients, who had a mean TC level of 5.99 mmol/: (231.6 mg/dL). Of 6761 (78.1%) patients who were not receiving statins at the end of the study, TC levels were above the cutoff in 5316 (78.6%), with a mean TC level of 6.24 mmol/L (241.4 mg/dL). CONCLUSIONS: In this long-term cardiovascular end point study in patients with moderate to severe hypertension and left ventricular hypertrophy, statins were not optimally administered and cholesterol levels were poorly controlled.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Cholesterol_MeSH S_blood_MeSH Cholesterol_blood_MeSH M_Double-Blind_Method_MeSH M_Endpoint_Determination_MeSH M_Female_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Regression_Analysis_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12812405
----K 5
----T Headache case studies for the primary care physician.
----A In a given year, over 5% of persons in the United States seek medical care for headaches, most often seeing their primary care physician. The five cases here review diagnosis and treatment of migraine and other primary headaches, medication rebound headaches, and headaches in the elderly including temporal arteritis. Although headaches (along with dizziness and back pain) may be one of the least preferred diseases internists see, the increasing number of effective treatments may favorably change this opinion and result in better care for their patients.
----P Case_Reports Journal_Article Review Review__Multicase 
----M M_Adult_MeSH M_Female_MeSH M_Headache_MeSH S_diagnosis_MeSH Headache_diagnosis_MeSH S_therapy_MeSH Headache_therapy_MeSH M_Human_MeSH M_Middle_Aged_MeSH M_Physicians__Family_MeSH S_education_MeSH Physicians__Family_education_MeSH 
****** 12771007
----K 5
----T Distal myocardial protection during percutaneous coronary intervention with an intracoronary beta-blocker.
----A BACKGROUND: Experimental studies have demonstrated that intravenous beta-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. METHODS AND RESULTS: Patients undergoing PCI (n=150) were randomly assigned in a double-blind fashion to receive IC propranolol (n=75) or placebo (n=75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (P=0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (P=0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, P=0.004). CONCLUSIONS: IC administration of propranolol protects the myocardium during PCI, significantly reducing the incidence of MI and improving short-term clinical outcomes.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH P_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH S_adverse_effects_MeSH Angioplasty__Transluminal__Percutaneous_Coronary_adverse_effects_MeSH M_Aspirin_MeSH S_administration_&_dosage_MeSH Aspirin_administration_&_dosage_MeSH M_Biological_Markers_MeSH S_analysis_MeSH Biological_Markers_analysis_MeSH M_Coronary_Arteriosclerosis_MeSH S_therapy_MeSH Coronary_Arteriosclerosis_therapy_MeSH M_Creatine_Kinase_MeSH S_analysis_MeSH Creatine_Kinase_analysis_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Human_MeSH M_Injections__Intra-Arterial_MeSH M_Isoenzymes_MeSH S_analysis_MeSH Isoenzymes_analysis_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Myocardial_Infarction_MeSH S_etiology_MeSH Myocardial_Infarction_etiology_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_administration_&_dosage_MeSH Platelet_Aggregation_Inhibitors_administration_&_dosage_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Risk_MeSH M_Sample_Size_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12815569
----K 5
----T Survival and hospitalization in heart failure patients with or without diabetes treated with beta-blockers.
----A BACKGROUND: Physicians are still concerned about prescribing beta-blockers in diabetic patients with heart failure. METHODS: In the outcome research study (the Beta-Blockers in Patients With Congestive Heart Failure: Guided Use in Clinical Practice [BRING-UP] study), the responsible clinicians could decide whether to start beta-blocker treatment and which agent to use. A total of 3091 patients were enrolled by 202 cardiologic centers: 25% of the recruited patients were already on beta-blockers, 28% started treatment at the enrollment visit, and 47% were not started on beta-blockers. RESULTS: The 1-year mortality, hospitalization rate, and the combined end point of mortality or hospitalization were higher in diabetic patients (15.8% versus 10.9%; relative risk [RR] = 1.44; 95% confidence intervals [CI] 1.16-1.78, P =.001) (31.0% versus 24.0%; RR = 1.28; 95% CI 1.11-1.49; P =.0009) (40.5% versus 30.1%; RR = 1.35; 95% CI 1.19-1.51; P =.0001). The event-free analysis of the 4 groups (diabetic patients not treated with beta-blockers, diabetic patients treated with beta-blockers, nondiabetic patients not treated with beta-blockers, nondiabetic patients treated with beta-blockers) showed that patients treated with beta-blockers had a higher event-free probability than patients not treated with beta-blockers regardless the presence of diabetes (P <.0001). CONCLUSIONS: On the basis of post hoc analysis, diabetic patients with chronic heart failure benefit from beta-blockers even if at a lower degree. Thus, there are no justifications to avoid beta-blockers in heart failure patients in the presence of diabetes.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Diabetes_Mellitus_MeSH S_drug_therapy_MeSH Diabetes_Mellitus_drug_therapy_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH S_mortality_MeSH Diabetes_Mellitus_mortality_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH S_statistics_&_numerical_data_MeSH Hospitalization_statistics_&_numerical_data_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Outcome_and_Process_Assessment_(Health_Care)_MeSH M_Retrospective_Studies_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Rate_MeSH 
****** 12815570
----K E
----T Tolerability to beta-blocker therapy among heart failure patients in clinical practice.
----A BACKGROUND: Although beta-blockers were well-tolerated by heart failure (HF) patients in clinical trials, tolerability of these drugs in a general population of HF patients is not well-described. METHODS: We studied a total of 308 encounters with beta-blockers therapy in 268 ambulatory HF patients. Side effects and frequency and predictors of discontinuation of therapy were studied. Independent predictors of discontinuation were assessed. RESULTS: Weight gain (59%), fatigue (56%), dizziness (41%), and dyspnea (29%) were the most common side effects. Fifty-one patients (19%) were discontinued on therapy with any 1 particular beta-blocker. Fatigue (30%) and hypotension (28%) were the most common reasons for discontinuation. Forty (78%) of these were given a trial with a different beta-blocker. Of these, 22 (55%) attempts with a different beta-blocker were tolerated. Thus the overall absolute discontinuation rate was only 7% for patients who were given a trial with different beta-blockers or 11% for the entire study population. Independent predictors of discontinuation of therapy included advanced symptoms, nonischemic etiology, history of pulmonary disease, and higher diuretic doses. CONCLUSION: Side effects with beta-blockers in a general population of HF patients are common; however, with changes in medical management, most patients can tolerate them eventually. In case of intolerance to one kind, a trial with a different beta-blocker is indicated.
----P Journal_Article Multicenter_Study 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Algorithms_MeSH M_Dizziness_MeSH S_chemically_induced_MeSH Dizziness_chemically_induced_MeSH M_Dyspnea_MeSH S_chemically_induced_MeSH Dyspnea_chemically_induced_MeSH M_Fatigue_MeSH S_chemically_induced_MeSH Fatigue_chemically_induced_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Weight_Gain_MeSH 
****** 12818283
----K 5
----T Portal pressure response to losartan compared with propranolol in patients with cirrhosis.
----A OBJECTIVES: Losartan, an angiotensin II receptor blocker, has portal hypotensive effects. This study evaluates the effect of losartan on portal pressure after 14 days and compares it with that of propranolol. METHODS: A total of 39 individuals with cirrhosis were randomized into two groups of 19 and 20 patients each and were treated with losartan and propranolol, respectively. Hepatic venous pressure gradient was measured at baseline and on day 14 of therapy. Responders to therapy had hepatic venous pressure gradient reduction of >/=20% of baseline value. RESULTS: With losartan, 15 of 19 (78.94%) patients were responders and with propranolol, nine of 20 (45%) patients were responders (p < 0.05). Although the hepatic venous pressure gradient reduction (i.e., percentage from baseline) with losartan (26.74 +/- 21.7%) was higher than with propranolol (14.52 +/- 32%), the difference was not significant. The reduction in hepatic venous pressure gradient with losartan was contributed mainly by a significant drop of wedge hepatic venous pressure from 32.42 +/- 6.61 mm of Hg to 28.31 +/- 5.09 mm of Hg (p < 0.05) compared to that with propranolol, which was from 34.55 +/- 5.41 mm of Hg to 32.75 +/- 8.13 mm of Hg (p > 0.05). Responders among alcohol-abusing patients were significantly higher with losartan (81.8%) compared to those on propranolol (27.2%; p < 0.05). In the losartan group, all seven nonascitic cirrhotic individuals, as compared with two of five in the propranolol group, responded to the drugs. During the study, no significant side effects were observed in either group (who were not receiving diuretics) or in follow-up with diuretics. CONCLUSIONS: Losartan is as effective as propranolol in reducing portal pressure in cirrhotic patients who are not receiving diuretics. Losartan is also superior to propranolol for achieving target level hepatic venous gradient for prevention of variceal bleeding in nonascitic and alcohol-abusing cirrhotic patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Adult_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Comparative_Study_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_etiology_MeSH Esophageal_and_Gastric_Varices_etiology_MeSH S_physiopathology_MeSH Esophageal_and_Gastric_Varices_physiopathology_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH S_physiopathology_MeSH Hypertension__Portal_physiopathology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH S_physiopathology_MeSH Liver_Cirrhosis_physiopathology_MeSH M_Losartan_MeSH S_pharmacology_MeSH Losartan_pharmacology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Portal_Vein_MeSH S_physiology_MeSH Portal_Vein_physiology_MeSH M_Propranolol_MeSH S_pharmacology_MeSH Propranolol_pharmacology_MeSH 
****** 12820820
----K 5
----T Calcium channel blockers as the treatment of choice for hypertension in renal transplant recipients: fact or fiction.
----A Posttransplantation hypertension has been identified as an independent risk factor for chronic allograft dysfunction and loss. Based on available morbidity and mortality data, posttransplantation hypertension must be identified and managed appropriately. During the past decade, calcium channel blockers have been recommended by some as the antihypertensive agents of choice in this population, because it was theorized that their vasodilatory effects would counteract the vasoconstrictive effects of the calcineurin inhibitors. With increasing data becoming available, reexamining the use of traditional antihypertensive agents, including diuretics and beta-blockers, or the newer agents, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers, may be beneficial. Transplant clinicians must choose antihypertensive agents that will provide their patients with maximum benefit, from both a renal and a cardiovascular perspective. Beta-blockers, diuretics, and ACE inhibitors have all demonstrated significant benefit on morbidity and mortality in patients with cardiovascular disease. Calcium channel blockers have been shown to possess the ability to counteract cyclosporine-induced nephrotoxicity. When compared with beta-blockers, diuretics, and ACE inhibitors, however, the relative risk of cardiovascular events is increased with calcium channel blockers. With the long-term benefits of calcium channel blockers on the kidney unknown and a negative cardiovascular profile, these agents are best reserved as adjunctive therapy to beta-blockers, diuretics, and ACE inhibitors.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH P_Kidney_Transplantation_MeSH P_Postoperative_Complications_MeSH M_Treatment_Outcome_MeSH 
****** 12820824
----K 5
----T Better living through chemistry: does it still apply to patients after myocardial infarction?
----A Sudden cardiac death is an elusive process that claims a significant number of lives annually in the United States. It is often associated with increased mortality within the first year after myocardial infarction, with the highest frequency occurring among patients with left ventricular dysfunction. Therefore, increasing survival rates in patients with a history of both disorders is an important goal of therapy. Recent trials suggested that an implantable cardioverter-defibrillator (ICD) in these patients may be superior to medical intervention in reducing the high mortality rate. Four major trials measured the benefits of an ICD for patients at risk for life-threatening ventricular arrhythmias. We assessed whether patients in these trials received adequate drug therapy as directed by American College of Cardiology-American Heart Association guidelines. One aim was to determine if medicated patients who served as controls in the trials were fairly represented. Furthermore, the need for improved overall guideline adherence was apparent.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH P_Defibrillators__Implantable_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH M_Platelet_Aggregation_Inhibitors_MeSH M_Randomized_Controlled_Trials_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 12821958
----K 5
----T Why not prescribe the best drugs for hypertension now?
----A As Westernised societies have become more affluent, the attitudes of the population have become more risk-aware. People are now intolerant of small risks as well as the physical or mental discomforts from drug side effects. Safety and tolerability are now major forces driving the development of new medicines for the treatment of chronic illnesses and the prevention of increasingly rare events. For example, over the past decades, lower and lower treatment thresholds have been recommended in hypertension. Public perception of risk strongly influences the acceptability of lifetime treatment, especially for mild hypertension. This era has also witnessed great advances in the development of antihypertensive drugs that combine efficacy with unsurpassed tolerability. However, the philosophy of Scottish teachers of Materia medica still appears to be followed-'never be the first or the last to prescribe a new drug'. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists are as safe and as efficacious as other antihypertensive medications and better tolerated. Large trials (HOT, HOPE, UKPDS and PROGRESS) point to the need for rigorous control of blood pressure particularly in high-risk individuals. Antihypertensive drugs that act on the renin-angiotensin system will probably impact significantly on achieving optimal blood pressure levels. Should it not now be accepted that high-risk patients should have ACE inhibitors and angiotensin II receptor antagonists prescribed as first-line agents? We review the evidence for the use of ACE inhibitors and angiotensin II receptor antagonists as antihypertensive agents.
----P Journal_Article Review Review_Literature 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Patient_Acceptance_of_Health_Care_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH 
****** 12824091
----K 5
----T Progression of chronic renal failure.
----A Chronic renal failure is characterized by a persistently abnormal glomerular filtration rate. The rate of progression varies substantially. Several morphologic features are prominent: fibrosis, loss of native renal cells, and infiltration by monocytes and/or macrophages. Mediators of the process include abnormal glomerular hemodynamics, hypoxia, proteinuria, hypertension, and several vasoactive substances (ie, cytokines and growth factors). Several predisposing host factors may also contribute to the process. Treatments to delay progression are aimed at treating the primary disease and at strictly controlling the systemic blood pressure and proteinuria. The role of antihypertensive agents, statins, and use of other maneuvers such as protein restriction and novel approaches are also discussed herein.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anoxia_MeSH M_Cell_Death_MeSH M_Complement_Activation_MeSH M_Disease_Progression_MeSH M_Hemodynamic_Processes_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Kidney_Failure__Chronic_MeSH S_etiology_MeSH Kidney_Failure__Chronic_etiology_MeSH S_physiopathology_MeSH Kidney_Failure__Chronic_physiopathology_MeSH S_therapy_MeSH Kidney_Failure__Chronic_therapy_MeSH M_Proteinuria_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Smoking_MeSH S_adverse_effects_MeSH Smoking_adverse_effects_MeSH 
****** 12823642
----K 5
----T Microalbuminuria and hypertension with focus on type 1 and type 2 diabetes.
----A Microalbuminuria and hypertension with Over the past decade, there has been considerable focus on the concept of microalbuminuria, not only because it predicts renal disease in type 1 and type 2 diabetes, but also because it relates to premature mortality in the diabetic and in the general population. More importantly, intervention at this stage is now possible with the perspective of preserving glomerular filtration rate (GFR) and ameliorating cardiovascular disease and ensuing strong end-points. INITIAL STUDIES: The concept of microalbuminuria was introduced about 20 years ago and since then there has been a multitude of studies and papers on this subject using the original definition, but not always, in the US. Before that time it was suggested, mainly from the US, that diabetic renal disease was an untreatable relentlessly progressive condition. GENETIC STUDIES: There is an overwhelming number of studies on genetics and diabetes and also covering the genetics of diabetic complications including nephropathy. However, so far the results are extremely disappointing. Patients at risk cannot be identified and genetic analyses are of no value as a guide to treatment. The notion that the development of complications is controlled mainly by a special genetic pattern is increasingly doubtful. In genetic studies, it is rather phenotypic well-accepted risk factors that dominate. STRUCTURAL BASIS OF MICROALBUMINURIA: Patients with microalbuminuria have significant abnormalities in the kidney, including glomeruli. This is quite clear in patients with type 1 diabetes, but is also seen in type 2 diabetes, where on the other hand, other risk factors such as hypertension and dyslipidaemia also seem to be of importance, including loss of autoregulation. Renal biopsies are generally not indicated in the management of diabetic patients. MICROALBUMINURIA AND EARLY MORTALITY: It is quite clear that microalbuminuria predicts early mortality both in type 1 and type 2 diabetes. The association to other risk factors may partly explain this--but this does not account for the whole picture. Endothelial dysfunction as well as inflammatory and arteriosclerotic abnormalities in blood vessels may be a relevant hypothesis that needs to be further explored along with other possibilities. CLINICAL COURSE AND ASSOCIATED ABNORMALITIES: The risk factor for progression in normoalbuminuric patients to microalbuminuria is higher than normal albumin excretion (strongest factor), poor glycaemic control, elevated blood pressure, and to some extent smoking. The clinical course of microalbuminuria is usually progressive, but with the more effective intervention now available we encounter that the so-called natural history (without intervention) is increasingly difficult to study. Microalbuminuria is clearly associated with a number of abnormalities, almost in all organs, but GFR is generally well preserved in spite of more advanced structural lesions. Therefore, microalbuminuria is an important marker for more pronounced diabetic vascular disease in general as well as for nephropathy. Regression to normoalbuminuria only rarely occurs during standard unchanged nonintensive treatment. TREATMENT STRATEGIES: The best possible glycaemic control is important in preventing and ameliorating the course of normo- and micro-albuminuria. Another major treatment strategy, especially in microalbuminuric patients, is antihypertensive treatment including inhibition of the renal angiotensin aldosterone system. Numerous new studies are available, both in type 1 and type 2 diabetes, documenting that not only microalbuminuria but also renal and cardiovascular complications in these patient are also far better controlled by early detection and treatment. Therefore, screening for microalbuminuria should be a strategy in all diabetes management followed by effective intervention as outlined in this paper.
----P Journal_Article Review Review__Tutorial 
----M M_Albuminuria_MeSH S_etiology_MeSH Albuminuria_etiology_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Diabetes_Mellitus__Type_I_MeSH S_complications_MeSH Diabetes_Mellitus__Type_I_complications_MeSH M_Diabetes_Mellitus__Type_II_MeSH S_complications_MeSH Diabetes_Mellitus__Type_II_complications_MeSH M_Diabetic_Nephropathies_MeSH S_complications_MeSH Diabetic_Nephropathies_complications_MeSH M_Diet__Protein-Restricted_MeSH M_Diet__Sodium-Restricted_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Male_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Risk_Factors_MeSH 
****** 12826772
----K 5
----T Treatment of heart failure in older persons. Dilemmas with coexisting conditions: diabetes mellitus, chronic obstructive pulmonary disease, and arthritis.
----A Diabetes mellitus is a risk factor for congestive heart failure. Diabetics with congestive heart failure should have good glycemic control, treatment of hypertension and dyslipidemia, and treatment with diuretics, angiotensin-converting enzyme inhibitors, and beta blockers as well as digoxin, if the left ventricular ejection fraction is abnormal. Patients with chronic obstructive pulmonary disease may have left ventricular failure because of a coexistent cardiac disorder or right ventricular failure from pulmonary hypertension. An acute respiratory tract infection may precipitate right ventricular failure and should be treated. Alveolar hypoxia should be corrected by improving alveolar ventilation through relieving airflow obstruction with bronchodilators and by increasing inspired oxygen concentration. Loop diuretics should be used cautiously. Beta blockers may be given to patients with chronic obstructive pulmonary disease and left ventricular failure if bronchospasm is not present. Angiotensin-converting enzyme inhibitors should be used to treat left ventricular failure. Digitalis should not be used in patients with right ventricular failure due to chronic obstructive pulmonary disease. Nonsteroidal anti-inflammatory drugs are contraindicated in patients with congestive heart failure. There are controversial data about the negative interaction between aspirin and angiotensin-converting enzyme inhibitors in patients with congestive heart failure. Patients with arthritis and congestive heart failure needing large doses of aspirin for pain relief may be treated instead with acetaminophen, tramadol, or Percocet if necessary for chronic severe pain.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Arthritis_MeSH S_epidemiology_MeSH Arthritis_epidemiology_MeSH M_Comorbidity_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH M_Pulmonary_Disease__Chronic_Obstructive_MeSH S_epidemiology_MeSH Pulmonary_Disease__Chronic_Obstructive_epidemiology_MeSH 
****** 12826775
----K 5
----T Depression and congestive heart failure.
----A The prevalence rates of depression in congestive heart failure patients range from 24%-42%. Depression is a graded, independent risk factor for readmission to the hospital, functional decline, and mortality in patients with congestive heart failure. Physicians can assess depression by using the SIG E CAPS + mood mnemonic, or any of a number of easily administered and scored self-report inventories. Cognitive-behavior therapy is the preferred psychological treatment. Cognitive-behavior therapy emphasizes the reciprocal interactions among physiology, environmental events, thoughts, and behaviors, and how these may be altered to produce changes in mood and behavior. Pharmacologically, the selective serotonin reuptake inhibitors are recommended, whereas the tricyclic antidepressants are not recommended for depression in congestive heart failure patients. The combination of a selective serotonin reuptake inhibitor with cognitive-behavior therapy is often the most effective treatment.
----P Journal_Article Review Review__Tutorial 
----M M_Antidepressive_Agents_MeSH S_therapeutic_use_MeSH Antidepressive_Agents_therapeutic_use_MeSH M_Cognitive_Therapy_MeSH M_Comorbidity_MeSH M_Depression_MeSH S_drug_therapy_MeSH Depression_drug_therapy_MeSH S_epidemiology_MeSH Depression_epidemiology_MeSH S_therapy_MeSH Depression_therapy_MeSH M_Drug_Interactions_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH M_Human_MeSH 
****** 12826780
----K 5
----T The JNC 7: stepped care is alive and well.
----A 
----P Editorial 
----M M_Alcohol_Drinking_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Diet_MeSH M_Diet__Sodium-Restricted_MeSH M_Exercise_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_therapy_MeSH Hypertension_therapy_MeSH 
****** 12826781
----K 5
----T The ANBP2 and ALLHAT: conflicting or consistent?
----A 
----P Journal_Article 
----M M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Australia_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH M_United_States_MeSH 
****** 12826782
----K 4
----T Response to six classes of antihypertensive medications by body mass index in a randomized controlled trial.
----A Blood pressure increases with increasing body mass index (BMI) and BMI is linearly related to blood pressure in population studies. Obesity has been said to cause resistance to antihypertensive medications. We compared short-term and 1-year blood pressure response by BMI category and weight change with hydrochlorothiazide, atenolol, diltiazem-SR, captopril, clonidine, prazosin, or placebo in 1292 male veterans. Drug doses were titrated to achieve goal diastolic blood pressure <90 mm Hg over 4-8 weeks. Patients who achieved goal blood pressure were maintained for 1 year. BMI did not predict change in systolic, diastolic or pulse pressures during titration for any drug. At 1 year obese patients (BMI >30) were 2.5 times more likely to have diastolic blood pressure controlled by atenolol than normal weight (BMI <27) patients (p=0.01). Only prazosin patients gained weight: 1.7 lb (end-titration, p<0.0001; 1-year, p=0.02). Obesity does not appear to cause resistance to antihypertensive medications.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH P_Body_Mass_Index_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Obesity_MeSH S_metabolism_MeSH Obesity_metabolism_MeSH S_physiopathology_MeSH Obesity_physiopathology_MeSH 
****** 12826791
----K 5
----T What should we advise our patients about taking antioxidants?
----A The safety and tolerability of clozapine combined with lithium were investigated because of potential additive risks as well as frequent usage in clinical practice. Ten hospitalized schizophrenic and 10 schizoaffective patients receiving clozapine maintenance therapy with partial therapeutic response were studied in a randomized controlled trial. CGI and PANSS outcome ratings were employed and a cognitive battery was administered at baseline and after 4 weeks of lithium and placebo administration. Barnes and UKU side effect ratings and laboratory safety data were obtained. Combined lithium-clozapine treatment was well tolerated except for reversible neurotoxic reactions in two schizophrenic patients. Safety measures showed no significant variations, even during lithium toxicity. Total WBC and absolute granulocyte counts increased with lithium and declined with placebo. Schizoaffective patients improved with lithium on CGI and PANSS total and negative symptom scales and the cognitive measures, whereas schizophrenic patients did not. Lithium added to clozapine in treatment regimens for hospitalized, treatment-resistant, schizoaffective patients appears to afford potential benefit without harmful effects; for schizophrenic patients, however, it did not afford improvement but posed a risk of lithium toxicity.
----P Journal_Article 
----M M_Animals_MeSH M_Antioxidants_MeSH S_therapeutic_use_MeSH Antioxidants_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_physiopathology_MeSH Cardiovascular_Diseases_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_metabolism_MeSH Hypertension_metabolism_MeSH M_Rats_MeSH M_Rats__Inbred_SHR_MeSH M_Reactive_Oxygen_Species_MeSH S_metabolism_MeSH Reactive_Oxygen_Species_metabolism_MeSH S_therapeutic_use_MeSH Reactive_Oxygen_Species_therapeutic_use_MeSH 
****** 12831340
----K 5
----T A review of the clinical efficacy and tolerability of almotriptan in acute migraine.
----A Almotriptan is a serotonin (5-hydroxytryptamine, 5HT)(1B/1D)-receptor agonist approved for the acute treatment of migraine. In 3500 acute migraine patients enrolled in short-term trials and 1500 patients in long-term open-label trials, almotriptan 12.5 mg was effective and well-tolerated. Almotriptan maintains a consistency of response across three attacks and patients continue to respond to almotriptan for up to 1 year. Results from two comparative studies and a meta-analysis of 53 randomised, placebo-controlled studies of oral triptans in > 24,000 patients, confirm that almotriptan 12.5 mg demonstrates comparable efficacy with sumatriptan 50 and 100 mg. The incidence of treatment-related adverse events with almotriptan is comparable to that of placebo and significantly lower than that with sumatriptan. Drug-drug interaction studies indicate that almotriptan may be coadministered with other commonly prescribed drugs without dose modification. Almotriptan can be recommended as first-line treatment for acute migraine.
----P Journal_Article Review Review__Tutorial 
----M M_Acute_Disease_MeSH M_Adult_MeSH M_Aged_MeSH M_Area_Under_Curve_MeSH M_Biological_Availability_MeSH P_Expert_Testimony_MeSH M_Female_MeSH M_Half-Life_MeSH M_Human_MeSH P_Indoles_MeSH S_administration_&_dosage_MeSH Indoles_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Indoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Randomized_Controlled_Trials_MeSH M_Serotonin_Agonists_MeSH S_administration_&_dosage_MeSH Serotonin_Agonists_administration_&_dosage_MeSH S_pharmacokinetics_MeSH Serotonin_Agonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12832990
----K 5
----T Myocardial revascularization before carotid endarterectomy.
----A Diffuse atherosclerosis involving more than 1 vascular bed is a challenging problem. The natural histories of carotid and coronary atherosclerosis are clearly intertwined. The optimal strategies for treatment of patients who present with carotid artery stenoses and co-existent coronary artery disease (CAD) remain controversial. Minimally invasive screening tests for CAD are often unreliable, and patients presenting with significant extracranial carotid artery stenoses should usually be assumed to harbor some degree of CAD. Numerous studies have confirmed, however, that in contrast to peripheral artery stenoses, hemodynamically significant stenoses of the coronary arteries are not necessarily the index lesions that produce myocardial infarctions (MIs). Although there are some anecdotal reports that myocardial revascularization prior to carotid endarterectomy (CEA) improves the short- and long-term cardiac outcomes of patients after CEA, no prospective, randomized, controlled studies have proven this hypothesis. Numerous adverse cardiac events can occur in the perioperative period including congestive heart failure (CHF), arrhythmias, unstable angina pectoris and both nonfatal and fatal MIs. Of these, only MIs are truly "hard" endpoints. The incidence of MI after CEA is much lower than after other commonly performed peripheral arterial operations such as aortic or infrainguinal procedures. The perioperative nonfatal and fatal MI rates after CEA average about 1.0% and 0.4%, respectively. The Coronary Artery Revascularization Prophylaxis (CARP) study is currently ongoing in the United States as a multicentered randomized prospective controlled trial sponsored by the Department of Veterans Affairs. In this study, patients with significant CAD who are undergoing operations for peripheral arterial disease are randomized to myocardial revascularization versus best medical care; however, CEA procedures are excluded from this study because cardiac morbidity is low. Based on the low incidence of adverse cardiac events in CEA patients, it is generally prudent to treat their CAD with best medical care rather than routine prophylactic myocardial revascularization.
----P Journal_Article Review Review__Academic 
----M M_Carotid_Stenosis_MeSH S_mortality_MeSH Carotid_Stenosis_mortality_MeSH S_surgery_MeSH Carotid_Stenosis_surgery_MeSH M_Combined_Modality_Therapy_MeSH M_Comparative_Study_MeSH M_Coronary_Arteriosclerosis_MeSH S_mortality_MeSH Coronary_Arteriosclerosis_mortality_MeSH S_surgery_MeSH Coronary_Arteriosclerosis_surgery_MeSH P_Endarterectomy__Carotid_MeSH M_Human_MeSH M_Myocardial_Infarction_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Infarction_prevention_&_control_MeSH P_Myocardial_Revascularization_MeSH M_Postoperative_Complications_MeSH S_mortality_MeSH Postoperative_Complications_mortality_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH M_United_States_MeSH 
****** 12834148
----K 5
----T Movement disorders.
----A Movement disorders are commonly encountered in clinical practice. The diagnosis of movement disorders relies on a focused history and neurologic examination. Diagnostic steps include (1) identification of the phenomenology of the movements (eg, tremor); (2) characterization of appropriate clinical syndromes; and (3) differential diagnosis of specific disease entities. Accurate diagnosis is essential because symptomatic treatment exists for most movement disorders.
----P Case_Reports Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Anticonvulsants_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Atrophy_MeSH S_pathology_MeSH Atrophy_pathology_MeSH M_Brain_MeSH S_pathology_MeSH Brain_pathology_MeSH M_Child_MeSH M_Clonazepam_MeSH S_therapeutic_use_MeSH Clonazepam_therapeutic_use_MeSH M_Diagnosis__Differential_MeSH M_Female_MeSH M_Human_MeSH M_Huntington_Disease_MeSH S_diagnosis_MeSH Huntington_Disease_diagnosis_MeSH M_Lewy_Body_Disease_MeSH S_diagnosis_MeSH Lewy_Body_Disease_diagnosis_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multiple_System_Atrophy_MeSH S_diagnosis_MeSH Multiple_System_Atrophy_diagnosis_MeSH M_Myoclonus_MeSH S_diagnosis_MeSH Myoclonus_diagnosis_MeSH S_drug_therapy_MeSH Myoclonus_drug_therapy_MeSH S_physiopathology_MeSH Myoclonus_physiopathology_MeSH M_Neurologic_Examination_MeSH M_Parkinson_Disease_MeSH S_diagnosis_MeSH Parkinson_Disease_diagnosis_MeSH S_drug_therapy_MeSH Parkinson_Disease_drug_therapy_MeSH M_Spine_MeSH S_physiopathology_MeSH Spine_physiopathology_MeSH M_Torticollis_MeSH S_diagnosis_MeSH Torticollis_diagnosis_MeSH S_drug_therapy_MeSH Torticollis_drug_therapy_MeSH M_Tourette_Syndrome_MeSH S_diagnosis_MeSH Tourette_Syndrome_diagnosis_MeSH S_drug_therapy_MeSH Tourette_Syndrome_drug_therapy_MeSH M_Treatment_Failure_MeSH M_Tremor_MeSH S_diagnosis_MeSH Tremor_diagnosis_MeSH S_drug_therapy_MeSH Tremor_drug_therapy_MeSH S_psychology_MeSH Tremor_psychology_MeSH 
****** 12834362
----K 5
----T Current treatment of patients with hypertension: therapeutic implications of INSIGHT.
----A When planning treatment for patients with hypertension, current guidelines emphasise the importance of risk stratification, based on blood pressure, the presence of end-organ damage and other cardiovascular risk factors. Because the beneficial effect of antihypertensive therapy seems to be linked to the degree of blood pressure reduction, guidelines recommend reducing blood pressure below 140/90mm Hg, with a lower target in patients who are young or who have diabetes mellitus (with or without nephropathy) or non-diabetic nephropathy. Blood pressure reduction can be achieved with several classes of drugs, including diuretics, beta-blockers, ACE inhibitors, angiotensin II antagonists and calcium channel antagonists. Calcium channel antagonists have been shown to reduce the risk of stroke and major cardiovascular events. However, it is still controversial whether different treatment regimens based on different drug classes can offer advantages beyond similar degrees of blood pressure control in preventing cardiovascular morbidity and mortality. The International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) was a controlled clinical trial aimed at comparing the efficacy of a long-acting calcium channel antagonist, nifedipine gastrointestinal-transport-system (GITS), versus co-amilozide, a combination of the diuretics hydrochlorothiazide (HCTZ) and amiloride, on morbidity and mortality in high-risk hypertensive patients. Nifedipine GITS and HCTZ/amiloride were equally effective at reducing blood pressure and the risk of primary outcomes (a composite of death from any cardiovascular or cerebrovascular cause, non-fatal stroke, myocardial infarction and heart failure). Results from other studies indicate that there may be greater benefits for stroke and smaller benefits for coronary artery disease with calcium channel antagonist-based regimens than with diuretic or beta-blocker-based regimens. However, there is at present insufficient evidence to recommend a specific drug choice based on patient risk profile. Thus, the choice of antihypertensive drug(s) should be according to efficacy and tolerability. In addition to the reductions in cardiovascular risk, two substudies of INSIGHT showed that nifedipine GITS was able to prevent the progression of intima media thickness in the common carotid artery and slow the progression of coronary calcification. The clinical significance of this effect in the prevention of cardiovascular events still remains to be established.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_physiopathology_MeSH Cardiovascular_Diseases_physiopathology_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Clinical_Trials_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Nifedipine_MeSH S_pharmacology_MeSH Nifedipine_pharmacology_MeSH S_therapeutic_use_MeSH Nifedipine_therapeutic_use_MeSH 
****** 12834366
----K 5
----T Rate control in atrial fibrillation: choice of treatment and assessment of efficacy.
----A The clinical relevance and high social costs of atrial fibrillation have boosted interest in rate control as a cost-effective alternative to long-term maintenance of sinus rhythm (i.e. rhythm control). Prospective studies show that rate control (coupled with thromboembolic prophylaxis) is a valuable treatment option for all forms of atrial fibrillation. The rationale for rate control is that high ventricular rates, frequently found in atrial fibrillation, lead to haemodynamic impairment, consisting of a variable combination of loss of atrial kick, irregularity in ventricular response and inappropriately rapid ventricular rate, depending on the type of underlying heart disease. Long-term persistence of tachycardia at a high ventricular rate can lead to various degrees of ventricular dysfunction and even to tachycardiomyopathy-related heart failure. Identification of this reversible and often concealed form of left ventricular dysfunction can permit effective management by rate (or rhythm) control. Although acute rate control (to reduce ventricular rate within hours) is still often based on digoxin administration, for patients without left ventricular dysfunction, calcium channel antagonists or beta-adrenoceptor antagonists (beta-blockers) are generally more appropriate and effective. In chronic atrial fibrillation, long-term rate control (to reduce morbidity/mortality and improve quality of life) must be adapted to patients' individual characteristics to grant control during daily activities, including exercise. According to current guidelines, the clinical target of rate control should be a ventricular rate below 80-90 bpm at rest. However, in many patients, assessment of the appropriateness of different drugs should include exercise testing and 24h-Holter monitoring, for which specific guidelines are needed. In practice, rate control is considered a valid alternative to rhythm control. Recent prospective trials (e.g. the Pharmacological Intervention in Atrial Fibrillation [PIAF] and the Atrial Fibrillation Follow-up Investigation of Rhythm Management [AFFIRM] trials) have shown that in selected patients, rate control provides similar benefits, more economically, in terms of quality of life and long-term mortality. The choice of a rate control medication (digoxin, beta-blockers, calcium channel antagonists or possibly amiodarone) or a non-pharmacological approach (mainly atrioventricular node ablation coupled with pacing) must currently be based on clinical assessment, which includes assessing the presence of underlying heart disease and haemodynamic impairment. Definite guidelines are required for each different subset of patients. Rate control is particularly tricky in patients with heart failure, for whom non-pharmacological options can also be considered. The preferred pharmacological options are beta-blockers for stabilised heart failure and digoxin for unstabilised forms.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Anti-Arrhythmia_Agents_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Disease_Management_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Monitoring__Physiologic_MeSH S_methods_MeSH Monitoring__Physiologic_methods_MeSH 
****** 12836809
----K 4
----T Comparison of brimonidine/latanoprost and timolol/dorzolamide: two randomized, double-masked, parallel clinical trials.
----A Two double-masked, randomized, parallel, multicenter trials of similar design were conducted to compare the IOP-lowering efficacy of dual therapy with brimonidine 0.2% and latanoprost 0.005% with the fixed combination of timolol 0.5%/dorzolamide 2% in patients with glaucoma or ocular hypertension. The combination of brimonidine and latanoprost produced significantly greater mean IOP reductions at each visit in both trials. In study 1, the mean reduction at peak drug effect after 6 weeks was 9.2 mm Hg (34.7%) with brimonidine and latanoprost and 6.7 mm Hg (26.1%) with timolol/dorzolamide (P=.024); respective reductions at week 12 were 9.0 mm Hg (33.9%) and 6.5 mm Hg (25.3%) (P=.044). At the month 1 visit in study 2, the mean peak IOP reduction was 10.6 mm Hg (39.0%) with dual therapy and 6.3 mm Hg (25.1%) with the fixed combination (P=.001). After 3 months, reductions were 9.1 mm Hg (33.4%) and 6.6 mm Hg (26.3%) (P=.047). In these studies, the combination of brimonidine and latanoprost provided IOP control superior to that of the fixed combination of timolol/dorzolamide.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Exfoliation_Syndrome_MeSH S_drug_therapy_MeSH Exfoliation_Syndrome_drug_therapy_MeSH S_physiopathology_MeSH Exfoliation_Syndrome_physiopathology_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_physiopathology_MeSH Glaucoma__Open-Angle_physiopathology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Ocular_Hypertension_physiopathology_MeSH M_Patient_Satisfaction_MeSH S_statistics_&_numerical_data_MeSH Patient_Satisfaction_statistics_&_numerical_data_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_adverse_effects_MeSH Prostaglandins_F__Synthetic_adverse_effects_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Quinoxalines_MeSH S_administration_&_dosage_MeSH Quinoxalines_administration_&_dosage_MeSH S_adverse_effects_MeSH Quinoxalines_adverse_effects_MeSH S_therapeutic_use_MeSH Quinoxalines_therapeutic_use_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_adverse_effects_MeSH Sulfonamides_adverse_effects_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_adverse_effects_MeSH Thiophenes_adverse_effects_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_adverse_effects_MeSH Timolol_adverse_effects_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12840118
----K 5
----T Emergency management of atrial fibrillation.
----A Atrial fibrillation is the most common cardiac arrhythmia managed by emergency and acute general physicians. There is increasing evidence that selected patients with acute atrial fibrillation can be safely managed in the emergency department without the need for hospital admission. Meanwhile, there is significant variation in the current emergency management of acute atrial fibrillation. This review discusses evidence based emergency management of atrial fibrillation. The principles of emergency management of acute atrial fibrillation and the subset of patients who may not need hospital admission are reviewed. Finally, the need for evidence based guidelines before emergency department based clinical pathways for the management of acute atrial fibrillation becomes routine clinical practice is highlighted.
----P Journal_Article Review Review__Tutorial 
----M M_Ambulatory_Care_MeSH M_Atrial_Fibrillation_MeSH S_classification_MeSH Atrial_Fibrillation_classification_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Clinical_Protocols_MeSH M_Electric_Countershock_MeSH S_methods_MeSH Electric_Countershock_methods_MeSH M_Emergencies_MeSH M_Emergency_Service__Hospital_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Patient_Selection_MeSH M_Recurrence_MeSH 
****** 12842244
----K 5
----T Fibrin D-dimer levels in atrial fibrillation as an index of thrombogenesis: a possible test to exclude left atrial thrombus?
----A 
----P Comment Journal_Article 
----M M_Atrial_Fibrillation_MeSH S_blood_MeSH Atrial_Fibrillation_blood_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH M_Coronary_Thrombosis_MeSH S_diagnosis_MeSH Coronary_Thrombosis_diagnosis_MeSH S_etiology_MeSH Coronary_Thrombosis_etiology_MeSH M_Fibrin_Fibrinogen_Degradation_Products_MeSH S_analysis_MeSH Fibrin_Fibrinogen_Degradation_Products_analysis_MeSH M_Heart_Atria_MeSH M_Human_MeSH M_Predictive_Value_of_Tests_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12782643
----K 5
----T Pharmacological modulation of platelet function in hypertension.
----A Platelets exert a considerable influence on human morbidity and mortality. The rationale for their study in hypertension follows the observation that the major consequences of hypertension are stroke and myocardial infarction. However, the etiology of these consequences in hypertension is, paradoxically, not hemorrhagic (as might be expected from the effects of high blood pressure), but occlusive, with thrombus being the culprit lesion. Mechanisms of platelet activation include high shear force, activation of the renin-angiotensin system, endothelial changes, and the presence of comorbidity, such as atrial fibrillation. The treatment of high blood pressure brings about a reversal of the changes seen in the cell. This could be in part due to the direct effect of the drug on the megakaryocyte and/or the platelets themselves, or it might simply be due to the reduction in blood pressure. Some drugs, such as calcium channel antagonists and angiotensin II receptor blockers, however, might have direct effects on platelet biochemistry other than reducing blood pressure. Finally, antiplatelet drugs are becoming an important part of the management of high-risk hypertensives, which aim to minimize vascular complications.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Platelets_MeSH S_drug_effects_MeSH Blood_Platelets_drug_effects_MeSH S_physiology_MeSH Blood_Platelets_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Models__Cardiovascular_MeSH M_Platelet_Activation_MeSH S_drug_effects_MeSH Platelet_Activation_drug_effects_MeSH M_Platelet_Aggregation_Inhibitors_MeSH S_therapeutic_use_MeSH Platelet_Aggregation_Inhibitors_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12849655
----K 5
----T Restoring sinus rhythm in atrial fibrillation: a Pyrrhic victory?
----A 
----P Comment Editorial 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_drug_therapy_MeSH Atrial_Fibrillation_drug_therapy_MeSH S_physiopathology_MeSH Atrial_Fibrillation_physiopathology_MeSH M_Endpoint_Determination_MeSH M_Human_MeSH 
****** 12851520
----K 2
----T The effects of antihypertensive agents on endometrial thickness in asymptomatic, hypertensive, postmenopausal women.
----A OBJECTIVE: The aim of this study was to investigate, by using transvaginal ultrasonography, the possible effects on endometrial thickness of antihypertensive agents in asymptomatic postmenopausal women. DESIGN: A prospective study in an outpatient menopause clinic of a university hospital. We included 288 postmenopausal women in this study, and we compared three groups of postmenopausal women as follows: (1) normotensive postmenopausal women, (2) hypertensive women treated with an antihypertensive drug (beta-blocker, non-beta-blocker, or beta-blocker plus non-beta-blocker), and (3) untreated hypertensive women who had had hypertension for at least 1 year. Hypertensive women treated with a drug had been receiving treatment for 1 year. All women were interviewed and examined. Measurements of endometrial thickness were carried out by vaginal ultrasonography. RESULTS: Sixty-two women (22%) were normotensive, and 226 (78%) of 288 women were hypertensive. Of the 226 women, 122 (54%) were receiving an antihypertensive drug. The mean (+/- SD) endometrial thicknesses in groups A, B, and C were 4.5 (+/- 1.3), 5.4 (+/- 1.5), and 6.4 (+/- 1.7) mm, respectively. Significant difference was obtained among the groups (P = 0.004). CONCLUSIONS: Our data indicate that the mean endometrial thickness is significantly greater in asymptomatic, hypertensive women receiving antihypertensive drugs than among untreated hypertensive and normotensive women.
----P Journal_Article 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Comparative_Study_MeSH M_Endometrium_MeSH S_drug_effects_MeSH Endometrium_drug_effects_MeSH S_ultrasonography_MeSH Endometrium_ultrasonography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Middle_Aged_MeSH P_Postmenopause_MeSH M_Prospective_Studies_MeSH 
****** 12853188
----K 5
----T Beta blockers in heart failure.
----A 
----P Comment Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH 
****** 12853193
----K I
----T Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial.
----A BACKGROUND: Beta blockers reduce mortality in patients who have chronic heart failure, systolic dysfunction, and are on background treatment with diuretics and angiotensin-converting enzyme inhibitors. We aimed to compare the effects of carvedilol and metoprolol on clinical outcome. METHODS: In a multicentre, double-blind, and randomised parallel group trial, we assigned 1511 patients with chronic heart failure to treatment with carvedilol (target dose 25 mg twice daily) and 1518 to metoprolol (metoprolol tartrate, target dose 50 mg twice daily). Patients were required to have chronic heart failure (NYHA II-IV), previous admission for a cardiovascular reason, an ejection fraction of less than 0.35, and to have been treated optimally with diuretics and angiotensin-converting enzyme inhibitors unless not tolerated. The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality or all-cause admission. Analysis was done by intention to treat. FINDINGS: The mean study duration was 58 months (SD 6). The mean ejection fraction was 0.26 (0.07) and the mean age 62 years (11). The all-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard ratio 0.83 [95% CI 0.74-0.93], p=0.0017). The reduction of all-cause mortality was consistent across predefined subgroups. The composite endpoint of mortality or all-cause admission occurred in 1116 (74%) of 1511 on carvedilol and in 1160 (76%) of 1518 on metoprolol (0.94 [0.86-1.02], p=0.122). Incidence of side-effects and drug withdrawals did not differ by much between the two study groups. INTERPRETATION: Our results suggest that carvedilol extends survival compared with metoprolol.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Cause_of_Death_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_adverse_effects_MeSH Metoprolol_adverse_effects_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12853194
----K I
----T Myocardial viability as a determinant of the ejection fraction response to carvedilol in patients with heart failure (CHRISTMAS trial): randomised controlled trial.
----A BACKGROUND: The improvement in left-ventricular ejection fraction (LVEF) in response to beta blockers is heterogeneous in patients with heart failure due to ischaemic heart disease, possibly indicating variations in the myocardial substrate underlying left-ventricular dysfunction. We investigated whether improvement in LVEF was associated with the volume of hibernating myocardium (viable myocardium with contractile failure). METHODS: We did a double-blind, randomised trial to compare placebo and carvedilol for 6 months in individuals with stable, chronic heart failure due to ischaemic left-ventricular systolic dysfunction. We enrolled 489 patients, of whom 387 were randomised. Patients were designated hibernators or non-hibernators according to the volume of hibernating myocardium. The primary endpoint was change in LVEF, measured by radionuclide ventriculography, in hibernators versus non-hibernators, on carvedilol compared with placebo. Analysis was by intention to treat. RESULTS: 82 patients dropped out of the study because of adverse events, withdrawal of consent, or failure to complete the investigation. Thus, 305 (79%) were analysed. LVEF was unchanged with placebo (mean change -0.4 [SE 0.9] and -0.4 [0.8] for non-hibernators and hibernators, respectively) but increased with carvedilol (2.5 [0.9] and 3.2 [0.8], respectively; p<0.0001 compared with baseline). Mean placebo-subtracted change in LVEF was 3.2% (95% CI 1.8-4.7; p=0.0001) overall, and 2.9% (0.7-5.1; p=0.011) and 3.6% (1.7-5.4; p=0.0002) in non-hibernators and hibernators, respectively. Effect of hibernator status on response of LVEF to carvedilol was not significant (0.7 [-2.2 to 3.5]; p=0.644). However, patients with more myocardium affected by hibernation or by hibernation and ischaemia had a greater increase in LVEF on carvedilol (p=0.0002 and p=0.009, respectively). INTERPRETATION: Some of the effect of carvedilol on LVEF might be mediated by improved function of hibernating or ischaemic myocardium, or both. Medical treatment might be an important adjunct or alternative to revascularisation for patients with hibernating myocardium.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Stunning_MeSH S_complications_MeSH Myocardial_Stunning_complications_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Ventricular_Dysfunction__Left_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12853233
----K 4
----T A multicenter randomized crossover multiple-dose comparison study of arotinolol and propranolol in essential tremor.
----A BACKGROUND: A new medication is needed to treat essential tremor. Preliminary evidence suggests that arotinolol may be effective in the treatment of this disorder. OBJECTIVE: To study the effect of arotinolol and propranolol in a crossover, multiple dose comparative trial of patients with essential tremor. PATIENTS AND METHODS: One hundred and seventy-five outpatients, with essential tremor were included in the study; 161 patients completed the study. Patients were identically evaluated at eight consecutive visits. The study consisted of two treatments, which were arranged according to a crossover design that evaluated the dose of each (arotinolol 10 mg per day and propranolol 40 mg per day, arotinolol 20 mg per day and propranolol 80 mg per day, arotinolol 30 mg per day and propranolol 160 mg per day). Each course of treatment lasted 6 weeks. Major outcome evaluations consisted of a self-reported disability scale, and motor performance score obtained before drug intake and 14 days after each treatment. The treatment effects were evaluated by analysis of variance using the Hills-Armitage test. RESULTS: Arotinolol was found to be as effective as propranolol at reducing tremor. Drug effects as evaluated using motor-task performance scores revealed that arotinolol had a more significant effect than propranolol. CONCLUSIONS: Arotinolol may be more useful than propranolol for the treatment of essential tremor.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Essential_Tremor_MeSH S_drug_therapy_MeSH Essential_Tremor_drug_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Psychomotor_Performance_MeSH S_drug_effects_MeSH Psychomotor_Performance_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Task_Performance_and_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12857042
----K 5
----T Implication of cardiac remodeling in heart failure: mechanisms and therapeutic strategies.
----A The concept and clinical implication of left ventricular remodeling have been gradually extended. Cardiac remodeling plays important roles in the progression of cardiovascular diseases including myocardial infarction, valvular heart diseases, myocarditis, and dilated cardiomyopathy. In addition to cardiac myocytes, fibroblasts, extracellular matrix proteins and coronary vasculature are also involved in the remodeling process. Cardiac remodeling is associated with alterations of many mediators such as neurohumoral factors, cytokines, enzymes, ion channels, oxidative stress and mechanical stress. Although remodeling is initially an adaptive response to maintain normal cardiac function, it gradually becomes maladaptive and leads to progressive decompensation. Recent research has attempted to elucidate underlying molecular mechanisms of cardiac remodeling and to develop novel therapeutic strategies for heart failure. The modulation of remodeling process is effective for preventing the progression of heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Adaptation__Physiological_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Animals_MeSH M_Cytokines_MeSH S_metabolism_MeSH Cytokines_metabolism_MeSH M_Disease_Progression_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Male_MeSH M_Matrix_Metalloproteinases_MeSH S_metabolism_MeSH Matrix_Metalloproteinases_metabolism_MeSH M_Prognosis_MeSH M_Risk_Assessment_MeSH M_Severity_of_Illness_Index_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH S_physiology_MeSH Ventricular_Remodeling_physiology_MeSH 
****** 12858071
----K 5
----T The evolving management of migraine.
----A PURPOSE OF REVIEW: To review recent advances in acute and preventive migraine treatment. RECENT FINDINGS: The number of migraine drugs continues to expand, allowing for more flexible and tolerable treatment plans. Two new triptans, frovatriptan and eletriptan, and a nasal formulation of zolmitriptan have been recently developed. Eletriptan is effective for acute migraine treatment and may have some pharmacologic and clinical advantages. Frovatriptan has a longer half-life and lower headache recurrence rates compared with other triptans. It may be useful for patients who have prolonged attacks and high headache recurrence rate. Zolmitriptan nasal spray has a rapid onset of action and high efficacy. It should be considered when patients have rapid-onset attacks, especially when associated with severe nausea or vomiting. The butyrophenone neuroleptic droperidol is very effective in aborting acute migraine attacks. Central nervous system side effects are common, however, and the ECG should be monitored. Botulinum toxin type A shows promise as a safe, tolerable and effective drug for migraine prevention, with the unique advantages of almost no systemic adverse events and a long interval between treatments. The anticonvulsant topiramate is effective for migraine prevention. Cognitive side effects are of less concern with the lower doses needed for migraine. The angiotensin converting enzyme receptor blocker candesartan appears to be effective and highly tolerable in the prevention of migraine, but needs to be further evaluated. SUMMARY: New drugs expand the spectrum of migraine treatment both for the acute attack and for prevention.
----P Journal_Article Review Review__Tutorial 
----M M_Anticonvulsants_MeSH S_therapeutic_use_MeSH Anticonvulsants_therapeutic_use_MeSH M_Antipsychotic_Agents_MeSH S_therapeutic_use_MeSH Antipsychotic_Agents_therapeutic_use_MeSH M_Botulinum_Toxin_Type_A_MeSH S_therapeutic_use_MeSH Botulinum_Toxin_Type_A_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Droperidol_MeSH S_therapeutic_use_MeSH Droperidol_therapeutic_use_MeSH M_Fructose_MeSH S_analogs_&_derivatives_MeSH Fructose_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Fructose_therapeutic_use_MeSH M_Human_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Neuromuscular_Agents_MeSH S_therapeutic_use_MeSH Neuromuscular_Agents_therapeutic_use_MeSH M_Oxazolidinones_MeSH S_therapeutic_use_MeSH Oxazolidinones_therapeutic_use_MeSH M_Pyrrolidines_MeSH S_therapeutic_use_MeSH Pyrrolidines_therapeutic_use_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Serotonin_Agonists_MeSH S_therapeutic_use_MeSH Serotonin_Agonists_therapeutic_use_MeSH 
****** 12859261
----K 4
----T Timolol 0.5%/dorzolamide 2% fixed combination versus timolol 0.5%/pilocarpine 2% fixed combination in primary open-angle glaucoma or ocular hypertensive patients.
----A PURPOSE: To establish the efficacy and safety of timolol maleate/dorzolamide fixed combination (TDFC) versus timolol maleate/pilocarpine fixed combination (TPFC), each given twice daily, in primary open-angle glaucoma or ocular hypertensive patients. METHODS: In this prospective, multicentred, double-masked trial, 37 patients were treated twice daily with timolol for 4 weeks. They were then randomized to one of the treatment medications for 6 weeks, after which they were treated with timolol again for 2 weeks before being placed on the opposite treatment medication for 6 weeks. RESULTS: A total of 36 patients completed the trial. Their mean baseline intraocular pressure (IOP) was 22.3 +/- 3.7 mmHg. Following 6 weeks of treatment, the mean trough (08.00 hours) IOP was 18.0 +/- 2.2 mmHg for TDFC and 17.4 +/- 2.0 mmHg for TPFC (p = 0.22). The mean diurnal curve IOP was 18.1 +/- 2.2 mmHg for TDFC and 16.7 +/- 1.9 mmHg for TPFC (p = 0.0007). At the remaining time-points (10.00, 18.00 and 20.00 hours), TPFC IOPs were statistically lower than TDFC IOPs (p < 0.03). There were statistically more unsolicited reports of vision change and ocular pain associated with TPFC (p = 0.04). Six patients were discontinued early from TPFC therapy (17%) versus two from TDFC (6%) (p = 0.13). CONCLUSIONS: This study suggests that TPFC can provide at least a similar efficacious reduction in IOP as TDFC in patients with primary open-angle glaucoma or ocular hypertension.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Pilocarpine_MeSH S_administration_&_dosage_MeSH Pilocarpine_administration_&_dosage_MeSH S_therapeutic_use_MeSH Pilocarpine_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12860230
----K 5
----T Choosing metoprolol or carvedilol in heart failure (a pre-COMET commentary).
----A 
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comparative_Study_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Outcome_Assessment_(Health_Care)_MeSH M_Patient_Selection_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Rest_MeSH S_physiology_MeSH Rest_physiology_MeSH M_Retrospective_Studies_MeSH 
****** 12864722
----K 5
----T Digoxin in heart failure and cardiac arrhythmias.
----A HEART FAILURE: Digoxin therapy has no effect on mortality in heart failure. Digoxin may be useful for maintaining clinical stability and exercise capacity in patients with symptomatic heart failure. Digoxin appears to be of most benefit in patients with severe heart failure, cardiomegaly and a third heart sound. Digoxin should be used as a second-line drug after diuretics, angiotensin-converting enzyme inhibitors and beta-blockers in patients with congestive heart failure who are in sinus rhythm. Digoxin should be used as a first-line drug in patients with congestive heart failure who are in atrial fibrillation. ARRHYTHMIAS: Digoxin has a limited, but useful, role, either alone or in combination with other agents such as beta-blockers, diltiazem or verapamil, in achieving satisfactory resting ventricular rate control in patients with chronic atrial fibrillation. In patients who lead a predominantly sedentary lifestyle (perhaps particularly in those who are elderly), digoxin alone may be the agent of choice.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_adverse_effects_MeSH Anti-Arrhythmia_Agents_adverse_effects_MeSH S_pharmacology_MeSH Anti-Arrhythmia_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH M_Digoxin_MeSH S_adverse_effects_MeSH Digoxin_adverse_effects_MeSH S_pharmacology_MeSH Digoxin_pharmacology_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH 
****** 12866134
----K 3
----T Effect of right atrial pacing, intravenous amiodarone and beta blockers for suppression of atrial fibrillation after coronary artery bypass surgery: a pilot study.
----A OBJECTIVE: This pilot study aimed to compare right atrial pacing, intravenous amiodarone and oral beta-blockers in the prevention, time to onset, duration and effect on hospital stay of postoperative atrial fibrillation (AF) after coronary artery bypass graft surgery (CABG) at our center. BACKGROUND: AF is the most common arrhythmic complication after CABG and is related to increased morbidity, length of hospital stay and costs. Trials with different drugs and other therapeutic modalities including beta-blockers, intravenous amiodarone and override suppression of automatic atrial foci by atrial pacing have shown partial success as preventive measures. However, a comparison between those three interventions has not been reported. METHODS: Thirty-six consecutive patients that underwent CABG at our institution were randomly assigned to atrial pacing (18 patients) and intravenous amiodarone (18 patients) after baseline clinical, electrocardiographic and hemodynamic assessment. All patients received concomitant oral metoprolol or atenolol right after extubation. Thirty-three patients who had CABG at our center in the previous two months and that only received beta-blockers during their perioperative period served as a control group. RESULTS: The majority of baseline clinical and hemodynamic characteristics were similar in all groups. Only one patient (5.6%) developed AF in the atrial pacing group versus five (27.8%) on amiodarone and six (18.2%) who only received beta-blockers. That finding, however, did not attain statistical significance (p > 0.05). After adjusting for potential confounders, the odds of occurrence of AF was 77% lower in atrial pacing patients (OR = 0.23; 95% CI: 0.02, 2.20; p = 0.09) and 2.36 times higher in those on amiodarone (95% CI: 0.55, 10.24; P = 0.053) when compared to patients which only received beta blockers. Since only one patient on right atrial pacing developed atrial fibrillation, the analysis of the median time to onset and median duration of atrial fibrillation was restricted to those assigned to amiodarone and those who only received beta-blockers showing no statistically significant differences (p > 0.05). Although no statistical significance was achieved, the median hospital stay was one-day shorter in the beta-blockers group. Most of the side effects were minor and resolved without sequelae. CONCLUSION: This pilot study showed a trend in favor of atrial pacing versus intravenous amiodarone or beta-blockers in the prevention of postoperative AF after CABG in our center. Randomization of a larger patient sample would be required in order to ascertain the true value of the observed trend.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Administration__Oral_MeSH M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Amiodarone_MeSH S_administration_&_dosage_MeSH Amiodarone_administration_&_dosage_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_administration_&_dosage_MeSH Anti-Arrhythmia_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Cardiac_Pacing__Artificial_MeSH S_methods_MeSH Cardiac_Pacing__Artificial_methods_MeSH M_Comparative_Study_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Female_MeSH M_Heart_Atria_MeSH M_Human_MeSH M_Injections__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Treatment_Outcome_MeSH 
****** 12867118
----K 5
----T Demographics and concomitant disorders in heart failure.
----A Chronic heart failure is an increasingly common cause of premature death and poor quality of life. Community-based epidemiological studies have provided much-needed information on the demography of chronic heart failure, providing insight into its influence on public health. In most patients, chronic heart failure is accompanied by a range of concomitant disorders that both contribute to the cause of the disease and have a key role in its progression and response to treatment. Information on the most common comorbidities in chronic heart failure--ischaemic heart disease, hypertension, and diabetes mellitus--is presented for prespecified subgroups in the reports of many large-scale, multicentre trials; despite their limitations, these subanalyses provide guidance in therapeutic decision-making. Similarly, because chronic heart failure is commonly an endpoint in intervention trials of both hypertension and diabetes, such studies afford important information on the prevention of chronic heart failure in these common diseases.
----P Journal_Article Review Review__Academic 
----M M_Age_Factors_MeSH M_Comorbidity_MeSH M_Disease_Progression_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12867391
----K 4
----T Twenty-four-hour diurnal curve comparison of commercially available latanoprost 0.005% versus the timolol and dorzolamide fixed combination.
----A PURPOSE: To evaluate the efficacy and safety of commercially available latanoprost 0.005% given every evening versus timolol 0.5% and dorzolamide 2% fixed combination (TDFC) given twice daily to white Greeks with primary open-angle glaucoma and ocular hypertensive patients. DESIGN: A single-masked, two-center, crossover comparison with two 6-week treatment periods occurring after at least a 3-week medicine-free period. Diurnal curve intraocular pressures were taken at 2:00 AM, 6:00 AM, 10:00 AM, 2:00 PM, 6:00 PM, and 10:00 PM. PARTICIPANTS: Thirty-four subjects with primary open-angle glaucoma or ocular hypertension were enrolled. INTERVENTIONS: Latanoprost 0.005% given every evening and TDFC twice daily. MAIN OUTCOME MEASURES: The primary efficacy variable was diurnal intraocular pressure. RESULTS: Thirty-three patients completed the study. On the last day of treatment, the mean diurnal intraocular pressure for latanoprost was 15.9 +/- 2.3 mmHg and for TDFC was 15.3 +/- 2.0 mmHg (P = 0.05). Individual time points for intraocular pressure were not statistically different between groups except at the 10:00 PM time point, when the mean for TDFC was 14.6 +/- 2.7 mmHg and for latanoprost was 16.6 +/- 3.1 mmHg (P < 0.006). Eighteen patients overall preferred latanoprost versus 2 patients for the fixed combination, generally because of the greater convenience of once daily dosing. Adverse events were not significantly different between groups except that a bitter taste was found more frequently with TDFC (n = 9) than with latanoprost (n = 0; P = 0.009). Despite screening to exclude intolerance to beta-blockers, a single patient had to discontinue the TDFC because of new-onset asthma. CONCLUSIONS: This study indicates that the 24-hour diurnal intraocular pressure is lowered more, by a small but statistically significant amount, with TDFC compared with latanoprost in primary open-angle glaucoma and ocular hypertensive patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Circadian_Rhythm_MeSH S_drug_effects_MeSH Circadian_Rhythm_drug_effects_MeSH M_Comparative_Study_MeSH M_Cross-Over_Studies_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Prostaglandins_F__Synthetic_MeSH S_administration_&_dosage_MeSH Prostaglandins_F__Synthetic_administration_&_dosage_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Safety_MeSH M_Single-Blind_Method_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH S_therapeutic_use_MeSH Sulfonamides_therapeutic_use_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH S_therapeutic_use_MeSH Thiophenes_therapeutic_use_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12872859
----K 5
----T Transjugular renal biopsy in an unconscious patient maintained on mechanical ventilation.
----A 
----P Case_Reports Journal_Article 
----M P_Biopsy__Needle_MeSH S_methods_MeSH Biopsy__Needle_methods_MeSH M_Human_MeSH M_Jugular_Veins_MeSH M_Kidney_MeSH S_pathology_MeSH Kidney_pathology_MeSH P_Respiration__Artificial_MeSH P_Unconsciousness_MeSH 
****** 12873287
----K 5
----T The renin-angiotensin system and the long-term complications of diabetes: pathophysiological and therapeutic considerations.
----A The relationship between the renin-angiotensin system (RAS) and the progression of diabetic renal disease has been a major focus of investigation over the past 20 years. More recently, experimental and clinical studies have also suggested that the RAS may have a pathogenetic role at other sites of micro- and macrovascular injury in diabetes. Complementing major advances into the understanding of the local, as distinct from the systemic RAS, a number of large clinical trials have examined whether blockade of the RAS might provide protection from the long-term complications of diabetes, beyond that due to blood pressure reduction alone. While some controversy remains, these studies have, in general, suggested that angiotensin converting enzyme (ACE) inhibition and more recently, angiotensin receptor blockade reduce the development and progression of diabetic nephropathy, cardiovascular disease and possibly retinopathy. This review will focus on recent developments in our understanding of the tissue-based RAS and its role in end-organ injury in diabetes, the results of recent clinical trials and newer strategies for the pharmacological manipulation of the RAS.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Diabetic_Angiopathies_MeSH S_drug_therapy_MeSH Diabetic_Angiopathies_drug_therapy_MeSH S_etiology_MeSH Diabetic_Angiopathies_etiology_MeSH M_Diabetic_Nephropathies_MeSH S_drug_therapy_MeSH Diabetic_Nephropathies_drug_therapy_MeSH S_etiology_MeSH Diabetic_Nephropathies_etiology_MeSH M_Diabetic_Retinopathy_MeSH S_drug_therapy_MeSH Diabetic_Retinopathy_drug_therapy_MeSH S_etiology_MeSH Diabetic_Retinopathy_etiology_MeSH M_Growth_Substances_MeSH S_physiology_MeSH Growth_Substances_physiology_MeSH M_Human_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Renin-Angiotensin_System_MeSH S_genetics_MeSH Renin-Angiotensin_System_genetics_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12875785
----K 5
----T Valvular heart disease.
----A 
----P Congresses 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiac_Surgical_Procedures_MeSH S_trends_MeSH Cardiac_Surgical_Procedures_trends_MeSH M_Cardiology_MeSH S_trends_MeSH Cardiology_trends_MeSH M_Disease_Progression_MeSH M_Heart_Valve_Diseases_MeSH S_etiology_MeSH Heart_Valve_Diseases_etiology_MeSH S_therapy_MeSH Heart_Valve_Diseases_therapy_MeSH M_Heart_Valve_Prosthesis_MeSH S_trends_MeSH Heart_Valve_Prosthesis_trends_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12879116
----K E
----T Clopidogrel: a selective inhibitor of platelet ADP receptors.
----A Platelets play a key role in the development of ischemic complications in the arterial circulation. Antiplatelet therapy has proven effective in the treatment and prevention of ischemic events. Numerous clinical studies have confirmed the therapeutic efficacy of aspirin to such a point that this antiplatelet agent has become the gold standard in clinical practice. Clopidogrel is a thienopyridine compound that inhibits platelet aggregation by selectively binding to adenylate cyclase-coupled ADP receptors. Results of a large, double-blind, randomized study (CAPRIE) confirm that administration of clopidogrel to patients with atherosclerotic vascular disease is more effective than aspirin in reducing the combined risk of ischemic stroke, myocardial infarction or vascular death. The present article highlights the importance of activation of platelets through ADP receptors and reviews the pharmacology and clinical studies of clopidogrel, a selective inhibitor of these mechanisms.
----P Journal_Article 
----M 
****** 12877761
----K 5
----T Epidemiology, pathophysiology, prognosis, and treatment of systolic and diastolic heart failure in elderly patients.
----A American College of Cardiology/American Heart Association class I recommendations for treating patients with heart failure (HF) and abnormal left ventricular ejection fraction are diuretics in patients with fluid retention, an angiotensin-converting enzyme (ACE) inhibitor unless contraindicated, a beta-blocker unless contraindicated, digoxin for the treatment of symptoms of HF, and withdrawal of drugs known to precipitate or aggravate HF such as nonsteroidal anti-inflammatory drugs, calcium channel blockers, and most antiarrhythmic drugs. Class II(a) recommendations for treating HF with abnormal left ventricular ejection fraction are spironolactone in patients with class IV symptoms, preserved renal function, and normal serum potassium; exercise training as an adjunctive approach to improve clinical status in ambulatory patients; an angiotensin receptor blocker in patients who cannot be given an ACE inhibitor because of cough, rash, altered taste sensation, or angioedema; and hydralazine plus nitrates in patients being treated with diuretics, a beta-blocker, and digoxin who cannot be given an ACE inhibitor or an angiotensin receptor blocker because of hypotension or renal insufficiency. Patients with diastolic HF should be treated with cautious use of diuretics and with a beta-blocker. An ACE inhibitor should be added if HF persists or an angiotensin receptor blocker if the patient cannot tolerate an ACE inhibitor because of cough, angioedema, rash, or altered taste sensation. Isosorbide dinitrate plus hydralazine should be added if HF persists. A calcium channel blocker should be added if HF persists. Digoxin should be avoided in diastolic HF if sinus rhythm is present.
----P Journal_Article Review Review__Academic 
----M M_Age_Distribution_MeSH M_Aged_MeSH M_Cardiac_Output__Low_MeSH S_epidemiology_MeSH Cardiac_Output__Low_epidemiology_MeSH S_physiopathology_MeSH Cardiac_Output__Low_physiopathology_MeSH S_therapy_MeSH Cardiac_Output__Low_therapy_MeSH M_Diastole_MeSH S_physiology_MeSH Diastole_physiology_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Sex_Distribution_MeSH M_Survival_Rate_MeSH M_Systole_MeSH S_physiology_MeSH Systole_physiology_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH M_Ventricular_Dysfunction__Left_MeSH S_epidemiology_MeSH Ventricular_Dysfunction__Left_epidemiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_therapy_MeSH Ventricular_Dysfunction__Left_therapy_MeSH 
****** 12881589
----K 5
----T The role of omega-3 fatty acids in the secondary prevention of cardiovascular disease.
----A It has long been recognized from epidemiological studies that Greenland Eskimos have substantially reduced rates of acute myocardial infarction (MI) compared with Western controls. From these epidemiological observations, the benefits of fatty fish consumption have been explored in cell culture and animal studies, as well as randomized controlled trials investigating the cardioprotective effects of omega-3 fatty acids. Dietary omega-3 fatty acids seem to stabilize the myocardium electrically, resulting in reduced susceptibility to ventricular arrhythmias, thereby reducing the risk of sudden death. These fatty acids also have potent anti-inflammatory effects, and may also be antithrombotic and anti-atherogenic. Furthermore, the recent GISSI-Prevention study of 11 324 patients showed a marked decrease in risk of sudden cardiac death as well as a reduction in all-cause mortality in the group taking a highly purified form of omega-3 fatty acids, despite the use of other secondary prevention drugs, including beta-blockers and lipid-lowering therapy. The use of omega-3 fatty acids should be considered as part of a comprehensive secondary prevention strategy post-myocardial infarction.
----P Journal_Article Review Review_Literature 
----M M_Animals_MeSH M_Arrhythmia_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Coronary_Disease_MeSH S_diet_therapy_MeSH Coronary_Disease_diet_therapy_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Dogs_MeSH M_Fatty_Acids__Omega-3_MeSH S_administration_&_dosage_MeSH Fatty_Acids__Omega-3_administration_&_dosage_MeSH S_pharmacology_MeSH Fatty_Acids__Omega-3_pharmacology_MeSH M_Female_MeSH M_Forecasting_MeSH M_Human_MeSH M_Linoleic_Acid_MeSH S_physiology_MeSH Linoleic_Acid_physiology_MeSH M_Male_MeSH M_Nutrition_MeSH S_physiology_MeSH Nutrition_physiology_MeSH M_Randomized_Controlled_Trials_MeSH M_Rats_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12882875
----K 5
----T Heart failure: the frequent, forgotten, and often fatal complication of diabetes.
----A There is a high frequency of heart failure (HF) accompanied by an increased mortality risk for patients with diabetes. The poor prognosis of these patients has been explained by an underlying diabetic cardiomyopathy exacerbated by hypertension and ischemic heart disease. In these patients, activation of the sympathetic nervous system results in increased myocardial utilization of fatty acids and induction of fetal gene programs, decreasing myocardial function. Activation of the renin-angiotensin system results in myocardial remodeling. It is imperative for physicians to intercede early to stop the progression of HF, yet at least half of patients with left ventricular dysfunction remain undiagnosed and untreated until advanced disease causes disability. This delay is largely because of the asymptomatic nature of early HF, which necessitates more aggressive assessment of HF risk factors and early clinical signs. Utilization of beta-blockade, ACE inhibitors, or possibly angiotensin receptor blockers is essential in preventing remodeling with its associated decline in ventricular function. beta-Blockers not only prevent, but may also reverse, cardiac remodeling. Glycemic control may also play an important role in the therapy of diabetic HF. The adverse metabolic side effects that have been associated with beta-adrenergic inhibitors in the diabetic patient may be circumvented by use of a third-generation beta-blocker. Prophylactic utilization of ACE inhibitors and beta-blockers to avoid, rather than await, the need to treat HF should be considered in high-risk diabetic patients.
----P Journal_Article Review Review_Literature 
----M M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12888152
----K 2
----T Comparison of effects on systolic and diastolic left ventricular function of nebivolol versus atenolol in patients with uncomplicated essential hypertension.
----A This was a double-blind, randomized, prospective study comparing the effects of nebivolol and atenolol on systolic diastolic left ventricular function in patients with essential hypertension. A significant difference was seen in stroke volume between these 2 drugs. The blood pressure lowering effect of atenolol was strongly related to cardiac output and heart rate reduction. The blood pressure lowering effect of nebivolol was related to a reduction in peripheral resistance and an increase in stroke volume with preservation of cardiac output. This preservation of cardiac output, together with a reduced peripheral resistance, may be potentially important in treating heart failure.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Atenolol_MeSH S_pharmacology_MeSH Atenolol_pharmacology_MeSH M_Benzopyrans_MeSH S_pharmacology_MeSH Benzopyrans_pharmacology_MeSH M_Comparative_Study_MeSH M_Diastole_MeSH S_drug_effects_MeSH Diastole_drug_effects_MeSH M_Double-Blind_Method_MeSH M_Echocardiography_MeSH M_Ethanolamines_MeSH S_pharmacology_MeSH Ethanolamines_pharmacology_MeSH M_Female_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_ultrasonography_MeSH Hypertension_ultrasonography_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Systole_MeSH S_drug_effects_MeSH Systole_drug_effects_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH 
****** 12898491
----K 5
----T Care of children who have had surgery for congenital heart disease.
----A Children who have had surgical correction for congenital heart disease can present to the ED with an acute illness that could be associated with their cardiac lesion. There is no data available to summarize complications that could be associated with surgically corrected congenital heart disease. This work was undertaken to describe the common procedures used, list known complications of these procedures, and review general management principles in caring for the acutely ill child who has had heart surgery.
----P Journal_Article Review Review_Literature 
----M M_Child_MeSH M_Heart_Defects__Congenital_MeSH S_surgery_MeSH Heart_Defects__Congenital_surgery_MeSH M_Human_MeSH M_Postoperative_Complications_MeSH S_therapy_MeSH Postoperative_Complications_therapy_MeSH 
****** 12899584
----K 3
----T Effects of losartan or atenolol in hypertensive patients without clinically evident vascular disease: a substudy of the LIFE randomized trial.
----A BACKGROUND: Cardiovascular morbidity and mortality are reduced by treatment with the angiotensin II AT(1)-receptor antagonist losartan compared with conventional treatment with the beta-blocker atenolol in patients with hypertension and electrocardiogram-defined left ventricular hypertrophy, many of whom had known vascular disease. OBJECTIVE: To determine whether losartan reduces cardiovascular event rates in lower-risk hypertensive patients without clinically evident vascular disease. DESIGN: Subgroup analysis of a randomized trial. SETTING: The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study. PATIENTS: 6886 men and women (57% women) 55 to 80 years of age (average, 66 years) with essential hypertension (sitting blood pressure, 160 to 200/95 to 115 mm Hg [average, 174/98 mm Hg]) and electrocardiogram-defined left ventricular hypertrophy who did not have clinically evident vascular disease. INTERVENTION: Patients were randomly assigned to once-daily double-blind treatment with losartan or atenolol. MEASUREMENTS: An end point committee ascertained end points (cardiovascular death, stroke, or myocardial infarction). RESULTS: Blood pressure was reduced similarly by losartan and atenolol. The primary composite end point occurred in 282 losartan-treated patients (17.5 per 1000 patient-years) and 355 atenolol-treated patients (21.8 per 1000 patient-years; relative risk, 0.81 [95% CI, 0.69 to 0.95]; P = 0.008). Cardiovascular death occurred in 103 losartan-treated patients and 132 atenolol-treated patients (relative risk, 0.80 [CI, 0.62 to 1.04]; P = 0.092), stroke (nonfatal and fatal) occurred in 125 losartan-treated patients and 193 atenolol-treated patients (relative risk, 0.66 [CI, 0.53 to 0.82]; P < 0.001), and myocardial infarction (nonfatal and fatal) occurred in 110 losartan-treated patients and 100 atenolol-treated patients (relative risk, 1.14 [CI, 0.87 to 1.49]; P > 0.2). New-onset diabetes occurred less often in patients treated with losartan (n = 173) than in patients treated with atenolol (n = 254) (relative risk, 0.69 [CI, 0.57 to 0.84]; P < 0.001). Benefits of losartan treatment were numerically smaller, but not significantly so, in patients with preexisting vascular disease. CONCLUSION: In hypertensive patients without clinically evident vascular disease, losartan was more effective than atenolol in preventing cardiovascular morbidity and death, predominantly stroke, independent of blood pressure reduction.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_prevention_&_control_MeSH Cardiovascular_Diseases_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12906987
----K 5
----T Sympatholysis and cardiac sympathetic nerve function in the treatment of congestive heart failure.
----A 
----P Comment Editorial 
----M M_3-Iodobenzylguanidine_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Heart_MeSH S_innervation_MeSH Heart_innervation_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Radiopharmaceuticals_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH M_Sympatholytics_MeSH S_pharmacology_MeSH Sympatholytics_pharmacology_MeSH S_therapeutic_use_MeSH Sympatholytics_therapeutic_use_MeSH M_Ventricular_Dysfunction_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction_physiopathology_MeSH S_radionuclide_imaging_MeSH Ventricular_Dysfunction_radionuclide_imaging_MeSH 
****** 12885747
----K 3
----T Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study.
----A BACKGROUND: Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients. However, uncertainty persists as to how best to regress ECG LVH. METHODS AND RESULTS: Regression of ECG LVH with losartan versus atenolol therapy was assessed in 9193 hypertensive patients with ECG LVH by Sokolow-Lyon voltage or Cornell voltage-duration product criteria enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study. Patients had ECGs at study baseline and after 6 months, 1, 2, 3, 4, and 5 years of blinded losartan-based or atenolol-based therapy. After 6 months' follow-up, adjusting for baseline ECG LVH levels, baseline and in-treatment systolic and diastolic pressures, and for diuretic therapy, losartan-based therapy was associated with greater regression of both Cornell product (adjusted means, -200 versus -69 mm. ms, P<0.001) and Sokolow-Lyon voltage (-2.5 versus -0.7 mm, P<0.001) than was atenolol-based therapy. Greater regression of ECG LVH persisted at each subsequent annual evaluation in the losartan-treated group, with between 140 and 164 mm. ms greater mean reductions in Cornell product and from 1.7 to 2.2 mm greater mean reductions in Sokolow-Lyon voltage (all P<0.001). The effect of losartan was consistent across subgroups defined by gender, age, ethnicity, and diabetes. CONCLUSIONS: After adjusting for baseline and in-treatment blood pressure and baseline severity of ECG LVH, losartan-based antihypertensive therapy resulted in greater regression of ECG LVH by Cornell voltage-duration product and Sokolow-Lyon voltage criteria than did atenolol-based therapy. These findings support the value of angiotensin receptor blockade with losartan for reversing ECG LVH.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Age_Factors_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_adverse_effects_MeSH Atenolol_adverse_effects_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Continental_Population_Groups_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Double-Blind_Method_MeSH M_Electrocardiography_MeSH S_drug_effects_MeSH Electrocardiography_drug_effects_MeSH M_Female_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_diagnosis_MeSH Hypertrophy__Left_Ventricular_diagnosis_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Remission_Induction_MeSH M_Risk_Factors_MeSH M_Sex_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH M_Treatment_Outcome_MeSH 
****** 12912795
----K 5
----T Aortic dissection: new frontiers in diagnosis and management: Part II: therapeutic management and follow-up.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Aneurysm__Dissecting_MeSH S_complications_MeSH Aneurysm__Dissecting_complications_MeSH S_diagnosis_MeSH Aneurysm__Dissecting_diagnosis_MeSH S_therapy_MeSH Aneurysm__Dissecting_therapy_MeSH M_Aortic_Aneurysm_MeSH S_complications_MeSH Aortic_Aneurysm_complications_MeSH S_diagnosis_MeSH Aortic_Aneurysm_diagnosis_MeSH S_therapy_MeSH Aortic_Aneurysm_therapy_MeSH M_Blood_Vessel_Prosthesis_Implantation_MeSH S_adverse_effects_MeSH Blood_Vessel_Prosthesis_Implantation_adverse_effects_MeSH S_methods_MeSH Blood_Vessel_Prosthesis_Implantation_methods_MeSH S_mortality_MeSH Blood_Vessel_Prosthesis_Implantation_mortality_MeSH M_Cardiovascular_Surgical_Procedures_MeSH S_adverse_effects_MeSH Cardiovascular_Surgical_Procedures_adverse_effects_MeSH S_methods_MeSH Cardiovascular_Surgical_Procedures_methods_MeSH S_mortality_MeSH Cardiovascular_Surgical_Procedures_mortality_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Reoperation_MeSH M_Stents_MeSH S_adverse_effects_MeSH Stents_adverse_effects_MeSH M_Treatment_Outcome_MeSH 
****** 12914886
----K 5
----T Metoprolol CR/XL in black patients with heart failure (from the Metoprolol CR/XL randomized intervention trial in chronic heart failure).
----A A subgroup analysis was performed in black patients who participated in the Metoprolol CR/XL Randomized Intervention trial in Congestive Heart Failure trial. Results suggest a beneficial effect of beta blockade and support the use of beta blockers in black patients with clinically stable heart failure and left ventricular dysfunction.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH P_African_Americans_MeSH M_African_Continental_Ancestry_Group_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_ethnology_MeSH Heart_Failure__Congestive_ethnology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12915925
----K 5
----T The OPTIMAAL study, not so optimal: the lessons of LIFE, RENAAL and IDNT.
----A 
----P Editorial Evaluation_Studies 
----M M_Adult_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH S_therapeutic_use_MeSH Captopril_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Drug_Administration_Schedule_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_mortality_MeSH Hypertension_mortality_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_mortality_MeSH Hypertrophy__Left_Ventricular_mortality_MeSH M_Losartan_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Survival_Analysis_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_mortality_MeSH Ventricular_Dysfunction__Left_mortality_MeSH 
****** 12915830
----K 3
----T Long-term antiproteinuric and renoprotective efficacy and safety of losartan in children with proteinuria.
----A BACKGROUND: Angiotensin receptor antagonists are effective in reducing proteinuria by an action independent of blood pressure. As a consequence, such agents retard progressive renal dysfunction in adults with chronic proteinuria. Long-term efficacy and tolerability data in children are unavailable. METHODS: Efficacy of losartan in reducing proteinuria and in preserving renal function was prospectively assessed in 52 consecutive children under 18 years of age with chronic proteinuric renal disorders, an initial creatinine clearance > or =25 mL/min/1.73 m(2), and a minimum of two or more follow-up visits. Thirty had proteinuria (P), and 22 had proteinuria combined with hypertension (P+H). Adverse effects were also evaluated. RESULTS: Proteinuria had persisted or increased during a mean interval of 8.5 months before initiation of losartan at a mean dosage of 0.8 mg/kg/d. Mean protein excretion before starting losartan was 2453 mg/m(2)/d and fell by 34% at a mean follow-up time of six weeks (visit I, P<.05), and between 64% and 67% at mean follow-up periods of 0.38, 0.71, and 2.48 years corresponding to visits II, III, and IV (all P<.001 compared with baseline). The proportion of children with protein excretion exceeding 40 mg/m(2)/h (nephrotic range proteinuria) or nephrotic syndrome (>3500 mg/1.73 m(2)/d) fell from 42% and 40% at the start, to 24% and 8%, respectively, at visit IV (P<.01). Mean creatinine clearance as well as serum potassium and total CO(2) levels remained unchanged during the time of follow-up. Reduction in proteinuria in the P subgroup alone correlated with lowering in diastolic blood pressure at visit II and with both diastolic and systolic blood pressure at visits III and IV (all P<.05); it was largely independent of reduction in blood pressure in the P+H subgroup. The concomitant use of immunosuppressive agents in 28 of the 52 children had an influence on proteinuria only at baseline and at visit I (P<.05). There was no significant change in height or body mass index Z scores. Thirteen children had adverse effects potentially ascribed to losartan; most of these either improved or resolved with dosage adjustment or resulted in its discontinuation in 9 of the 52 children (17%). CONCLUSION: Losartan therapy was associated with a marked and sustained reduction in proteinuria and in preservation of GFR in children with chronic proteinuric disorders. The association between proteinuria and systemic blood pressure reduction was complex: it was largely limited to the first year of losartan therapy and was more pronounced in the normotensive subgroup. Losartan was generally well tolerated.
----P Clinical_Trial Journal_Article 
----M M_Adolescent_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Creatinine_MeSH S_blood_MeSH Creatinine_blood_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Kidney_Diseases_MeSH S_prevention_&_control_MeSH Kidney_Diseases_prevention_&_control_MeSH M_Losartan_MeSH S_administration_&_dosage_MeSH Losartan_administration_&_dosage_MeSH S_adverse_effects_MeSH Losartan_adverse_effects_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH M_Potassium_MeSH S_blood_MeSH Potassium_blood_MeSH M_Prospective_Studies_MeSH M_Proteinuria_MeSH S_diagnosis_MeSH Proteinuria_diagnosis_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH S_epidemiology_MeSH Proteinuria_epidemiology_MeSH M_Severity_of_Illness_Index_MeSH M_Time_MeSH 
****** 12916553
----K 5
----T Medical prevention of stroke, 2003.
----A Stroke is a preventable tragedy for nearly 750,000 people each year. Primary stroke prevention measures applicable to the general public include a healthy diet containing fruits, vegetables, fish, and low fat; exercise; smoking cessation; limiting alcohol to moderate use; and perhaps avoidance of stress. Screening for hypertension, cholesterol, heart disease, and carotid artery stenosiscan lead to even more effective stroke prevention in high-risk patients. Specific antihypertensive drugs such as angiotensin-converting enzyme inhibitors and angiotensin-converting enzyme receptor blockers may be especially protective against stroke. Secondary stroke prevention in patients who have already had a stroke or transient ischemic attack is even more effective in preventing more serious strokes. Measures include antihypertensive and cholesterol-lowering agents, carotid endarterectomy, anticoagulation for atrial fibrillation and other cardiac sources of embolic stroke, and antiplatelet therapy. Stroke prevention depends on the application of these well-known and widely available treatments to a large number of patients.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Inflammatory_Agents__Non-Steroidal_MeSH S_therapeutic_use_MeSH Anti-Inflammatory_Agents__Non-Steroidal_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Antilipemic_Agents_MeSH S_therapeutic_use_MeSH Antilipemic_Agents_therapeutic_use_MeSH M_Aspirin_MeSH S_therapeutic_use_MeSH Aspirin_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH P_Diet_MeSH M_Female_MeSH M_Human_MeSH P_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH S_drug_therapy_MeSH Hypercholesterolemia_drug_therapy_MeSH P_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Risk_Factors_MeSH 
****** 12918889
----K 5
----T Establishing principles for migraine management in primary care.
----A Published guidelines for the management of migraine in primary care were evaluated by an international advisory board of headache specialists, to establish evidence-based principles of migraine management that could be recommended for international use. Twelve principles of migraine management were identified, covering screening, diagnosis, management and treatments: Almost all headaches are benign/primary and can be managed by all practising clinicians. Use questions/a questionnaire to assess the impact on daily living and everyday activities, for diagnostic screening and to aid management decisions. Share migraine management between the clinician and the patient. Provide individualised care for migraine and encourage patients to manage their migraine. Follow up patients, preferably with migraine calendars or diaries. Regularly re-evaluate the success of therapy using specific outcome measures and monitor the use of acute and prophylactic medications regularly. Adapt migraine management to changes that occur in the illness and its presentation over the years. Provide acute medication to all migraine patients and recommend it is taken at the appropriate time, during the attack. Provide rescue medication/symptomatic treatment for when the initial therapy fails. Offer to prescribe prophylactic medications, as well as lifestyle changes, to patients who have four or more migraine attacks per month or who are resistant to acute medications. Consider concurrent co-morbidities in the choice of appropriate prophylactic medication. Work with the patient to achieve comfort with mutually agreed upon treatment and ensure that it is practical for their lifestyle and headache presentation. Using these principles, practising clinicians can screen and diagnose their headache patients effectively and manage their migraine patients over the long-term natural history of the migraine process. In this way, the majority of migraine patients can be well treated in primary care, ensuring a structured and individualised approach to headache management, and conserving valuable healthcare resources.
----P Consensus_Development_Conference Journal_Article Review 
----M M_Human_MeSH M_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_therapy_MeSH Migraine_therapy_MeSH M_Practice_Guidelines_MeSH M_Primary_Health_Care_MeSH S_methods_MeSH Primary_Health_Care_methods_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12923040
----K 5
----T Diagnostic accuracy of a new shorter dobutamine infusion protocol in stress echocardiography.
----A In the setting of acute myocardial infarction (MI) and cardiogenic shock in patients with significant unprotected left main coronary artery (LMCA) disease, treatment options are limited. In this report of a patient presenting in cardiogenic shock secondary to acute MI with critical LMCA stenosis, percutaneous coronary intervention with intra-aortic balloon pump support proved life saving.
----P Letter 
----M M_Angina_Pectoris_MeSH S_diagnosis_MeSH Angina_Pectoris_diagnosis_MeSH M_Cardiotonic_Agents_MeSH S_administration_&_dosage_MeSH Cardiotonic_Agents_administration_&_dosage_MeSH S_diagnostic_use_MeSH Cardiotonic_Agents_diagnostic_use_MeSH M_Clinical_Protocols_MeSH M_Dobutamine_MeSH S_administration_&_dosage_MeSH Dobutamine_administration_&_dosage_MeSH S_diagnostic_use_MeSH Dobutamine_diagnostic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Echocardiography_MeSH M_Echocardiography__Stress_MeSH M_Female_MeSH M_Human_MeSH M_Infusions__Intravenous_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Sensitivity_and_Specificity_MeSH 
****** 12923384
----K 5
----T New evidence on the importance of the renin-angiotensin system in the treatment of higher-risk patients with hypertension.
----A We reviewed the drug treatment of hypertension in the light of recent trials. beta-Blockers and diuretics clearly reduce mortality, strokes, and coronary heart disease (CHD) in hypertension. Recent trials assessed whether newer agents that block the renin-angiotensin-aldosterone system, or calcium blockers, offer any additional advantage, or have benefits in high-risk individuals with conventionally 'normal' blood pressure. The recent ALLHAT study claimed no differences in CHD or mortality when chlorthalidone, amlodipine, and lisinopril were compared. However, the decrease in blood pressure was not the same with the three agents, and a substantial proportion of patients enrolled did not have clinical disease. In contrast, the LIFE study (comparing losartan and a beta-blocker) and the ANBP-2 study [comparing angiotensin-converting enzyme (ACE) inhibition and a diuretic] reduced blood pressure similarly, yet demonstrated benefits in favour of angiotensin II type 1 receptor blockers (ARBs) and ACE inhibitors. Other trials indicated similar advantages of ACE inhibitors or ARBs in patients with diabetic nephropathy. Among high-risk patients with initial blood pressure in the 'normal' range, ACE inhibitors significantly reduce clinical events (mortality, strokes, and myocardial infarction), despite modest decreases in blood pressure, suggesting that additional mechanisms are responsible. Recent results of the Prospective Studies Collaboration show lower risk, even in the normal blood pressure range; high-risk patients will benefit further from ACE inhibitors and ARBs (and beta-blockers after myocardial infarction). Data for other blood pressure decreasing agents are unavailable in such populations. We conclude that blood pressure decreasing per se is of clinical benefit, but drugs that block the renin-angiotensin system offer additional advantages. Drug choice is best determined by the patient's clinical condition.
----P Journal_Article Review Review_Literature 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12923412
----K 5
----T Comparison of the SCOPE and LIFE results.
----A 
----P Comment Letter 
----M M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Cerebrovascular_Accident_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comparative_Study_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH P_Randomized_Controlled_Trials_MeSH 
****** 12924832
----K 5
----T Off-label applications for SSRIs.
----A Selective serotonin reuptake inhibitors (SSRIs) are widely used because of their safety, tolerability, and demonstrated efficacy across a broad range of clinical conditions. Medical literature supports the use of SSRIs for the treatment of many conditions outside of the indications approved by the U.S. Food and Drug Administration. SSRIs offer a reasonable alternative to traditional therapy for generalized anxiety disorder. A side effect of SSRIs coincidentally provides therapy for premature ejaculation. SSRIs may reduce the frequency and severity of migraine headaches and are possibly effective in reducing the pain of diabetic neuropathy. When taken in combination with tricyclic antidepressants, SSRis offer more potent therapy for fibromyalgia than either agent alone. SSRIs appear to be effective in some patients with neurocardiogenic syncope that is refractory to standard therapies. Clinical experience supported by ongoing research continues to expand on the broad array of therapeutic applications for this class of medication.
----P Journal_Article Review Review__Tutorial 
----M M_Antidepressive_Agents__Second-Generation_MeSH S_therapeutic_use_MeSH Antidepressive_Agents__Second-Generation_therapeutic_use_MeSH M_Anxiety_Disorders_MeSH S_drug_therapy_MeSH Anxiety_Disorders_drug_therapy_MeSH M_Clinical_Trials_MeSH M_Drug_Approval_MeSH M_Drug_Utilization_MeSH M_Fibromyalgia_MeSH S_drug_therapy_MeSH Fibromyalgia_drug_therapy_MeSH M_Human_MeSH M_Safety_MeSH M_Serotonin_Uptake_Inhibitors_MeSH S_therapeutic_use_MeSH Serotonin_Uptake_Inhibitors_therapeutic_use_MeSH 
****** 12933373
----K 4
----T Pharmacologic myocardial protection in patients undergoing noncardiac surgery: a quantitative systematic review.
----A A number of drugs have been tested in clinical trials to decrease cardiac complications in patients undergoing noncardiac surgery. To compare the results of these studies, we conducted a quantitative systematic review. Medline, Embase, and Cochrane databases were searched for randomized trials that assessed myocardial ischemia, myocardial infarction, 30-day cardiac mortality, and adverse effects. Data were combined using a fixed-effect model and expressed as Peto odds ratios (OR) with 95% confidence interval (CI) and as numbers-needed-to-treat/harm (NNT/H). Twenty-one trials involving 3646 patients were included: 11 trials using beta-blockers (6 drugs; 866 patients), 6 clonidine or mivazerol (614 patients), 3 diltiazem or verapamil (121 patients), and 1 nitroglycerin (45 patients). All trials had an inactive control; there were no direct comparisons. beta-blockers decreased ischemic episodes during surgery (7.6% versus 20.2% with placebo; OR 0.32 [95% CI, 0.17-0.58]; NNT 8) and after surgery (15.2% versus 27.9% with control; OR 0.46 [95% CI, 0.26-0.81]; NNT 8). alpha(2)-agonists decreased ischemia during surgery only (19.4% versus 32.8%; OR 0.47 [95% CI, 0.33-0.68]; NNT 7). beta-blockers reduced the risk of myocardial infarction (0.9% versus 5.2%; OR 0.19 [95% CI, 0.08-0.48]; NNT 23) but only when 2 trials with high-risk patients were included. The effect of alpha(2)-agonists on myocardial infarction was not significant (6.1% versus 7.3%; OR 0.85 [95% CI, 0.62-1.14]). beta-blockers significantly decreased the risk of cardiac death from 3.9% to 0.8% (OR 0.25 [95% CI, 0.09-0.73], NNT 32). alpha(2)-agonists significantly decreased the risk of cardiac death from 2.3% to 1.1% (OR 0.50 [95% CI, 0.28-0.91], NNT 83). For calcium channel blockers and nitroglycerin, evidence of any benefit was lacking. The most common adverse effect was bradycardia, which occurred in 24.5% of patients receiving a beta adrenergic blocker versus 9.1% of controls (OR 3.76 [95% CI, 2.45-5.77], NNH 6).
----P Journal_Article 
----M M_Adrenergic_alpha-Agonists_MeSH S_adverse_effects_MeSH Adrenergic_alpha-Agonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Agonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_adverse_effects_MeSH Adrenergic_beta-Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Myocardial_Diseases_MeSH S_mortality_MeSH Myocardial_Diseases_mortality_MeSH S_prevention_&_control_MeSH Myocardial_Diseases_prevention_&_control_MeSH M_Postoperative_Complications_MeSH S_prevention_&_control_MeSH Postoperative_Complications_prevention_&_control_MeSH M_Randomized_Controlled_Trials_MeSH M_Research_Design_MeSH M_Risk_Assessment_MeSH M_Support__Non-U_S__Gov't_MeSH M_Surgical_Procedures__Operative_MeSH S_adverse_effects_MeSH Surgical_Procedures__Operative_adverse_effects_MeSH 
****** 12934058
----K 3
----T Effects of moxonidine and metoprolol in penile circulation in hypertensive men with erectile dysfunction: results of a pilot study.
----A Centrally acting (moxonidine) and peripherally acting (metoprolol) sympatholytic agents might have different actions upon penile circulation in hypertensive men with erectile dysfunction. A total of 11 nonsmoking, hypertensive but otherwise healthy men with erectile dysfunction were studied after 8 weeks on moxonidine monotherapy (0.4 mg per day, increased to 0.6 mg if needed) and then after 8 weeks of metoprolol monotherapy (100 mg per day, increased to 200 mg if needed) in a crossover design. At the end of each treatment phase, the subjects were asked about their subjective erectile capacity (nocturnal and coital erections), and resting and stimulated (after intracavernosal injection of a mixture of alprostadil and phentolamine) penile deep artery diameters and systolic peak velocities were measured by color Doppler ultrasonography. There were no significant differences in blood pressure after either therapy. The change from earlier antihypertensive therapy, moxonidine produced significant subjective amelioration of sexual dysfunction in 9/11 of the men (< or = 0.001), whereas 9/11 returned to impaired dysfunction after crossover to metoprolol treatment. Resting and stimulated deep penile diameters and peak systolic velocities were higher after moxonidine treatment compared with metoprolol (diameters: < or = 0.004, < or = 0.0001; velocities: < or = 0.008, < or = 0.038). The centrally acting sympatholytic agent moxonidine seems to improve erectile function both subjectively and objectively and has a better effect on penile circulation compared with the peripherally acting sympatholytic agent metoprolol.
----P Journal_Article 
----M M_Adult_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Arteries_MeSH M_Blood_Flow_Velocity_MeSH S_drug_effects_MeSH Blood_Flow_Velocity_drug_effects_MeSH M_Cross-Over_Studies_MeSH M_Drug_Administration_Schedule_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Imidazoles_MeSH S_administration_&_dosage_MeSH Imidazoles_administration_&_dosage_MeSH M_Impotence_MeSH S_drug_therapy_MeSH Impotence_drug_therapy_MeSH S_etiology_MeSH Impotence_etiology_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Penis_MeSH S_blood_supply_MeSH Penis_blood_supply_MeSH S_ultrasonography_MeSH Penis_ultrasonography_MeSH M_Pilot_Projects_MeSH M_Regional_Blood_Flow_MeSH S_drug_effects_MeSH Regional_Blood_Flow_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sympatholytics_MeSH S_administration_&_dosage_MeSH Sympatholytics_administration_&_dosage_MeSH M_Ultrasonography__Doppler_MeSH 
****** 12932617
----K 5
----T Treatment of fetal tachycardia with sotalol: transplacental pharmacokinetics and pharmacodynamics.
----A OBJECTIVES: The aim of this study was to investigate the pharmacokinetics and pharmacodynamics of sotalol in the treatment of fetal tachycardia. BACKGROUND: Maternally administered, intrauterine therapy of fetal tachycardia is dependent on the transplacental passage of the antiarrhythmic agent. METHODS: In a prospective study of patients treated for fetal tachycardia with sotalol, concentrations of sotalol were determined in maternal and umbilical blood and in amniotic fluid, and the relationship between these concentrations and the occurrence of conversion to sinus rhythm was investigated. RESULTS: Eighteen fetal patients were studied, nine with atrial flutter and nine with supraventricular tachycardia. Fourteen were treated with sotalol; 13 converted to sinus rhythm, of whom 2 relapsed. There was one intrauterine death. Four patients were treated with sotalol and digoxin, of whom two were treated successfully. Mean birth weight was 3,266 g. The daily maternal sotalol dose was linearly related to the maternal plasma concentration. The mean fetal/maternal sotalol plasma concentration was 1.1 (range 0.67 to 2.87, SD 0.63), and the mean amniotic fluid/fetal blood ratio of sotalol was 3.2 (range 1.28 to 5.8, SD 1.4). The effectiveness of sotalol therapy could not be extrapolated from maternal blood levels. CONCLUSIONS: Sotalol is a potent antiarrhythmic agent in the treatment of fetal tachycardia. The placental transfer is excellent. Sotalol accumulates in amniotic fluid but not in the fetus itself. Therefore it seems that renal excretion in the fetus is efficient and greater than the oral absorption by fetal swallowing. The maternal blood level is not a reliable predictor of the chances of success of therapy. Sotalol is not associated with fetal growth restriction.
----P Journal_Article 
----M M_Amniotic_Fluid_MeSH S_chemistry_MeSH Amniotic_Fluid_chemistry_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Female_MeSH M_Fetal_Blood_MeSH S_chemistry_MeSH Fetal_Blood_chemistry_MeSH M_Fetal_Diseases_MeSH S_drug_therapy_MeSH Fetal_Diseases_drug_therapy_MeSH M_Human_MeSH M_Maternal-Fetal_Exchange_MeSH M_Placenta_MeSH S_physiology_MeSH Placenta_physiology_MeSH M_Pregnancy_MeSH M_Prospective_Studies_MeSH M_Sotalol_MeSH S_therapeutic_use_MeSH Sotalol_therapeutic_use_MeSH M_Tachycardia_MeSH S_complications_MeSH Tachycardia_complications_MeSH S_drug_therapy_MeSH Tachycardia_drug_therapy_MeSH 
****** 12943875
----K 5
----T Effects of cold exposure on submaximal exercise performance and adrenergic activation in patients with congestive heart failure and the effects of beta-adrenergic blockade (carvedilol or metoprolol).
----A Patients with congestive heart failure (CHF) exhibit a decrease in maximal exercise capacity in response to a cold environment. The aim of this study was to further investigate the impact of cold exposure on submaximal exercise capacity, systemic adrenergic drive, and the effects of long-term beta-adrenergic blockade on these parameters. Thirty-three patients with CHF, with exercise limited by dyspnea and left ventricular ejection fraction of 26 +/- 4%, were randomized to receive metoprolol or carvedilol for 6 months. The observations were compared with 12 age-matched healthy volunteers. Maximal exercise performance with gas exchange analyses were assessed using a ramp protocol, and endurance capacity was measured using 2 constant-load exercise tests performed randomly at 20 degrees C and -8 degrees C. Healthy volunteers increased their submaximal exercise time by 20% (1,353 +/- 455 [20 degrees C] vs 1,635 +/- 475 seconds [-8 degrees C]; p <0.05), whereas patients with CHF exhibited a 21% decrease in exercise time (1,182 +/- 549 [20 degrees C] vs 931 +/- 524 seconds [-8 degrees C]; p <0.05) at -8 degrees C. Beta blockers increased submaximal exercise duration at 20 degrees C (+261 +/- 617 seconds; p <0.05) and -8 degrees C (+374 +/- 729 seconds; p <0.05). Norepinephrine increased to a greater extent at 4 minutes and at the time of exhaustion (at -8 degrees C) only in patients with CHF. Beta-adrenergic blockade caused no significant decrease in plasma norepinephrine levels. Patients with symptomatic CHF exhibited a significant decrease in submaximal exercise time in response to moderate cold exposure. Beta-blocker therapy with either metoprolol or carvedilol significantly increases submaximal exercise time and attenuates the impact of cold exposure on functional capacity.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Blood_Gas_Analysis_MeSH M_Carbazoles_MeSH S_pharmacology_MeSH Carbazoles_pharmacology_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Case-Control_Studies_MeSH M_Cold_MeSH S_adverse_effects_MeSH Cold_adverse_effects_MeSH M_Dyspnea_MeSH S_etiology_MeSH Dyspnea_etiology_MeSH M_Exercise_Test_MeSH S_drug_effects_MeSH Exercise_Test_drug_effects_MeSH M_Exercise_Tolerance_MeSH S_drug_effects_MeSH Exercise_Tolerance_drug_effects_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Norepinephrine_MeSH S_blood_MeSH Norepinephrine_blood_MeSH M_Physical_Endurance_MeSH M_Propanolamines_MeSH S_pharmacology_MeSH Propanolamines_pharmacology_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Receptors__Adrenergic_MeSH S_drug_effects_MeSH Receptors__Adrenergic_drug_effects_MeSH S_physiology_MeSH Receptors__Adrenergic_physiology_MeSH M_Single-Blind_Method_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12943483
----K 5
----T Calcium antagonists in the treatment of hypertension in patients with ischaemic heart disease.
----A Are lives saved or heart attacks prevented by antihypertensive therapy, as a result of blood pressure reduction alone, or because of other properties of the antihypertensive medications which are independent of blood pressure lowering? Long-acting calcium antagonists seem to be as effective as thiazide diuretics and angiotensin-converting enzyme (ACE) inhibitors in preventing all-cause mortality and stroke in patients with hypertension, but are probably inferior to ACE inhibitors in preventing coronary artery disease. In patients with symptomatic coronary artery disease, calcium antagonists are generally as effective as beta-blockers in relieving angina and improving exercise time-to-onset of angina or ischaemia. Unstable angina or myocardial infarction require treatment with a beta-blocker, with an ACE inhibitor added when necessary for blood pressure control or if there is significant left ventricular (LV) dysfunction. If beta-blockers are contraindicated and if there is no LV dysfunction, a non-dihydropyridine calcium antagonist can be substituted.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_pharmacology_MeSH Calcium_Channel_Blockers_pharmacology_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Myocardial_Ischemia_MeSH S_complications_MeSH Myocardial_Ischemia_complications_MeSH 
****** 12944056
----K 5
----T Might losartan reduce sudden cardiac death in diabetic patients with hypertension?
----A 
----P Comment Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Clinical_Trials_MeSH M_Comorbidity_MeSH M_Comparative_Study_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_epidemiology_MeSH Diabetes_Mellitus_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Losartan_MeSH S_therapeutic_use_MeSH Losartan_therapeutic_use_MeSH M_Male_MeSH 
****** 12945222
----K 5
----T [Factors predicting blood pressure normalization in hypertensive patients treated with a fixed-dose combination of bisoprolol 2.5 mg/hydrochlorothiazide/6.25 mg]
----A It is not clear which duration of treatment is needed to achieve complete efficacy with fixed low dose antihypertensive therapy. The aim of this study was to compare blood pressure control rate in patients treated with bisoprolol 2.5 mg/HCTZ 6.25 mg, not controlled after 4 weeks, but treated at the same dosage for one more month to patients not controlled after 4 weeks, and uptitrated to bisoprolol 5 mg/HCTZ 6.25 mg for one month. The 641 patients who entered the study had a mean age of 58 +/- 12 with SBP/DBP at baseline of 165 +/- 12/96 +/- 7 mmHg. After 4 weeks, 252 (39%) where normalized (< 140/90) with SBP/DBP reductions of -27/-15 mmHg. In uncontrolled patients, 19% of those randomized to B 2.5 mg/H 6.25 mg and 33% of those treated with B 5 mg/H 6.25 mg where normalized at the end of the study (p < 0.001). Multivariate analysis indicates determinants of blood pressure normalisation after 4 weeks with B2.5 mg/HCTZ 6.25 mg as female gender, initial BP < 175/105 mmHg, previously untreated hypertension, age < 50 years. In conclusion, when the initial therapy with bisoprolol 2.5 mg/HCTZ 6.25 mg is not sufficient to control blood pressure, continuation with the same dosage 4 weeks longer increases the rate of blood pressure control. However, up-titration to bisoprolol 5 mg/6.25 mg is more efficacious to increase the number of patients with a final blood pressure < 140/90 mmHg.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Bisoprolol_MeSH S_administration_&_dosage_MeSH Bisoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Bisoprolol_pharmacology_MeSH M_Blood_Pressure_MeSH M_Drug_Administration_Schedule_MeSH M_English_Abstract_MeSH M_Female_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_administration_&_dosage_MeSH Hydrochlorothiazide_administration_&_dosage_MeSH S_pharmacology_MeSH Hydrochlorothiazide_pharmacology_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Multivariate_Analysis_MeSH M_Treatment_Outcome_MeSH 
****** 12954920
----K 5
----T Antihistamines.
----A Antihistamines and their drug-drug interactions are reviewed in depth. The metabolism of "classic" or sedating antihistamines is coming to light through in vivo and in vitro studies. The polymorphic CYP 2D6 metabolic enzyme appears to be potently inhibited by many of these over-the-counter medications. The history of the discontinued "second-generation" antihistamines terfenadine and astemizole is reviewed to remind the reader why the understanding of the cytochrome P450 system became increasingly important when the cardiotoxicity of these drugs became apparent. The "third-generation" nonsedating antihistamines are also listed and compared. They have been exhaustively scrutinized for drug-drug interactions and cardiotoxicity, and they appear to have no serious drug-drug interactions at recommended doses.
----P Journal_Article Review Review__Tutorial 
----M M_Astemizole_MeSH S_adverse_effects_MeSH Astemizole_adverse_effects_MeSH S_therapeutic_use_MeSH Astemizole_therapeutic_use_MeSH M_Cytochrome_P-450_CYP2D6_MeSH S_antagonists_&_inhibitors_MeSH Cytochrome_P-450_CYP2D6_antagonists_&_inhibitors_MeSH M_Drug_Interactions_MeSH M_Drugs__Non-Prescription_MeSH S_adverse_effects_MeSH Drugs__Non-Prescription_adverse_effects_MeSH S_therapeutic_use_MeSH Drugs__Non-Prescription_therapeutic_use_MeSH M_Histamine_H1_Antagonists_MeSH S_adverse_effects_MeSH Histamine_H1_Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Histamine_H1_Antagonists_therapeutic_use_MeSH M_Histamine_H1_Antagonists__Non-Sedating_MeSH S_adverse_effects_MeSH Histamine_H1_Antagonists__Non-Sedating_adverse_effects_MeSH S_therapeutic_use_MeSH Histamine_H1_Antagonists__Non-Sedating_therapeutic_use_MeSH M_Human_MeSH M_Terfenadine_MeSH S_adverse_effects_MeSH Terfenadine_adverse_effects_MeSH S_therapeutic_use_MeSH Terfenadine_therapeutic_use_MeSH 
****** 12956257
----K 4
----T Response to travoprost in black and nonblack patients with open-angle glaucoma or ocular hypertension.
----A Two prospective, controlled, multicenter, double-masked studies--one lasting 6 months (n=594) and the other, 12 months (n=787)--examined the intraocular pressure (IOP)-lowering efficacy of travoprost in 1381 black and nonblack patients with open-angle glaucoma or ocular hypertension. Investigated regimens were travoprost 0.004% once daily, latanoprost 0.005% once daily, and timolol 0:5% twice daily. In both studies, mean IOP was significantly lower in blacks treated with travoprost. The IOP reduction was also significantly greater in blacks after adjustments for age, sex, iris color, diagnosis, and corneal thickness. Timolol lowered mean IOP to a greater extent in nonblack patients. The significantly larger IOP reduction with travoprost compared with timolol in both racial groups was more pronounced in blacks. Travoprost also was superior to latanoprost in blacks. Mean changes from baseline generally were greater for black than for nonblack patients, although the differences did not achieve statistical significance. The response rate to travoprost was higher in blacks. The most common adverse effect was hyperemia.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH P_African_Continental_Ancestry_Group_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Child_MeSH M_Cloprostenol_MeSH S_analogs_&_derivatives_MeSH Cloprostenol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Cloprostenol_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Cornea_MeSH S_physiopathology_MeSH Cornea_physiopathology_MeSH M_Dose-Response_Relationship__Drug_MeSH M_Double-Blind_Method_MeSH P_European_Continental_Ancestry_Group_MeSH M_Female_MeSH M_Glaucoma__Open-Angle_MeSH S_drug_therapy_MeSH Glaucoma__Open-Angle_drug_therapy_MeSH S_ethnology_MeSH Glaucoma__Open-Angle_ethnology_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH S_ethnology_MeSH Ocular_Hypertension_ethnology_MeSH M_Prospective_Studies_MeSH M_Prostaglandins_F__Synthetic_MeSH S_therapeutic_use_MeSH Prostaglandins_F__Synthetic_therapeutic_use_MeSH M_Support__Non-U_S__Gov't_MeSH M_Time_Factors_MeSH M_Timolol_MeSH S_therapeutic_use_MeSH Timolol_therapeutic_use_MeSH M_Treatment_Outcome_MeSH 
****** 12958318
----K 5
----T Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the American Heart Association/American Stroke Association.
----A 
----P Guideline Journal_Article Practice_Guideline 
----M M_Brain_Ischemia_MeSH S_epidemiology_MeSH Brain_Ischemia_epidemiology_MeSH M_Carotid_Stenosis_MeSH S_epidemiology_MeSH Carotid_Stenosis_epidemiology_MeSH M_Clinical_Trials_MeSH S_statistics_&_numerical_data_MeSH Clinical_Trials_statistics_&_numerical_data_MeSH M_Comorbidity_MeSH M_Coronary_Arteriosclerosis_MeSH S_diagnosis_MeSH Coronary_Arteriosclerosis_diagnosis_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH S_therapy_MeSH Coronary_Arteriosclerosis_therapy_MeSH M_Human_MeSH M_Ischemic_Attack__Transient_MeSH S_epidemiology_MeSH Ischemic_Attack__Transient_epidemiology_MeSH M_Prevalence_MeSH M_Risk_MeSH M_Risk_Assessment_MeSH M_Risk_Factors_MeSH M_Risk_Reduction_Behavior_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 12964914
----K 5
----T Lowering blood pressure in 2003.
----A The foundation of treatment for patients with hypertension is ongoing use of lifestyle measures such as physical exercise, weight reduction, and salt restriction. There should be emphasis on reduction of total cardiovascular risk, including smoking cessation and achievement of goal blood pressures. There are now five classes of first-line blood-pressure-lowering drugs - diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and calcium antagonists. In most patients, the choice of drug will be guided by the clinical situation in the individual patient, including the presence of target organ damage, diabetes, established vascular or kidney disease, or other comorbidities. In the absence of such clinical indications, start drug therapy with a low-dose diuretic. Combination therapy will be needed in around two-thirds of patients, and a diuretic will normally form one element of most combinations, with the second or third drug coming from among the remaining four. Consider the use of fixed-dose combinations to improve adherence to therapy. Use long-acting, once-daily preparations.
----P Journal_Article Review Review_Literature 
----M M_Clinical_Trials_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12967547
----K 5
----T Do antiarrhythmics prevent sudden death in patients with heart failure?
----A 
----P Journal_Article 
----M M_Amiodarone_MeSH S_therapeutic_use_MeSH Amiodarone_therapeutic_use_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Death__Sudden__Cardiac_MeSH S_prevention_&_control_MeSH Death__Sudden__Cardiac_prevention_&_control_MeSH M_Evidence-Based_Medicine_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH 
****** 12968198
----K 5
----T Congestive heart failure: guidelines for the primary care physician.
----A Heart failure is a common medical condition affecting nearly 5 million people each year in the United States, of whom 500,000 are newly diagnosed. The impact of this disease on society and the health care system is immense. Inpatient and outpatient costs are approximately $40 billion annually, almost $500 million of which is spent on heart failure medications alone. Beyond the problem of financial costs, however, it is imperative for us as health care professionals to improve our ability to prevent disease progression, decrease morbidity and mortality, and optimize patients  quality of life. The use of a broad spectrum of treatments is reviewed in the context of a patient case study. Primary data justifying the use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, digoxin, as well as beta blockers and spironolactone, is reviewed, with special reference to the stage of heart failure.
----P Guideline Journal_Article 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Captopril_MeSH M_Diagnosis__Differential_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Losartan_MeSH P_Primary_Health_Care_MeSH M_Risk_Factors_MeSH 
****** 12974970
----K 5
----T Clinical review: the management of hypertensive crises.
----A Hypertension is an extremely common clinical problem, affecting approximately 50 million people in the USA and approximately 1 billion individuals worldwide. Approximately 1% of these patients will develop acute elevations in blood pressure at some point in their lifetime. A number of terms have been applied to severe hypertension, including hypertensive crises, emergencies, and urgencies. By definition, acute elevations in blood pressure that are associated with end-organ damage are called hypertensive crises. Immediate reduction in blood pressure is required only in patients with acute end-organ damage. This article reviews current concepts, and common misconceptions and pitfalls in the diagnosis and management of patients with acutely elevated blood pressure.
----P Journal_Article Review Review__Academic 
----M M_Acute_Disease_MeSH M_Antihypertensive_Agents_MeSH S_classification_MeSH Antihypertensive_Agents_classification_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_diagnosis_MeSH Hypertension_diagnosis_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH P_Intensive_Care_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 13678695
----K 5
----T A surgeon's guide to herbal supplements.
----A The use of herbal supplements has steadily increased in the United States over the last decade. Despite the increased awareness of alternative therapies by the government and lay public, many physicians do not ask their patients about their use of these alternative medications. In addition, many physicians are unaware of the possible side effects that may occur when a patient consumes these substances. Considering a number of these supplements have been associated with adverse reactions in the perioperative period, it is important for a surgeon to understand all of the herbs a patient may be taking. The purpose of this article is to discuss the growing trend of herbal use among surgical patients and give the reader some background on the most commonly used herbs.
----P Journal_Article Review Review__Tutorial 
----M P_Dietary_Supplements_MeSH P_Drug_Interactions_MeSH M_Female_MeSH M_Human_MeSH M_Intraoperative_Complications_MeSH M_Male_MeSH P_Medicine__Herbal_MeSH P_Plants__Medicinal_MeSH M_Postoperative_Complications_MeSH P_Surgery_MeSH 
****** 13678871
----K 3
----T Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial.
----A BACKGROUND: Half of patients with chronic heart failure (CHF) have preserved left-ventricular ejection fraction (LVEF), but few treatments have specifically been assessed in such patients. In previous studies of patients with CHF and low LVEF or vascular disease and preserved LVEF, inhibition of the renin-angiotensin system is beneficial. We investigated the effect of addition of an angiotensin-receptor blocker to current treatments. METHODS: Between March, 1999, and July, 2000, we randomly assigned 3023 patients candesartan (n=1514, target dose 32 mg once daily) or matching placebo (n=1509). Patients had New York Heart Association functional class II-IV CHF and LVEF higher than 40%. The primary outcome was cardiovascular death or admission to hospital for CHF. Analysis was done by intention to treat. FINDINGS: Median follow-up was 36.6 months. 333 (22%) patients in the candesartan and 366 (24%) in the placebo group experienced the primary outcome (unadjusted hazard ratio 0.89 [95% CI 0.77-1.03], p=0.118; covariate adjusted 0.86 [0.74-1.0], p=0.051). Cardiovascular death did not differ between groups (170 vs 170), but fewer patients in the candesartan group than in the placebo group were admitted to hospital for CHF once (230 vs 279, p=0.017) or multiple times. Composite outcomes that included non-fatal myocardial infarction and non-fatal stroke showed similar results to the primary composite (388 vs 429; unadjusted 0.88 [0.77-1.01], p=0.078; covariate adjusted 0.86 [0.75-0.99], p=0.037). INTERPRETATION: Candesartan has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_therapeutic_use_MeSH Benzimidazoles_therapeutic_use_MeSH M_Cardiovascular_Diseases_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Hospitalization_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Outcome_Assessment_(Health_Care)_MeSH M_Placebos_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Stroke_Volume_MeSH S_physiology_MeSH Stroke_Volume_physiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Function__Left_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 14499775
----K 5
----T N-2-butyl-cyanoacrylate for bleeding gastric varices: a United States pilot study and cost analysis.
----A OBJECTIVES: N-butyl-2-cyanoacrylate has been reported to be effective for bleeding varices but is not available in the United States. We report the initial US experience with cyanoacrylate in this prospective trial and evaluate its safety, efficacy, and relative costs. METHODS: Patients with active or recent gastric variceal bleeding were eligible. Cyanoacrylate therapy was performed until variceal occlusion was achieved. Rebleeding was assessed at 72 h (acute phase), 6 wk (subacute phase), and 1 yr (chronic phase). Survival was assessed at 3 months and 1 yr. Cost analysis was performed comparing the first 17 patients to historical control patients not treated with cyanoacrylate. RESULTS: A total of 44 patients were enrolled, 37 with cirrhosis and seven with noncirrhotic portal hypertension (NCPH). In cirrhotic patients, rebleeding was seen in two of 37 (5%) at 72 h, one of 30 (3%) at 6 wk, and five of 28 (18%) at 1 yr. Survival without shunt at 3 months was 30 of 34 (88%) and at 1 yr was 24 of 31 (77%). In NCPH patients, rebleeding was seen in two of seven (29%) at 72 h. These patients received definitive therapy for NCPH after diagnosis. Mortality and costs were substantially higher in the non-cyanoacrylate group. The odds of death were greater by 7-fold in the non-cyanoacrylate group than within the cyanoacrylate group (95% CI = 1.18-41.36, p = 0.0318). At 3 months, there was a 3.18-fold difference (95% CI = 1.05-9.64, p = 0.0411) in accrued costs; at 1 yr, the difference was 2.55-fold (95% CI = 0.96-6.94, p = 0.0585). The cost-effective ratio was estimated as 108,237 US dollars/death averted, reflecting marked cost reduction with improved survival in the cyanoacrylate-treated group. This is believed to result largely from avoidance of shunt interventions. CONCLUSIONS: Cyanoacrylate treatment of gastric varices is safe, clinically effective, and cost effective.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Case-Control_Studies_MeSH M_Cost-Benefit_Analysis_MeSH M_Cyanoacrylates_MeSH S_economics_MeSH Cyanoacrylates_economics_MeSH S_therapeutic_use_MeSH Cyanoacrylates_therapeutic_use_MeSH M_Esophageal_and_Gastric_Varices_MeSH S_complications_MeSH Esophageal_and_Gastric_Varices_complications_MeSH S_diagnosis_MeSH Esophageal_and_Gastric_Varices_diagnosis_MeSH S_economics_MeSH Esophageal_and_Gastric_Varices_economics_MeSH S_therapy_MeSH Esophageal_and_Gastric_Varices_therapy_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Gastrointestinal_Hemorrhage_MeSH S_complications_MeSH Gastrointestinal_Hemorrhage_complications_MeSH S_diagnosis_MeSH Gastrointestinal_Hemorrhage_diagnosis_MeSH S_economics_MeSH Gastrointestinal_Hemorrhage_economics_MeSH S_therapy_MeSH Gastrointestinal_Hemorrhage_therapy_MeSH M_Hemostasis__Endoscopic_MeSH S_economics_MeSH Hemostasis__Endoscopic_economics_MeSH S_methods_MeSH Hemostasis__Endoscopic_methods_MeSH M_Human_MeSH M_Logistic_Models_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pilot_Projects_MeSH M_Risk_Assessment_MeSH M_Sampling_Studies_MeSH M_Sclerosing_Solutions_MeSH M_Sclerotherapy_MeSH S_economics_MeSH Sclerotherapy_economics_MeSH S_methods_MeSH Sclerotherapy_methods_MeSH M_Treatment_Outcome_MeSH 
****** 14500332
----K 5
----T Antiarrhythmic drug target choices and screening.
----A Most antiarrhythmic drugs are ion channel blockers, and to date, those tested in large randomized placebo-controlled clinical trials have shown no decrease in mortality outcome. This apparent lack of survival benefit may result from the significant liabilities associated with these agents that offset any long-term benefit. Despite the current success of implantable defibrillators and the future promise of gene therapy, there is still a pressing need for new antiarrhythmic drugs. An improved understanding of cardiac ion channels and novel approaches to target selection and compound screening will provide new opportunities for drug discovery in the near future. Here, we briefly review the multiple mechanisms of arrhythmia, the history of drug failures, and the possibilities that evolving technologies may provide in the search for more efficacious and safer antiarrhythmic drugs.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_drug_therapy_MeSH Arrhythmia_drug_therapy_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Calcium_Channels__T-Type_MeSH S_metabolism_MeSH Calcium_Channels__T-Type_metabolism_MeSH M_Drug_Delivery_Systems_MeSH M_Drug_Evaluation__Preclinical_MeSH M_Human_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Failure_MeSH 
****** 14504154
----K 5
----T Influence of thoracic epidural analgesia on cardiovascular autonomic control after thoracic surgery.
----A BACKGROUND: Thoracic epidural analgesia (TEA) is effective in alleviating pain after major thoracoabdominal surgery and may also reduce postoperative mortality and morbidity. This study investigated cardiovascular autonomic control in patients undergoing elective thoracic surgery and its modulation by continuous TEA. METHODS: Thirty-eight patients were randomly assigned to receive patient-controlled analgesia (PCA group) or thoracic epidural analgesia (TEA group) with doses of bupivacaine (0.25% during operation, 0.125% after operation) and fentanyl (2 microg ml(-1)). Heart rate variability (HRV), baroreflex function and pressure response to nitroglycerine and phenylephrine were assessed before operation, 4 h after the end of surgery (POD 0) and on the first and second postoperative days (POD 1 and POD 2). RESULTS: Early after surgery, all HRV variables and baroreflex sensitivities were markedly decreased in both groups. In the TEA group, total HRV and its high-frequency components (HF) increased towards preoperative values at POD 1 and POD 2, whereas the ratio of low to high frequencies (LF/HF) was significantly reduced (mean (SD), -44 (15)% at POD 0, -38 (17)% at POD 1, -37 (18%) at POD 2) and associated with blunting of the postoperative increase in heart rate and blood pressure. In the PCA group, the ratio of LF/HF remained unchanged and the decrements in HRV variables persisted until POD 2. In the two groups, baroreflex sensitivities and pressure responses recovered preoperative values at POD 2. CONCLUSIONS: In contrast with PCA management, TEA using low concentrations of bupivacaine and fentanyl blunted cardiac sympathetic neural drive, resulting in vagal predominance, while HRV variables were better restored after surgery.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Analgesia__Epidural_MeSH S_methods_MeSH Analgesia__Epidural_methods_MeSH M_Analgesia__Patient-Controlled_MeSH S_methods_MeSH Analgesia__Patient-Controlled_methods_MeSH M_Anesthesia__General_MeSH S_methods_MeSH Anesthesia__General_methods_MeSH M_Baroreflex_MeSH S_physiology_MeSH Baroreflex_physiology_MeSH M_Blood_Pressure_MeSH S_physiology_MeSH Blood_Pressure_physiology_MeSH M_Heart_Rate_MeSH S_physiology_MeSH Heart_Rate_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH M_Hypotension_MeSH S_etiology_MeSH Hypotension_etiology_MeSH M_Lung_MeSH S_surgery_MeSH Lung_surgery_MeSH M_Lung_Neoplasms_MeSH S_physiopathology_MeSH Lung_Neoplasms_physiopathology_MeSH S_surgery_MeSH Lung_Neoplasms_surgery_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Postoperative_Complications_MeSH S_etiology_MeSH Postoperative_Complications_etiology_MeSH M_Sympathetic_Nervous_System_MeSH S_physiopathology_MeSH Sympathetic_Nervous_System_physiopathology_MeSH M_Tachycardia_MeSH S_etiology_MeSH Tachycardia_etiology_MeSH P_Thoracic_Surgical_Procedures_MeSH M_Time_Factors_MeSH 
****** 14508818
----K 5
----T Breast carcinoma and antihypertensive therapy.
----A 
----P Comment Editorial 
----M M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Breast_Neoplasms_MeSH S_chemically_induced_MeSH Breast_Neoplasms_chemically_induced_MeSH S_epidemiology_MeSH Breast_Neoplasms_epidemiology_MeSH M_Carcinoma_MeSH S_chemically_induced_MeSH Carcinoma_chemically_induced_MeSH S_epidemiology_MeSH Carcinoma_epidemiology_MeSH M_Cardiovascular_Diseases_MeSH S_drug_therapy_MeSH Cardiovascular_Diseases_drug_therapy_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Incidence_MeSH M_Middle_Aged_MeSH M_Prognosis_MeSH M_Randomized_Controlled_Trials_MeSH M_Risk_Assessment_MeSH 
****** 14511900
----K 5
----T Cytochrome P450 enzyme polymorphisms and adverse drug reactions.
----A Adverse drug reactions (ADR) are common and many are thought to have a genetic predisposition. There has been a great deal of interest in the role of P450 enzyme gene polymorphisms in the pathogenesis of adverse reactions. The major impact to date of polymorphic P450 expression has been on pre-clinical drug development. However, the direct clinical impact of P450 polymorphisms on prediction of ADRs has been limited, largely because studies have been small and retrospective, and the literature shows an abundance of contradictory data. Furthermore, the clinical- and cost-effectiveness of pre-prescription genotyping for P450 polymorphisms has not been convincingly demonstrated. Further studies that address these deficiencies are urgently needed--only then will prospective P450 genotyping become routine in clinical practice.
----P Journal_Article Review Review__Tutorial 
----M M_Animals_MeSH M_Cytochrome_P-450_Enzyme_System_MeSH S_genetics_MeSH Cytochrome_P-450_Enzyme_System_genetics_MeSH S_metabolism_MeSH Cytochrome_P-450_Enzyme_System_metabolism_MeSH M_Human_MeSH M_Pharmaceutical_Preparations_MeSH S_adverse_effects_MeSH Pharmaceutical_Preparations_adverse_effects_MeSH M_Polymorphism_(Genetics)_MeSH S_genetics_MeSH Polymorphism_(Genetics)_genetics_MeSH 
****** 14517152
----K 5
----T Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: Part II.
----A This issue brief reviews hospital reporting initiatives designed for consumer use and discusses how employers can encourage greater transparency and disclosure in health care.
----P Journal_Article Review Review__Tutorial 
----M M_Arteriosclerosis_MeSH S_diagnosis_MeSH Arteriosclerosis_diagnosis_MeSH S_etiology_MeSH Arteriosclerosis_etiology_MeSH S_therapy_MeSH Arteriosclerosis_therapy_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH M_Coronary_Arteriosclerosis_MeSH S_etiology_MeSH Coronary_Arteriosclerosis_etiology_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Diabetic_Angiopathies_MeSH S_diagnosis_MeSH Diabetic_Angiopathies_diagnosis_MeSH S_physiopathology_MeSH Diabetic_Angiopathies_physiopathology_MeSH S_therapy_MeSH Diabetic_Angiopathies_therapy_MeSH M_Female_MeSH M_Human_MeSH M_Male_MeSH M_Peripheral_Vascular_Diseases_MeSH S_etiology_MeSH Peripheral_Vascular_Diseases_etiology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 14557343
----K 5
----T Aldosterone blockade in patients with systolic left ventricular dysfunction.
----A 
----P Case_Reports Journal_Article Review Review__Tutorial 
----M M_Aldosterone_MeSH S_physiology_MeSH Aldosterone_physiology_MeSH M_Aldosterone_Antagonists_MeSH S_pharmacology_MeSH Aldosterone_Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Forecasting_MeSH M_Heart_Failure__Congestive_MeSH S_etiology_MeSH Heart_Failure__Congestive_etiology_MeSH M_Human_MeSH M_Hypercholesterolemia_MeSH S_complications_MeSH Hypercholesterolemia_complications_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_pathology_MeSH Myocardial_Infarction_pathology_MeSH M_Patient_Selection_MeSH M_Randomized_Controlled_Trials_MeSH M_Spironolactone_MeSH S_analogs_&_derivatives_MeSH Spironolactone_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Systole_MeSH M_Ventricular_Dysfunction__Left_MeSH S_complications_MeSH Ventricular_Dysfunction__Left_complications_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 14557344
----K 5
----T ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).
----A 
----P Duplicate_Publication Guideline Journal_Article Practice_Guideline 
----M M_Adolescent_MeSH M_Adult_MeSH M_Age_of_Onset_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_classification_MeSH Arrhythmia_classification_MeSH S_diagnosis_MeSH Arrhythmia_diagnosis_MeSH S_epidemiology_MeSH Arrhythmia_epidemiology_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Case_Management_MeSH S_standards_MeSH Case_Management_standards_MeSH M_Catheter_Ablation_MeSH M_Child_MeSH M_Child__Preschool_MeSH M_Diagnosis__Differential_MeSH M_Electric_Countershock_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Heart_Conduction_System_MeSH S_physiopathology_MeSH Heart_Conduction_System_physiopathology_MeSH M_Human_MeSH M_Infant_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Pregnancy_MeSH M_Pregnancy_Complications__Cardiovascular_MeSH S_epidemiology_MeSH Pregnancy_Complications__Cardiovascular_epidemiology_MeSH S_therapy_MeSH Pregnancy_Complications__Cardiovascular_therapy_MeSH 
****** 14562566
----K 5
----T New treatments for perioperative cardiac arrhythmias.
----A Cardiac arrhythmias remain a major source of morbidity, mortality, and prolonged postoperative hospital stay in surgical patients. Recent studies in patients experiencing out-of-hospital cardiac arrest have expanded our knowledge in the management of cardiac arrhythmias. Future advances require additional studies focused on the unique proarrhythmic substrates in surgical patients, to provide a clear rationale for antiarrhythmic drug therapy in the perioperative period.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Child_MeSH M_Heart_Defects__Congenital_MeSH S_surgery_MeSH Heart_Defects__Congenital_surgery_MeSH M_Human_MeSH M_Intraoperative_Complications_MeSH S_physiopathology_MeSH Intraoperative_Complications_physiopathology_MeSH S_therapy_MeSH Intraoperative_Complications_therapy_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tachycardia__Supraventricular_MeSH S_etiology_MeSH Tachycardia__Supraventricular_etiology_MeSH S_therapy_MeSH Tachycardia__Supraventricular_therapy_MeSH 
****** 14564329
----K 5
----T Metoprolol CR/XL in postmyocardial infarction patients with chronic heart failure: experiences from MERIT-HF.
----A BACKGROUND: The benefit of beta-blockers post-myocardial infarction (MI) was established in the late 1970s. Major advances in the treatment of MI have since occurred. However, patients with chronic heart failure (CHF) were excluded from those trials. The purpose of this study was to assess the effect of beta-blockers in post-MI patients with CHF receiving contemporary management. METHODS: This was a prespecified subgroup analysis of a double-blind, randomized trial: the Metoprolol CR/XL Randomized Intervention Trial in Heart Failure (MERIT-HF). Patients with CHF in New York Heart Association class II to IV with an ejection fraction (EF) < or =0.40 and a history of being hospitalized for an acute MI (n = 1926) were randomized to metoprolol succinate controlled release/extended release (CR/XL) versus placebo. Mean EF was 0.28, and the mean follow-up was 1 year. RESULTS: Metoprolol CR/XL reduced total mortality by 40% (95% CI 0.20-0.55, P =.0004), and sudden death by 50% (95% CI 0.26-0.66, P =.0004). The combined end point of all-cause mortality/hospitalization for worsening CHF was reduced by 31% (95% CI 0.16-0.44, P <.0001), and cardiac death/nonfatal acute MI by 45% (95% CI 0.26-0.58, P <.0001). A post-hoc analysis showed that the outcome in patients with earlier revascularization (44%) and outcome in those with more severe CHF (20%) was similar to the entire post-MI population. CONCLUSIONS: In post-MI patients with symptomatic CHF, beta-blockade continues to exert a profound reduction in mortality and morbidity in the presence of contemporary management that includes early and late revascularization, angiotensin-converting enzyme inhibitors, aspirin, and statins.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angioplasty__Transluminal__Percutaneous_Coronary_MeSH M_Coronary_Artery_Bypass_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_analogs_&_derivatives_MeSH Metoprolol_analogs_&_derivatives_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_mortality_MeSH Myocardial_Infarction_mortality_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 14563505
----K 5
----T Update on therapy for heart failure.
----A The success of angiotensin-converting enzyme (ACE) inhibitors in reducing morbidity and mortality in patients with heart failure has led to investigations of other inhibitors of the renin-angiotensin-aldosterone system. Although ACE inhibitors remain first-line drugs in the treatment of heart failure and left ventricular dysfunction, clinical evidence suggests that a newer class of agents--angiotensin II receptor blockers--may provide additional benefit by blocking the adverse effects of angiotensin II more completely. An improved adverse-effect profile also makes angiotensin II receptor blockers appropriate in patients who cannot tolerate ACE inhibitors. Clinical trials have demonstrated the beneficial effects of angiotensin II receptor blockers on the combined endpoints of morbidity and mortality in patients with heart failure. Aldosterone antagonism with spironolactone has additive benefits in patients receiving an ACE inhibitor. The most recent treatment guidelines for heart failure recommend the use of angiotensin II receptor blockers and spironolactone in selected patients.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin_II_MeSH S_antagonists_&_inhibitors_MeSH Angiotensin_II_antagonists_&_inhibitors_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Human_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH 
****** 14563595
----K 4
----T Acute beta-blockade reduces the extent and severity of myocardial perfusion defects with dipyridamole Tc-99m sestamibi SPECT imaging.
----A OBJECTIVES: The goal of this study was to examine the effect of acute beta-blockade on dipyridamole Tc-99m sestamibi myocardial perfusion imaging (DMPI). BACKGROUND: Studies suggest that antianginal drugs may reduce the presence and severity of myocardial perfusion defects with dipyridamole stress. However, there are no data regarding specific drugs. METHODS: Patients with catheterization-proven coronary artery disease (CAD) were enrolled in this prospective, double-blind, placebo-controlled study and randomly assigned to DMPI after placebo, low-dose metoprolol (up to 10 mg), and high-dose metoprolol (up to 20 mg). Patients underwent one Tc-99m sestamibi study at rest on a separate day. The interval between DMPI studies was <or=14 days. Images were interpreted by three observers blinded to clinical data using a 17-segment, five-point model. For each image, a summed stress score (SSS), summed rest score (SRS), and summed difference score (SDS) were calculated (SDS = SSS - SRS). Images with an SSS <4 were considered normal. RESULTS: Twenty-one patients completed all four Tc-99m sestamibi studies. The sensitivity of DMPI for detection of CAD was 85.7% with placebo versus 71.4% with low- and high-dose metoprolol. In comparison with placebo, the SSS was significantly lower (p < 0.05) with low- and high-dose metoprolol (12.0 +/- 10.1 vs. 8.7 +/- 9.0 and 9.3 +/- 10.6, respectively). The SDS also was significantly lower (8.4 +/- 8.8 with placebo vs. 5.0 +/- 6.7 [p < 0.001] and 5.4 +/- 7.9 [p < 0.01] with low- and high-dose metoprolol, respectively). CONCLUSIONS: The presence and severity of CAD may be underestimated in patients receiving beta-blocker therapy undergoing dipyridamole stress myocardial perfusion imaging.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radionuclide_imaging_MeSH Coronary_Disease_radionuclide_imaging_MeSH M_Dipyridamole_MeSH S_diagnostic_use_MeSH Dipyridamole_diagnostic_use_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Female_MeSH M_Hemodynamic_Processes_MeSH S_drug_effects_MeSH Hemodynamic_Processes_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Technetium_Tc_99m_Sestamibi_MeSH S_diagnostic_use_MeSH Technetium_Tc_99m_Sestamibi_diagnostic_use_MeSH P_Tomography__Emission-Computed__Single-Photon_MeSH M_Vasodilator_Agents_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 14563596
----K 3
----T Reduction in dipyridamole-induced single-photon emission computed tomography myocardial defect size by beta-blockers: time to re-examine the patient preparation protocol for pharmacologic stress testing.
----A 
----P Clinical_Trial Comment Editorial Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_beta-Antagonists_administration_&_dosage_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH M_Coronary_Disease_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH S_radionuclide_imaging_MeSH Coronary_Disease_radionuclide_imaging_MeSH M_Dipyridamole_MeSH S_diagnostic_use_MeSH Dipyridamole_diagnostic_use_MeSH M_Double-Blind_Method_MeSH M_Exercise_Test_MeSH M_Human_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH S_pharmacology_MeSH Metoprolol_pharmacology_MeSH M_Prospective_Studies_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Technetium_Tc_99m_Sestamibi_MeSH S_diagnostic_use_MeSH Technetium_Tc_99m_Sestamibi_diagnostic_use_MeSH P_Tomography__Emission-Computed__Single-Photon_MeSH M_Vasodilator_Agents_MeSH S_diagnostic_use_MeSH Vasodilator_Agents_diagnostic_use_MeSH 
****** 14585943
----K 5
----T Schizophrenia.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Adolescent_MeSH M_Adult_MeSH M_Antipsychotic_Agents_MeSH S_adverse_effects_MeSH Antipsychotic_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antipsychotic_Agents_therapeutic_use_MeSH M_Brain_MeSH S_drug_effects_MeSH Brain_drug_effects_MeSH S_physiopathology_MeSH Brain_physiopathology_MeSH M_Child_MeSH M_Clozapine_MeSH S_therapeutic_use_MeSH Clozapine_therapeutic_use_MeSH M_Dopamine_MeSH S_physiology_MeSH Dopamine_physiology_MeSH M_Dopamine_Antagonists_MeSH S_adverse_effects_MeSH Dopamine_Antagonists_adverse_effects_MeSH S_therapeutic_use_MeSH Dopamine_Antagonists_therapeutic_use_MeSH M_Human_MeSH M_Pyramidal_Cells_MeSH S_drug_effects_MeSH Pyramidal_Cells_drug_effects_MeSH S_physiopathology_MeSH Pyramidal_Cells_physiopathology_MeSH M_Receptors__Dopamine_D2_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Dopamine_D2_antagonists_&_inhibitors_MeSH M_Schizophrenia_MeSH S_drug_therapy_MeSH Schizophrenia_drug_therapy_MeSH S_genetics_MeSH Schizophrenia_genetics_MeSH S_physiopathology_MeSH Schizophrenia_physiopathology_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__Non-P_H_S__MeSH M_Support__U_S__Gov't__P_H_S__MeSH 
****** 14602883
----K 5
----T Implantable cardioverter-defibrillators.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Arrhythmia_MeSH S_therapy_MeSH Arrhythmia_therapy_MeSH M_Clinical_Trials_MeSH P_Defibrillators__Implantable_MeSH S_adverse_effects_MeSH Defibrillators__Implantable_adverse_effects_MeSH S_contraindications_MeSH Defibrillators__Implantable_contraindications_MeSH S_standards_MeSH Defibrillators__Implantable_standards_MeSH S_trends_MeSH Defibrillators__Implantable_trends_MeSH M_Equipment_Failure_MeSH M_Human_MeSH M_Postoperative_Complications_MeSH 
****** 12605549
----K 5
----T Pharmacogenomics of angiotensin converting enzyme inhibitors in renal disease--pathophysiological considerations.
----A Angiotensin converting enzyme (ACE) inhibitors preserve native kidney function in patients with renal disease better than other antihypertensive drugs, most likely because they more effectively reduce proteinuria. The plasma concentration of the ACE inhibitors target is, at least in part, under genetic control. A polymorphism of the ACE gene based on the presence or absence of a 287 base pair element in intron 16 accounts for 47% of the total phenotypic variance in the plasma ACE levels of healthy individuals. Unfortunately, pharmacogenetic studies performed so far do not provide a clear answer as to whether the efficacy of the reduction of proteinuria by ACE inhibitors is influenced by the ACE genotype - probably because these studies were not primarily designed to answer this question. This paper will try to outline some aspects that should be considered before an appropriate study on this topic is initiated.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_metabolism_MeSH Angiotensin-Converting_Enzyme_Inhibitors_metabolism_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Genotype_MeSH M_Human_MeSH M_Kidney_Diseases_MeSH S_enzymology_MeSH Kidney_Diseases_enzymology_MeSH S_physiopathology_MeSH Kidney_Diseases_physiopathology_MeSH M_Kidney_Failure_MeSH S_drug_therapy_MeSH Kidney_Failure_drug_therapy_MeSH S_physiopathology_MeSH Kidney_Failure_physiopathology_MeSH P_Pharmacogenetics_MeSH M_Phenotype_MeSH M_Proteinuria_MeSH S_drug_therapy_MeSH Proteinuria_drug_therapy_MeSH S_enzymology_MeSH Proteinuria_enzymology_MeSH M_Renin_MeSH S_blood_MeSH Renin_blood_MeSH S_genetics_MeSH Renin_genetics_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH 
****** 12745796
----K 5
----T Women--a neglected risk group for atherosclerosis and vascular disease.
----A Women are a neglected group for cardiovascular disease. Whereas young women tend to have lower incidences of coronary artery disease, stroke and myocardial infarctions than men, the situation changes drastically at menopause, after which women are at greater risk than men. Despite this, women at all ages receive less treatment, less attention and not enough information about health risks. Most risk factors, e.g. hypertension, elevated blood lipid levels, diabetes and changes in oestrogen levels, differ between women and men. As a consequence of this, secondary prevention from coronary artery disease is likely to have different effects in women to those in men. Different kinds of antihypertensive therapy, hormone-replacement therapy and lipid-lowering treatment may be more or less suitable in women than in men. The recent development of angiotensin-receptor blockers may have beneficial effects which make them particularly effective in women.
----P Journal_Article Review Review__Tutorial 
----M M_Arteriosclerosis_MeSH S_complications_MeSH Arteriosclerosis_complications_MeSH S_epidemiology_MeSH Arteriosclerosis_epidemiology_MeSH S_physiopathology_MeSH Arteriosclerosis_physiopathology_MeSH S_prevention_&_control_MeSH Arteriosclerosis_prevention_&_control_MeSH M_Female_MeSH M_Human_MeSH M_Menopause_MeSH S_physiology_MeSH Menopause_physiology_MeSH P_Sex_Characteristics_MeSH M_Vascular_Diseases_MeSH S_complications_MeSH Vascular_Diseases_complications_MeSH S_epidemiology_MeSH Vascular_Diseases_epidemiology_MeSH S_physiopathology_MeSH Vascular_Diseases_physiopathology_MeSH S_prevention_&_control_MeSH Vascular_Diseases_prevention_&_control_MeSH 
****** 12797840
----K 5
----T Exercise in hypertension. A clinical review.
----A The current exercise prescription for the treatment of hypertension is: cardiovascular mode, for 20-60 minutes, 3-5 days per week, at 40-70% of maximum oxygen uptake (VO2(max)). Cardiovascular exercise training is the most effective mode of exercise in the prevention and treatment of hypertension. Resistance exercise is not the preferred mode of exercise treatment, but can be incorporated into an exercise regime provided the diastolic blood pressure response is within safe limits. It is inconclusive whether durations longer than 30 minutes produce significantly greater reductions in blood pressure. A frequency of three exercise sessions per week has been considered to be the minimal frequency for blood pressure reduction. Higher frequencies tended to produce greater reductions, although not significantly different. Evidence still exists that high intensity exercise (>75% VO2(max)) may not be as effective as low intensity exercise (<70% VO2(max)) in reducing elevated blood pressures. Exercise can be effective without a change in bodyweight or body fat. Bodyweight or body fat loss and anti-hypertensive medications do not have an added effect on blood pressure reduction associated with exercise. beta-blockade is not the recommended anti-hypertensive medication for effective exercise performance in non-cardiac patients. Not all hypertensive patients respond to exercise treatment. Differences in genetics and pathophysiology may be responsible for the inability of some hypertensive patients to respond to exercise. Ambulatory technology may allow advances in individualising a more effective exercise prescription for low-responders and non-responders.
----P Journal_Article Review Review__Tutorial 
----M M_Exercise_Therapy_MeSH S_methods_MeSH Exercise_Therapy_methods_MeSH M_Human_MeSH M_Hypertension_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH 
****** 12821221
----K 3
----T The effect of statin therapy on ventricular late potentials in acute myocardial infarction.
----A AIMS: To determine whether early statin therapy in acute myocardial infarction has any effect on ventricular late potentials which are considered as a noninvasive tool for evaluation of arrhythmogenic substrate. METHODS AND RESULTS: Study population consisted of prospectively enrolled 72 patients presenting with acute myocardial infarction (<6 h). Thirty-four of the patients were randomized to pravastatin (40 mg/day) on admission irrespective of lipid levels. All patients received thrombolytic therapy. Signal-averaged ECG recordings were obtained serially prior to thrombolytic therapy, 48 h after and 10 days later. Late potentials were defined as positive if signal-averaged ECG met at least two of Gomes criteria: filtered total QRS duration >114 ms, root mean square voltage of the last 40 ms of the QRS <20 mV, or the duration of the terminal low (<40 mV) amplitude signals >38 ms. Changes observed in signal-averaged ECG recordings after thrombolysis were evaluated statistically with regard to statin usage. There were no significant differences between the clinical characteristics of the two randomized groups. There was a significant decrease in the rates of late potentials between the first and third signal-averaged ECG recordings after thrombolytic therapy in pravastatin group. Pravastatin group also had lower incidence of ventricular arrhythmias compared with control group (26 vs. 63%, P=0.021). The in-hospital cardiovascular event rates were also lower in statin group. CONCLUSION: Early use of pravastatin reduces the incidence of late potentials following thrombolytic therapy in acute myocardial infarction. Statin therapy also seems to be reducing the incidence of in-hospital ventricular arrhythmias. These beneficial effects of statins might be explained through prevention of new myocardial ischemic episodes due to early plaque stabilization or regulation of endothelial and platelet functions.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Arrhythmia_MeSH S_etiology_MeSH Arrhythmia_etiology_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH S_prevention_&_control_MeSH Arrhythmia_prevention_&_control_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Therapy__Combination_MeSH M_Electrocardiography_MeSH M_Female_MeSH M_Fibrinolytic_Agents_MeSH S_administration_&_dosage_MeSH Fibrinolytic_Agents_administration_&_dosage_MeSH S_therapeutic_use_MeSH Fibrinolytic_Agents_therapeutic_use_MeSH M_Human_MeSH M_Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_MeSH S_administration_&_dosage_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_administration_&_dosage_MeSH S_therapeutic_use_MeSH Hydroxymethylglutaryl-CoA_Reductase_Inhibitors_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Myocardial_Infarction_MeSH S_complications_MeSH Myocardial_Infarction_complications_MeSH S_drug_therapy_MeSH Myocardial_Infarction_drug_therapy_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Pravastatin_MeSH S_administration_&_dosage_MeSH Pravastatin_administration_&_dosage_MeSH S_therapeutic_use_MeSH Pravastatin_therapeutic_use_MeSH M_Prospective_Studies_MeSH M_Time_Factors_MeSH M_Ventricular_Dysfunction__Left_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH S_prevention_&_control_MeSH Ventricular_Dysfunction__Left_prevention_&_control_MeSH 
****** 12862505
----K 3
----T Drug interactions with angiotensin receptor blockers: a comparison with other antihypertensives.
----A The ever-increasing introduction of new therapeutic agents means that the potential for drug interactions is likely to escalate. Numerous different classes of drugs are currently used to treat hypertension. The angiotensin receptor blockers offer one of the newest approaches to the management of patients with high blood pressure. Compared with other classes of antihypertensive agents, the angiotensin receptor blockers appear overall to have a low potential for drug interactions, but variations within the class have been detected. Losartan and irbesartan have a greater affinity for cytochrome p450 (CYP) isoenzymes and, thus, are more likely to be implicated in drug interactions. There is pharmacokinetic evidence to suggest that such interactions could have a clinical impact. Candesartan cilexetil, valsartan and eprosartan have variable but generally modest affinity and telmisartan has no affinity for any of the CYP isoenzymes. In vitro studies and pharmacokinetic/pharmacodynamic evaluation can provide evidence for some interactions, but only a relatively small number of drug combinations are usually studied in this way. The absence of any pharmacokinetic evidence of drug interaction, however, should not lead to complacency. Patients should be made aware of possible interactions, especially involving the concurrent use of over-the-counter products, and it may be prudent for all patients receiving antihypertensive treatment to be monitored for possible drug interactions at their regular check-ups. The physician can help by prescribing agents with a low potential for interaction, such as angiotensin receptor blockers.
----P Journal_Article Review Review__Tutorial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_adverse_effects_MeSH Angiotensin-Converting_Enzyme_Inhibitors_adverse_effects_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Comparative_Study_MeSH M_Drug_Interactions_MeSH M_Human_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 12888704
----K 5
----T Drug therapy of heart failure in the elderly.
----A Heart failure is a disorder that predominantly affects older adults, with more than 50% of heart failure hospitalizations occurring in persons over 75 years of age. Unfortunately, most of the major heart failure clinical trials have targeted middle-aged patients with systolic heart failure, and the applicability of these studies to elderly patients, particularly those with preserved left ventricular systolic function, remains uncertain. In this paper, current data on the pharmacotherapy of heart failure in older adults are reviewed, recommended approaches to managing systolic and diastolic heart failure are outlined, and the importance of preventive measures is emphasized.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Diastole_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_prevention_&_control_MeSH Heart_Failure__Congestive_prevention_&_control_MeSH M_Human_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_prevention_&_control_MeSH Hypertrophy__Left_Ventricular_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Spironolactone_MeSH S_therapeutic_use_MeSH Spironolactone_therapeutic_use_MeSH M_Systole_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH M_Ventricular_Dysfunction__Left_MeSH S_prevention_&_control_MeSH Ventricular_Dysfunction__Left_prevention_&_control_MeSH 
****** 12902554
----K 5
----T A practical approach to hypertension in the 21st century.
----A 
----P Journal_Article Review Review__Academic 
----M M_Adrenergic_alpha-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_alpha-Antagonists_therapeutic_use_MeSH M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Diuretics_MeSH S_therapeutic_use_MeSH Diuretics_therapeutic_use_MeSH M_Human_MeSH P_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Life_Style_MeSH M_Radiography__Interventional_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 13678427
----K 5
----T Adipocyte-derived leucine aminopeptidase genotype and response to antihypertensive therapy.
----A BACKGROUND: Adipocyte-derived leucine aminopeptidase (ALAP) is a recently identified member of the M1 family of zinc-metallopeptidases and is thought to play a role in blood pressure control through inactivation of angiotensin II and/or generation of bradykinin. The enzyme seems to be particularly abundant in the heart. Recently, the Arg528-encoding allele of the ALAP gene was shown to be associated with essential hypertension. METHODS: We evaluated the influence of this polymorphism on the change in left ventricular mass index in 90 patients with essential hypertension and echocardiographically diagnosed left ventricular hypertrophy, randomised in a double-blind study to receive treatment with either the angiotensin II type I receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol for 48 weeks. Genyotyping was performed using minisequencing. RESULTS: After adjustment for potential covariates (blood pressure and left ventricular mass index at baseline, blood pressure change, age, sex, dose and added antihypertensive treatment), there was a marked difference between the Arg/Arg and Lys/Arg genotypes in patients treated with irbesartan; those with the Arg/Arg genotype responded on average with an almost two-fold greater regression of left ventricular mass index than patients with the Lys/Arg genotype (-30.1 g/m2 [3.6] vs -16.7 [4.5], p = 0.03). CONCLUSIONS: The ALAP genotype seems to determine the degree of regression of left ventricular hypertrophy during antihypertensive treatment with the angiotensin II type I receptor antagonist irbesartan in patients with essential hypertension and left ventricular hypertrophy. This is the first report of a role for ALAP/aminopeptidases in left ventricular mass regulation, and suggests a new potential target for antihypertensive drugs.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adipocytes_MeSH S_enzymology_MeSH Adipocytes_enzymology_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_enzymology_MeSH Hypertension_enzymology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_enzymology_MeSH Hypertrophy__Left_Ventricular_enzymology_MeSH M_Leucyl_Aminopeptidase_MeSH S_genetics_MeSH Leucyl_Aminopeptidase_genetics_MeSH M_Male_MeSH M_Middle_Aged_MeSH P_Polymorphism_(Genetics)_MeSH M_Remission_Induction_MeSH M_Single-Blind_Method_MeSH M_Support__Non-U_S__Gov't_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 14530617
----K 5
----T Primary and secondary stroke prevention in nonrheumatic atrial fibrillation by oral anticoagulation.
----A The risk of stroke or embolism in atrial fibrillation (AF) patients can be reduced by 68% by oral anticoagulation (OAC). This review is aimed to (1) summarize indications for OAC in patients with AF, (2) give an overview of the current knowledge of risk factors for bleeding complications of OAC and (3) give practical recommendations for an optimal OAC therapy in the neurological setting. Indications for OAC are increased age (>75 years), arterial hypertension, diabetes mellitus, previous thromboembolism, heart failure and, probably, coronary heart disease. Risk factors for bleeding complications are overanticoagulation with international normalized ratios (INRs) >3.0, increased age, arterial hypertension, diabetes mellitus, previous thromboembolism, polypharmacy, the early phase of OAC therapy and a lack of patients' education. Before initiation of OAC, the patient should be screened for potential bleeding sites. Careful monitoring of OAC comprises fixed appointments for the INR value determination, tracking for the patient, if he does not attend, advices about pain therapy, information about the influence of diet on the INR value and drug interaction, unscheduled INR determination in case of acute disorders and regular assessment if OAC is still indicated. Monitoring of OAC needs an effort, which has to be adequately estimated by the health care system.
----P Journal_Article Review Review__Tutorial 
----M M_Administration__Oral_MeSH M_Age_Factors_MeSH M_Anticoagulants_MeSH S_adverse_effects_MeSH Anticoagulants_adverse_effects_MeSH S_contraindications_MeSH Anticoagulants_contraindications_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_complications_MeSH Atrial_Fibrillation_complications_MeSH M_Cerebrovascular_Accident_MeSH S_etiology_MeSH Cerebrovascular_Accident_etiology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Drug_Administration_Schedule_MeSH M_Drug_Interactions_MeSH M_Embolism_MeSH S_etiology_MeSH Embolism_etiology_MeSH S_prevention_&_control_MeSH Embolism_prevention_&_control_MeSH M_Heart_Failure__Congestive_MeSH S_complications_MeSH Heart_Failure__Congestive_complications_MeSH M_Hemorrhage_MeSH S_etiology_MeSH Hemorrhage_etiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH P_Primary_Prevention_MeSH S_methods_MeSH Primary_Prevention_methods_MeSH M_Risk_Factors_MeSH 
****** 14575221
----K 5
----T ACE inhibitors and beta blockers in chronic congestive cardiac failure: therapeutic basis.
----A Congestive cardiac failure (CCF) is a common problem through out the globe and is associated with high morbidity and mortality. The rapid progression of the disease due to neurohormonal activation can be blunted by use of angiotensin-converting enzyme inhibitor (ACEI) and beta blockers (BB) with a major impact on morbidity and mortality. Besides CCF, they are also useful in asymptomatic left ventricular dysfunction (LVD) and in prevention of heart failure in high risk patients without LVD. Both ACEI and BB are highly underutilised therapy in CCF and there is an urgent necessity to spread message among the medical fraternity for their enhanced use.
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_pharmacology_MeSH Adrenergic_beta-Antagonists_pharmacology_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_pharmacology_MeSH Angiotensin-Converting_Enzyme_Inhibitors_pharmacology_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Chronic_Disease_MeSH M_Heart_MeSH S_drug_effects_MeSH Heart_drug_effects_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_mortality_MeSH Heart_Failure__Congestive_mortality_MeSH M_Human_MeSH 
****** 14580043
----K 5
----T Botulinum toxins in the treatment of migraine and tension-type headaches.
----A Botulinum toxins are promising preventive treatments for patients with moderate to severe episodic and chronic migraine and chronic daily headache. The recommended indications for botulinum toxins as preventive therapy lend themselves to the following patient types: those who demonstrate a lack of improvement from preventive (prophylactic) pharmacotherapy; those who experience severe and intolerable adverse events from preventive medications; those who refuse to use daily medications; those who have contraindications to acute migraine therapy, and elderly patients with chronic migraine. Both open-label and double-blind placebo-controlled studies using fixed-site, "follow the pain." or a combination approach have demonstrated significant reduction in migraine frequency, severity, and duration, as well as decreased use of acute medications. The most prominent reductions have been noted in those with reportedly the most severe migraine headaches. Large, well-designed, double-blind, placebo-controlled studies are recommended to further clarify optimum dosage and location of injection, reduce treatment frequency and duration, and address other primary headache disorders that may benefit from this therapy.
----P Journal_Article Review Review__Tutorial 
----M M_Analgesics__Non-Narcotic_MeSH S_therapeutic_use_MeSH Analgesics__Non-Narcotic_therapeutic_use_MeSH M_Botulinum_Toxin_Type_A_MeSH S_therapeutic_use_MeSH Botulinum_Toxin_Type_A_therapeutic_use_MeSH M_Botulinum_Toxins_MeSH S_therapeutic_use_MeSH Botulinum_Toxins_therapeutic_use_MeSH M_Human_MeSH M_Migraine_MeSH S_drug_therapy_MeSH Migraine_drug_therapy_MeSH M_Tension_Headache_MeSH S_drug_therapy_MeSH Tension_Headache_drug_therapy_MeSH 
****** 14587131
----K 5
----T Congestive heart failure and the elderly.
----A As patients age, congestive heart failure becomes an increasingly important problem and accounts for up to 20% of hospital admissions for patients over 65 years. With technological improvements in the treatment of coronary artery disease, improved survival after myocardial infarction, and better hypertension therapy, patients are living longer, thus the need for successful management of older patients with chronic heart failure. The elderly, especially minorities, tend to be under-represented in congestive heart failure trials. This article will focus on the care of the geriatric patient with congestive heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH P_Aging_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Defibrillators__Implantable_MeSH M_Digoxin_MeSH S_therapeutic_use_MeSH Digoxin_therapeutic_use_MeSH M_Exercise_MeSH P_Heart_Failure__Congestive_MeSH S_diagnosis_MeSH Heart_Failure__Congestive_diagnosis_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_therapy_MeSH Heart_Failure__Congestive_therapy_MeSH M_Human_MeSH M_Pacemaker__Artificial_MeSH M_Terminal_Care_MeSH 
****** 14597461
----K 5
----T Pathogenesis of hypertension.
----A 
----P Journal_Article Review Review__Academic 
----M M_Human_MeSH M_Hypertension_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Risk_Factors_MeSH 
****** 12635070
----K 5
----T The pathophysiology of perioperative myocardial infarction: facts and perspectives.
----A 
----P Journal_Article Review Review__Academic 
----M M_Human_MeSH M_Intraoperative_Complications_MeSH S_pathology_MeSH Intraoperative_Complications_pathology_MeSH S_physiopathology_MeSH Intraoperative_Complications_physiopathology_MeSH M_Myocardial_Infarction_MeSH S_pathology_MeSH Myocardial_Infarction_pathology_MeSH S_physiopathology_MeSH Myocardial_Infarction_physiopathology_MeSH M_Postoperative_Complications_MeSH S_pathology_MeSH Postoperative_Complications_pathology_MeSH S_physiopathology_MeSH Postoperative_Complications_physiopathology_MeSH M_Surgical_Procedures__Operative_MeSH S_adverse_effects_MeSH Surgical_Procedures__Operative_adverse_effects_MeSH 
****** 12640257
----K 3
----T B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial.
----A OBJECTIVE: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy. DESIGN AND METHODS: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol. RESULTS: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 +/- 4.6 versus -21.6 +/- 2.2 g/m2, P = 0.03). CONCLUSIONS: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Biphenyl_Compounds_MeSH S_therapeutic_use_MeSH Biphenyl_Compounds_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Genotype_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_genetics_MeSH Hypertension_genetics_MeSH S_pathology_MeSH Hypertension_pathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH S_genetics_MeSH Hypertrophy__Left_Ventricular_genetics_MeSH S_pathology_MeSH Hypertrophy__Left_Ventricular_pathology_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Organ_Weight_MeSH S_drug_effects_MeSH Organ_Weight_drug_effects_MeSH M_Polymorphism_(Genetics)_MeSH M_Receptor__Angiotensin__Type_1_MeSH S_antagonists_&_inhibitors_MeSH Receptor__Angiotensin__Type_1_antagonists_&_inhibitors_MeSH M_Receptor__Bradykinin_B2_MeSH S_genetics_MeSH Receptor__Bradykinin_B2_genetics_MeSH M_Support__Non-U_S__Gov't_MeSH M_Sweden_MeSH M_Tetrazoles_MeSH S_therapeutic_use_MeSH Tetrazoles_therapeutic_use_MeSH 
****** 12663237
----K 3
----T Effects of long-term Irbesartan in reducing portal pressure in cirrhotic patients: comparison with propranolol in a randomised controlled study.
----A BACKGROUND/AIMS: The role of angiotensin II (AT-II) type I receptor antagonists in the treatment of portal hypertension remains controversial. We tested the efficacy of Irbesartan (Irb) vs. Propranolol (Pro) in reducing portal pressure and evaluated its systemic haemodynamic effects. METHODS: Thirty-four patients were randomly assigned to receive either Irb 300 mg/day (19 patients) or Pro 40-120 mg/day (15 patients) for 2 months. RESULTS: Irb was discontinued in five patients (26%). No major side effect occurred in the Pro group. On an average, the portal pressure gradient decreased significantly more in the Pro than in the Irb group (median -19.5%, range -11/-31% vs. -4.8%, +2.5/-10%, P<0.001). A clinically significant decrease was seen in one (7%) of the patients given Irb vs. five (33%) given Pro (P<0.02). The fall in mean arterial pressure was significantly higher with Irb than with Pro (median -29%, range -15/-45% vs. -4.9%, +8/-19%, P<0.02). Irb significantly modified the blood creatinine clearance (median -29 ml/m, range +9/-61 ml/m, -30, -24/-35% P<0.0001 vs. basal). CONCLUSIONS: Irb offers no advantage over Pro in the control of portal hypertension. Moreover, its therapeutic profile is limited by important side effects.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adult_MeSH M_Aged_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH M_Biphenyl_Compounds_MeSH S_administration_&_dosage_MeSH Biphenyl_Compounds_administration_&_dosage_MeSH S_adverse_effects_MeSH Biphenyl_Compounds_adverse_effects_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension__Portal_MeSH S_drug_therapy_MeSH Hypertension__Portal_drug_therapy_MeSH S_etiology_MeSH Hypertension__Portal_etiology_MeSH M_Hypotension_MeSH S_chemically_induced_MeSH Hypotension_chemically_induced_MeSH M_Kidney_MeSH S_physiology_MeSH Kidney_physiology_MeSH M_Liver_Cirrhosis_MeSH S_complications_MeSH Liver_Cirrhosis_complications_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propranolol_MeSH S_administration_&_dosage_MeSH Propranolol_administration_&_dosage_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH S_adverse_effects_MeSH Tetrazoles_adverse_effects_MeSH 
****** 12670819
----K 5
----T Ventricular tachycardia during general anesthesia in a patient with congenital long QT syndrome.
----A PURPOSE: Congenital long QT syndrome is characterized by a corrected QT interval of at least 440 msec on the electrocardiogram and has been associated with recurrent syncope, documented ventricular arrhythmia and sudden death. There have been numerous articles over the past 20 years describing isolated instances of surgical and anesthesia related complications but the general anesthetic management of the condition remains unclear. CLINICAL FEATURES: An 11-yr-old female with documented long QT syndrome, with two episodes of syncope in the past, was admitted for emergency drainage of left periorbital cellulitis. Anesthesia was induced with propofol, fentanyl and rocuronium, and initially maintained with nitrous oxide and halothane. After 20 min, the patient developed ventricular tachycardia (torsade de pointes). Lidocaine 1 mg.kg(-1) iv was given and the rhythm reverted to normal sinus. Halothane was discontinued and the surgery proceeded without further incident. CONCLUSIONS: Our review of the literature revealed that patients with long QT syndrome whose symptoms are well controlled prior to surgery tend to do well regardless of the anesthetic chosen. There are, however, theoretical reasons to avoid anesthetics which either sensitize the myocardium to catecholamines or which cause an increase in circulating levels of catecholamines.
----P Case_Reports Journal_Article 
----M M_Anesthesia__General_MeSH S_adverse_effects_MeSH Anesthesia__General_adverse_effects_MeSH M_Anesthetics__Inhalation_MeSH S_adverse_effects_MeSH Anesthetics__Inhalation_adverse_effects_MeSH M_Child_MeSH M_Female_MeSH M_Halothane_MeSH S_adverse_effects_MeSH Halothane_adverse_effects_MeSH M_Human_MeSH M_Long_QT_Syndrome_MeSH S_complications_MeSH Long_QT_Syndrome_complications_MeSH S_congenital_MeSH Long_QT_Syndrome_congenital_MeSH M_Nitrous_Oxide_MeSH S_adverse_effects_MeSH Nitrous_Oxide_adverse_effects_MeSH M_Tachycardia__Ventricular_MeSH S_etiology_MeSH Tachycardia__Ventricular_etiology_MeSH 
****** 12678857
----K 5
----T Arterial stiffness and cardiovascular drugs.
----A Arterial stiffness is the most important cause of increasing systolic and pulse pressure, and for decreasing diastolic pressure with ageing. Many measures can be applied to quantify arterial stiffness, but all are approximations only, on account of the nonhomogenous structure of the arterial wall, its variability in different locations, at different levels of distending pressure, and with changes in smooth muscle tone. This article summarizes those indices with a focus on newer non-invasive methods and provides an overview of physiological, pathological and pharmacological influences on arterial hemodynamics. In the near future, the ability to detect and monitor subclinical arterial damage will improve cardiovascular risk stratification and act as a better guide in assessing the efficacy of therapeutic interventions than monitoring blood pressure alone. However, large-scale clinical trials are needed to prove the hypothesis that treatment of these new therapeutic targets will translate into clinical benefit, expressed in cardiovascular events or even mortality.
----P Journal_Article Review Review__Tutorial 
----M M_Age_Factors_MeSH M_Arteries_MeSH S_physiopathology_MeSH Arteries_physiopathology_MeSH M_Arteriosclerosis_MeSH S_diagnosis_MeSH Arteriosclerosis_diagnosis_MeSH S_etiology_MeSH Arteriosclerosis_etiology_MeSH S_physiopathology_MeSH Arteriosclerosis_physiopathology_MeSH M_Blood_Flow_Velocity_MeSH S_physiology_MeSH Blood_Flow_Velocity_physiology_MeSH M_Cardiovascular_Agents_MeSH S_therapeutic_use_MeSH Cardiovascular_Agents_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Exercise_MeSH S_physiology_MeSH Exercise_physiology_MeSH M_Gender_Identity_MeSH M_Heart_Diseases_MeSH S_complications_MeSH Heart_Diseases_complications_MeSH S_diagnosis_MeSH Heart_Diseases_diagnosis_MeSH S_drug_therapy_MeSH Heart_Diseases_drug_therapy_MeSH M_Hemodynamic_Processes_MeSH S_physiology_MeSH Hemodynamic_Processes_physiology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_etiology_MeSH Hypertension_etiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Pulsatile_Flow_MeSH S_physiology_MeSH Pulsatile_Flow_physiology_MeSH 
****** 12729393
----K 5
----T Analysis of survival data with missing measurements of a time-dependent binary covariate.
----A The objective of this study was to investigate the influence of the number and timing of a binary time-dependent covariate on the bias using the last-observation carried forward in the proportional hazards model. Under various assumptions of censoring rates, transition probabilities of the time-dependent covariate, sample size, and the log hazard-ratio for the covariate, we empirically examined the impact that the number and timing have on the bias of the estimator of the covariate. An example from the Systolic Hypertension in the Elderly Program was used. Inference on the effect of systolic blood pressure on survival is strongly affected by the number and timing of systolic blood measurements.
----P Journal_Article 
----M M_Human_MeSH P_Proportional_Hazards_Models_MeSH M_Randomized_Controlled_Trials_MeSH S_methods_MeSH Randomized_Controlled_Trials_methods_MeSH S_statistics_&_numerical_data_MeSH Randomized_Controlled_Trials_statistics_&_numerical_data_MeSH M_Support__U_S__Gov't__P_H_S__MeSH P_Survival_Analysis_MeSH M_Time_Factors_MeSH 
****** 12731459
----K 5
----T Therapeutic impact of CYP2C19 pharmacogenetics on proton pump inhibitor-based eradication therapy for Helicobacter pylori.
----A Current regimens for the eradication of Helicobacter pylori consist of a proton pump inhibitor (PPI) plus one or two antibacterial agents, such as amoxicillin (AMPC), clarithromycin (CAM) or metronidazole (MNZ). PPIs are mainly metabolized by S-mephenytoin 4'-hydroxylase (CYP2C19) in the liver. The polymorphism of CYP2C19 is associated with the pharmacokinetics and pharmacodynamics of PPIs. Eradication rates by PPI-based therapies are also affected by this genotype, as well as bacterial resistance to antibiotics. An individualized treatment strategy based on CYP2C19-related pharmacogenetics or pharmacogenomics and bacterial resistance is expected to increase the cure rate of the initial treatment. It is also necessary to recognize that there is a possible drug-drug interaction between some of the drugs used in this treatment regimen.
----P Journal_Article Review Review__Tutorial 
----M M_Anti-Bacterial_Agents_MeSH S_therapeutic_use_MeSH Anti-Bacterial_Agents_therapeutic_use_MeSH M_Aryl_Hydrocarbon_Hydroxylases_MeSH S_genetics_MeSH Aryl_Hydrocarbon_Hydroxylases_genetics_MeSH S_metabolism_MeSH Aryl_Hydrocarbon_Hydroxylases_metabolism_MeSH M_Clinical_Trials_MeSH M_Drug_Interactions_MeSH M_Drug_Therapy__Combination_MeSH M_Gastrointestinal_Agents_MeSH S_pharmacokinetics_MeSH Gastrointestinal_Agents_pharmacokinetics_MeSH S_pharmacology_MeSH Gastrointestinal_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Gastrointestinal_Agents_therapeutic_use_MeSH M_Genotype_MeSH M_Helicobacter_Infections_MeSH S_drug_therapy_MeSH Helicobacter_Infections_drug_therapy_MeSH S_enzymology_MeSH Helicobacter_Infections_enzymology_MeSH M_Helicobacter_pylori_MeSH S_genetics_MeSH Helicobacter_pylori_genetics_MeSH M_Human_MeSH M_Mixed_Function_Oxygenases_MeSH S_genetics_MeSH Mixed_Function_Oxygenases_genetics_MeSH S_metabolism_MeSH Mixed_Function_Oxygenases_metabolism_MeSH M_Polymorphism_(Genetics)_MeSH M_Proton_Pumps_MeSH S_antagonists_&_inhibitors_MeSH Proton_Pumps_antagonists_&_inhibitors_MeSH 
****** 12766540
----K 5
----T Thyroid emergencies.
----A 
----P Journal_Article Review Review__Tutorial 
----M M_Coma_MeSH S_etiology_MeSH Coma_etiology_MeSH P_Critical_Care_MeSH M_Emergencies_MeSH M_Human_MeSH M_Myxedema_MeSH S_complications_MeSH Myxedema_complications_MeSH S_diagnosis_MeSH Myxedema_diagnosis_MeSH S_therapy_MeSH Myxedema_therapy_MeSH M_Thyroid_Crisis_MeSH S_diagnosis_MeSH Thyroid_Crisis_diagnosis_MeSH S_therapy_MeSH Thyroid_Crisis_therapy_MeSH M_Thyroid_Diseases_MeSH S_diagnosis_MeSH Thyroid_Diseases_diagnosis_MeSH M_Thyroid_Hormones_MeSH S_blood_MeSH Thyroid_Hormones_blood_MeSH 
****** 12858122
----K 5
----T Management of the hypertensive patient with coronary insufficiency but without atherosclerosis.
----A Arterial hypertension is a major risk factor for the clinical syndrome of angina pectoris, in which the ECG is abnormal but the coronary arteries are normal. Structural and functional abnormalities in coronary circulation as well as extravascular factors (eg, left-ventricular hypertrophy, fibrosis with diastolic dysfunction) compromise the adequate ratio of coronary blood flow to oxygen demand causing angina, dyspnea, and major cardiac events. Recent studies stress the importance to functional disturbances of coronary microvasculature leading to profound morphologic changes associated with impaired coronary conductance. In patients without epicardial coronary stenosis hypertensive microvascular disease can be qualitatively assessed by noninvasive diagnostic approaches based on new Doppler echocardiography techniques and may also be monitored by widely available stress tests. For ultimate quantitative assessment, invasive procedures are still required. Beyond guidelines to control blood pressure in hypertensive individuals, restoration of functional and structural integrity of the coronary microvasculature represents the ultimate therapeutic goal in hypertensive patients with coronary insufficiency and without angiographic evidence of atherosclerosis. Concomitant factors reducing coronary conductance such as left-ventricular hypertrophy and diastolic dysfunction should be reversed in parallel. Currently, therapeutic intervention in the renin-aldosterone-angiotensin-II-system using ACE inhibitors, angiotensin receptor blockers, and low doses of aldosterone antagonists represent the most promising strategy to achieve these goals. Using the knowledge of these recent results we should refine the overall management of our hypertensive patients with coronary insufficiency but without atherosclerosis.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH M_Coronary_Circulation_MeSH S_drug_effects_MeSH Coronary_Circulation_drug_effects_MeSH S_physiology_MeSH Coronary_Circulation_physiology_MeSH M_Coronary_Disease_MeSH S_diagnosis_MeSH Coronary_Disease_diagnosis_MeSH S_physiopathology_MeSH Coronary_Disease_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH S_therapy_MeSH Hypertension_therapy_MeSH M_Risk_Assessment_MeSH M_Ventricular_Function__Left_MeSH S_drug_effects_MeSH Ventricular_Function__Left_drug_effects_MeSH S_physiology_MeSH Ventricular_Function__Left_physiology_MeSH 
****** 12858124
----K 5
----T Treatment of hypertensive patients with coexisting coronary arterial disease.
----A Despite clear guidelines and an array of available antihypertensive medications, patients with hypertension and coronary artery disease are often inadequately treated. New data from HOPE, LIFE, and ALLHAT underscores the importance of blood pressure reduction for patients with coronary artery disease. Despite our improved understanding of the mechanism by which the various classes of antihypertensive medications achieve their effect, it remains the case that blood pressure reduction remains more important than the medication used to achieve the reduction. For most patients with coronary artery disease, combination therapy will be required to achieve a target blood pressure of less than 140/80. When tolerated, this therapy should include a beta-blocker and ACE inhibitor, both of which are of prognostic benefit for patients with coronary artery disease. There are also attractions in choosing calcium antagonists because of their efficacy in controlling anginal symptoms (Dihydropyridine calcium channel blockers if already on a beta-blocking agent and rate-limiting calcium channel blockers if beta blockers are contraindicated). Thiazide diuretics have proven themselves effective again in the ALLHAT study and are likely to be an integral part of treatment for the great majority of patients with coronary artery disease.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Comorbidity_MeSH M_Coronary_Arteriosclerosis_MeSH S_epidemiology_MeSH Coronary_Arteriosclerosis_epidemiology_MeSH S_physiopathology_MeSH Coronary_Arteriosclerosis_physiopathology_MeSH M_Diuretics__Thiazide_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 12858125
----K 5
----T Treatment of hypertension for patients with diastolic dysfunction.
----A Diastolic dysfunction is a poorly understood pathophysiological entity; its importance is magnified by the increasing prevalence of diastolic heart failure. Forty-six million people in the US are experiencing heart failure and 550000 new cases are diagnosed annually. A large percentage of these patients with heart failure have a normal or nearly normal left-ventricular ejection fraction. Isolated diastolic dysfunction may be associated with an increased mortality. One of the major causes of diastolic dysfunction is hypertension. Advances in diagnosis and treatment strategies may improve the clinical outcome for patients with diastolic dysfunction.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aldosterone_Antagonists_MeSH S_therapeutic_use_MeSH Aldosterone_Antagonists_therapeutic_use_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Comorbidity_MeSH M_Diastole_MeSH M_Heart_Failure__Congestive_MeSH S_epidemiology_MeSH Heart_Failure__Congestive_epidemiology_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH S_physiopathology_MeSH Hypertension_physiopathology_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_drug_therapy_MeSH Hypertrophy__Left_Ventricular_drug_therapy_MeSH M_Ventricular_Dysfunction__Left_MeSH S_epidemiology_MeSH Ventricular_Dysfunction__Left_epidemiology_MeSH S_physiopathology_MeSH Ventricular_Dysfunction__Left_physiopathology_MeSH 
****** 12871180
----K 5
----T A point of view: The need to identify an antigen in psyconeuroimmunological disorders.
----A Several lines of evidence support a mutual relationship between the nervous system and the immune system. Therefore, it is not surprising that some neuropsychiatric disorders are also characterized by immune abnormalities. In patients with phobic disorders and in patients with migraine without aura some common immune abnormalities have been detected and, in particular, natural immunity deficits, exaggerated release of proinflammatory cytokines and circulating bacterial endotoxins have been found. In other neurological disease, some etiologic factors have been detected as in the case of Guillain-Barre syndrome in which molecular mimicry between Campylobacter jejuni endotoxin and GM1 ganglioside may cause an acute inflammatory polyneuropathy. On the other hand, attempts to identify an antigen have been made in patients with Alzheimer's disease and schizophrenia. Finally, the chronic fatigue syndrome, an old illness in search for an antigen, risk factors and precipitating agents have been described but evidence for a specific antigen is still lacking.
----P Journal_Article Review Review__Tutorial 
----M M_Antigens_MeSH S_immunology_MeSH Antigens_immunology_MeSH M_Fatigue_Syndrome__Chronic_MeSH S_immunology_MeSH Fatigue_Syndrome__Chronic_immunology_MeSH M_Human_MeSH M_Mental_Disorders_MeSH S_immunology_MeSH Mental_Disorders_immunology_MeSH M_Neuroimmunomodulation_MeSH M_Psychoneuroimmunology_MeSH M_Risk_Factors_MeSH 
****** 12904089
----K 5
----T Carvedilol: a review of its use in chronic heart failure.
----A Carvedilol (Dilatrend) blocks beta(1)-, beta(2)- and alpha(1)-adrenoceptors, and has antioxidant and antiproliferative effects. Carvedilol improved left ventricular ejection fraction (LVEF) in patients with chronic heart failure (CHF) in numerous studies. Moreover, significantly greater increases from baseline in LVEF were seen with carvedilol than with metoprolol in a double-blind, randomised study and in a meta-analysis. Carvedilol also reversed or attenuated left ventricular remodelling in patients with CHF and in those with left ventricular dysfunction after acute myocardial infarction (MI). Combined analysis of studies in the US Carvedilol Heart Failure Trials Program (patients had varying severities of CHF; n = 1094) revealed that mortality was significantly lower in carvedilol than in placebo recipients. In addition, the risk of hospitalisation for any cardiovascular cause was significantly lower with carvedilol than with placebo. Mortality was significantly lower with carvedilol than with metoprolol in patients with mild to severe CHF in the Carvedilol Or Metoprolol European Trial (COMET) [n = 3029]. The Carvedilol Prospective Randomised Cumulative Survival (COPERNICUS) trial (n = 2289) demonstrated that compared with placebo, carvedilol was associated with significant reductions in all-cause mortality and the combined endpoint of death or hospitalisation for any reason in severe CHF. All-cause mortality was reduced in patients who received carvedilol in addition to conventional therapy compared with those who received placebo plus conventional therapy in the Carvedilol Post-Infarct Survival Control in LV Dysfunction (CAPRICORN) trial (enrolling 1959 patients with left ventricular dysfunction following acute MI). Carvedilol was generally well tolerated in patients with CHF. Adverse events associated with the alpha- and beta-blocking effects of the drug occurred more commonly with carvedilol than with placebo, whereas placebo recipients were more likely to experience worsening heart failure. In conclusion, carvedilol blocks beta(1)-, beta(2)- and alpha(1)-adrenoceptors and has a unique pharmacological profile. It is thought that additional properties of carvedilol (e.g. antioxidant and antiproliferative effects) contribute to its beneficial effects in CHF. Carvedilol improves ventricular function and reduces mortality and morbidity in patients with mild to severe CHF, and should be considered a standard treatment option in this setting. Administering carvedilol in addition to conventional therapy reduces mortality and attenuates myocardial remodelling in patients with left ventricular dysfunction following acute MI. Moreover, mortality was significantly lower with carvedilol than with metoprolol in patients with mild to severe CHF, suggesting that carvedilol may be the preferred beta-blocker.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_economics_MeSH Adrenergic_beta-Antagonists_economics_MeSH S_pharmacokinetics_MeSH Adrenergic_beta-Antagonists_pharmacokinetics_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Carbazoles_MeSH S_adverse_effects_MeSH Carbazoles_adverse_effects_MeSH S_pharmacokinetics_MeSH Carbazoles_pharmacokinetics_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Chronic_Disease_MeSH P_Drug_Administration_Schedule_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_metabolism_MeSH Heart_Failure__Congestive_metabolism_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Models__Biological_MeSH M_Propanolamines_MeSH S_adverse_effects_MeSH Propanolamines_adverse_effects_MeSH S_pharmacokinetics_MeSH Propanolamines_pharmacokinetics_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH P_Treatment_Outcome_MeSH 
****** 12957754
----K 5
----T Arrhythmias during acute and chronic exercise in chronic heart failure.
----A Exercise can induce or prevent arrhythmias depending upon several factors, related to patient's clinical characteristics and to exercise modalita (type, intensita, frequency, duration). In the present paper, the author reviews the mechanisms of arrhythmias during acute and chronic exercise in heart failure, and focuses on the relationship between exercise training programs and arrhythmias in chronic heart failure.
----P Journal_Article Review Review__Tutorial 
----M M_Arrhythmia_MeSH S_physiopathology_MeSH Arrhythmia_physiopathology_MeSH M_Exercise_Therapy_MeSH S_adverse_effects_MeSH Exercise_Therapy_adverse_effects_MeSH M_Heart_Failure__Congestive_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH S_rehabilitation_MeSH Heart_Failure__Congestive_rehabilitation_MeSH M_Human_MeSH 
****** 12972122
----K 5
----T Comparison of effectiveness of carvedilol versus metoprolol or atenolol for atrial fibrillation appearing after coronary artery bypass grafting or cardiac valve operation.
----A A retrospective review of 115 patients who underwent cardiac surgery demonstrated a marked reduction in postoperative atrial fibrillation (8% vs 32%, p <0.05) in patients who received carvedilol versus metoprolol or atenolol immediately after surgery. A prospective study examining the possibility of carvedilol's greater efficacy in preventing postoperative atrial fibrillation appears warranted.
----P Journal_Article 
----M M_Adult_MeSH M_Aged_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_etiology_MeSH Atrial_Fibrillation_etiology_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Coronary_Arteriosclerosis_MeSH S_surgery_MeSH Coronary_Arteriosclerosis_surgery_MeSH M_Coronary_Artery_Bypass_MeSH S_adverse_effects_MeSH Coronary_Artery_Bypass_adverse_effects_MeSH M_Female_MeSH M_Heart_Valve_Diseases_MeSH S_surgery_MeSH Heart_Valve_Diseases_surgery_MeSH M_Heart_Valve_Prosthesis_Implantation_MeSH S_adverse_effects_MeSH Heart_Valve_Prosthesis_Implantation_adverse_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_therapeutic_use_MeSH Metoprolol_therapeutic_use_MeSH M_Middle_Aged_MeSH M_Outcome_Assessment_(Health_Care)_MeSH P_Postoperative_Complications_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Retrospective_Studies_MeSH M_Vasodilator_Agents_MeSH S_therapeutic_use_MeSH Vasodilator_Agents_therapeutic_use_MeSH 
****** 14500864
----K 5
----T The ALLHAT study: results and clinical implications.
----A 
----P Journal_Article 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Disease_MeSH S_prevention_&_control_MeSH Coronary_Disease_prevention_&_control_MeSH M_Diuretics_MeSH S_administration_&_dosage_MeSH Diuretics_administration_&_dosage_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Hypertension_MeSH S_prevention_&_control_MeSH Hypertension_prevention_&_control_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Randomized_Controlled_Trials_MeSH 
****** 14522567
----K 6
----T Comparative impact of enalapril, candesartan or metoprolol alone or in combination on ventricular remodelling in patients with congestive heart failure.
----A AIMS: RESOLVD study patients were randomized to candesartan (C), enalapril (E), or C+E. Patients were later randomized to metoprolol CR (M) or placebo. Examine impact of C or E (C/E), C+E, C+M/E+M, C+E+M on ventricular remodelling in heart failure (HF) over 43 weeks. METHODS AND RESULTS: Four hundred and twenty-six of 768 patients receiving C, E, or C+E were randomized to either M or placebo. Patients were New York Heart Association class II-IV, ejection fraction (EF) <0.40 and 6-min walk distance <500 m. Ejection fraction (EF), cardiac volumes, blood pressures, heart rates, and neurohormones were measured. End diastolic volumes changed +29.4+/-6.4 ml for C/E, +16.6+/-10.4 ml for C+E, +19.7+/-6.5 ml for C+M/E+M, and -6.4+/-7.5 ml for C+E+M (P< or =0.01). End systolic volumes changed +22.9+/-5.8 ml for C/E, +11.9+/-9.1 ml for C+E, +6.0+/-5.7 ml for C+E/E+M, and -16.5+/-7.0 ml for C+E+M (P< or =0.001). Ejection fraction changed +0.01+/-0.01 for C/E, +0.01+/-0.01 for C+E, +0.03+/-0.01 for C+M/E+M, and +0.05+/-0.01 for C+E+M (P< or =0.0001). No significant differences for blood pressure or neurohormones; heart rate for C+M/E+M and C+E+M decreased (P< or =0.01) vs C/E or C+E. CONCLUSION: C+E+M had a modest but beneficial effect on cardiac function compared to the other groups. Combination of C+E+M has potential for providing HF patients with further benefit.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_administration_&_dosage_MeSH Angiotensin-Converting_Enzyme_Inhibitors_administration_&_dosage_MeSH M_Antihypertensive_Agents_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Benzimidazoles_MeSH S_administration_&_dosage_MeSH Benzimidazoles_administration_&_dosage_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cardiac_Volume_MeSH S_drug_effects_MeSH Cardiac_Volume_drug_effects_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Therapy__Combination_MeSH M_Enalapril_MeSH S_administration_&_dosage_MeSH Enalapril_administration_&_dosage_MeSH M_Female_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH M_Heart_Rate_MeSH S_drug_effects_MeSH Heart_Rate_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Receptors__Angiotensin_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Angiotensin_antagonists_&_inhibitors_MeSH M_Stroke_Volume_MeSH S_drug_effects_MeSH Stroke_Volume_drug_effects_MeSH M_Support__Non-U_S__Gov't_MeSH M_Survival_Analysis_MeSH M_Tetrazoles_MeSH S_administration_&_dosage_MeSH Tetrazoles_administration_&_dosage_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Remodeling_MeSH S_drug_effects_MeSH Ventricular_Remodeling_drug_effects_MeSH 
****** 14529610
----K 5
----T What medication best prevents migraine in children?
----A 
----P Journal_Article 
----M M_Amitriptyline_MeSH S_therapeutic_use_MeSH Amitriptyline_therapeutic_use_MeSH M_Child_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Migraine_MeSH S_prevention_&_control_MeSH Migraine_prevention_&_control_MeSH M_Propranolol_MeSH S_therapeutic_use_MeSH Propranolol_therapeutic_use_MeSH M_Valproic_Acid_MeSH S_therapeutic_use_MeSH Valproic_Acid_therapeutic_use_MeSH 
****** 14530474
----K 5
----T Efficacy of carvedilol treatment on cardiac function and cardiac sympathetic nerve activity in patients with dilated cardiomyopathy: comparison with metoprolol therapy.
----A Carvedilol and metoprolol have been reported to be effective in the treatment of patients with chronic heart failure. However, to our knowledge, there have been no studies comparing the effects of the 2 drugs on cardiac function, including cardiac sympathetic nerve activity. METHODS: We compared 15 patients with dilated cardiomyopathy (DCM) who were receiving carvedilol (group A) with 15 patients with DCM who were receiving metoprolol (group B). Before and after 1 y of treatment, cardiac (123)I-metaiodobenzylguanidine ((123)I-MIBG) uptake was assessed using the total defect score (TDS) and the heart-to-mediastinum (H/M) activity ratio from the delayed images. The New York Heart Association (NYHA) class and echocardiographic left ventricular ejection fraction (LVEF) also were assessed. RESULTS: In both groups, the TDS decreased (in group A, from 25 +/- 14 to 16 +/- 14, P < 0.01; in group B, from 27 +/- 9 to 19 +/- 10, P < 0.01), the H/M increased (in group A, from 1.67 +/- 0.31 to 2.01 +/- 0.36, P < 0.01; in group B, from 1.68 +/- 0.21 to 1.93 +/- 0.32, P < 0.01), the LVEF increased (in group A, from 31% +/- 10% to 48% +/- 10%, P < 0.01; in group B, from 28% +/- 9% to 47% +/- 15%, P < 0.01), and the NYHA functional class improved (in group A, from 2.9 +/- 0.3 to 1.7 +/- 0.5, P < 0.01; in group B, from 2.8 +/- 0.6 to 1.7 +/- 0.6, P < 0.01). The change in LVEF was mildly correlated with the change in the TDS in group A (r = 0.41) as well as in group B (r = 0.53). In the patients with a favorable response in the TDS or H/M, the NYHA class improved more than in the patients without a favorable response (P < 0.05). CONCLUSION: Carvedilol treatment can improve cardiac function, symptoms, and cardiac sympathetic nerve activity in patients with DCM to a similar extent as metoprolol treatment. The improvement of cardiac function and symptoms is related to the improvement of cardiac sympathetic nerve activity.
----P Clinical_Trial Controlled_Clinical_Trial Journal_Article 
----M M_3-Iodobenzylguanidine_MeSH S_diagnostic_use_MeSH 3-Iodobenzylguanidine_diagnostic_use_MeSH M_Adrenergic_Antagonists_MeSH S_administration_&_dosage_MeSH Adrenergic_Antagonists_administration_&_dosage_MeSH M_Adult_MeSH M_Aged_MeSH M_Carbazoles_MeSH S_administration_&_dosage_MeSH Carbazoles_administration_&_dosage_MeSH M_Cardiomyopathy__Congestive_MeSH S_complications_MeSH Cardiomyopathy__Congestive_complications_MeSH S_drug_therapy_MeSH Cardiomyopathy__Congestive_drug_therapy_MeSH S_radionuclide_imaging_MeSH Cardiomyopathy__Congestive_radionuclide_imaging_MeSH M_Comparative_Study_MeSH M_Female_MeSH M_Heart_Ventricles_MeSH S_drug_effects_MeSH Heart_Ventricles_drug_effects_MeSH S_innervation_MeSH Heart_Ventricles_innervation_MeSH S_radionuclide_imaging_MeSH Heart_Ventricles_radionuclide_imaging_MeSH M_Human_MeSH M_Male_MeSH M_Metoprolol_MeSH S_administration_&_dosage_MeSH Metoprolol_administration_&_dosage_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_administration_&_dosage_MeSH Propanolamines_administration_&_dosage_MeSH M_Radiopharmaceuticals_MeSH S_diagnostic_use_MeSH Radiopharmaceuticals_diagnostic_use_MeSH M_Sympathetic_Nervous_System_MeSH S_drug_effects_MeSH Sympathetic_Nervous_System_drug_effects_MeSH S_radionuclide_imaging_MeSH Sympathetic_Nervous_System_radionuclide_imaging_MeSH M_Technetium_Tc_99m_Sestamibi_MeSH S_diagnostic_use_MeSH Technetium_Tc_99m_Sestamibi_diagnostic_use_MeSH M_Treatment_Outcome_MeSH M_Ventricular_Dysfunction__Left_MeSH S_drug_therapy_MeSH Ventricular_Dysfunction__Left_drug_therapy_MeSH S_etiology_MeSH Ventricular_Dysfunction__Left_etiology_MeSH S_radionuclide_imaging_MeSH Ventricular_Dysfunction__Left_radionuclide_imaging_MeSH 
****** 14561016
----K 4
----T Cardioselective beta-blockers for chronic obstructive pulmonary disease: a meta-analysis.
----A Beta-blocker therapy has a mortality benefit in patients with hypertension, heart failure and coronary artery disease, as well as during the perioperative period. These drugs have traditionally been considered contraindicated in patients with chronic obstructive pulmonary disease (COPD). The objective of this study was to assess the effect of cardioselective beta-blockers on respiratory function of patients with COPD. Comprehensive searches were performed of the EMBASE, MEDLINE and CINAHL databases from 1966 to May 2001, and identified articles and related reviews were scanned. Randomised, blinded, controlled trials that studied the effects of cardioselective beta-blockers on the forced expiratory volume in 1 s (FEV1) or symptoms in patients with COPD were included in the analysis. Interventions studied were the administration of beta-blocker, given either as a single dose or for longer duration, and the use of beta2-agonist given after the study drug. Outcomes measured were the change in FEV1 from baseline and the number of patients with respiratory symptoms. Eleven studies of single-dose treatment and 8 of continued treatment were included. Cardioselective beta-blockers produced no significant change in FEV1 or respiratory symptoms compared to placebo, given as a single dose (-2.05% [95% CI, -6.05% to 1.96%]) or for longer duration (-2.55% [CI, -5.94% to 0.84]), and did not significantly affect the FEV1 treatment response to beta2-agonists. Subgroup analyses revealed no significant change in results for those participants with severe chronic airways obstruction or for those with a reversible obstructive component. In conclusion, cardioselective beta-blockers given to patients with COPD do not produce a significant reduction in airway function or increase the incidence of COPD exacerbations. Given their demonstrated benefit in conditions such as heart failure, coronary artery disease and hypertension, cardioselective beta-blockers should be considered for patients with COPD.
----P Journal_Article Meta-Analysis 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Double-Blind_Method_MeSH M_Female_MeSH M_Forced_Expiratory_Volume_MeSH S_drug_effects_MeSH Forced_Expiratory_Volume_drug_effects_MeSH M_Human_MeSH M_Male_MeSH M_Pulmonary_Disease__Chronic_Obstructive_MeSH S_drug_therapy_MeSH Pulmonary_Disease__Chronic_Obstructive_drug_therapy_MeSH S_physiopathology_MeSH Pulmonary_Disease__Chronic_Obstructive_physiopathology_MeSH M_Randomized_Controlled_Trials_MeSH M_Receptors__Adrenergic__beta-1_MeSH S_antagonists_&_inhibitors_MeSH Receptors__Adrenergic__beta-1_antagonists_&_inhibitors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 14562585
----K 5
----T Cyclic vomiting syndrome: a brain-gut disorder.
----A Despite the "black box" surrounding CVS, the authors' understanding of this clinical entity has advanced substantially in the last decade as a result of an international interdisciplinary clinical and research effort. Although CVS is now recognized as a unique clinical entity, patients still undergo innumerable hospitalizations and diagnostic tests. Although controlled therapeutic studies are lacking, reasonably effective empiric approaches have been developed by trial and error using anti-migraine, anti-emetic, and anti-epileptic regimens. The ongoing investigations of migraine mechanisms through NMR spectroscopy, mitochondrial DNA mutations and cellular energetics, corticotropin-releasing factor and gastric motility, and brainstem regulation of autonomic function may lead to breakthroughs in the understanding of and new therapies for CVS in the next decade.
----P Journal_Article Review Review__Tutorial 
----M M_Diagnosis__Differential_MeSH M_Human_MeSH P_Migraine_MeSH S_diagnosis_MeSH Migraine_diagnosis_MeSH S_etiology_MeSH Migraine_etiology_MeSH S_therapy_MeSH Migraine_therapy_MeSH M_Periodicity_MeSH M_Recurrence_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Syndrome_MeSH P_Vomiting_MeSH S_diagnosis_MeSH Vomiting_diagnosis_MeSH S_etiology_MeSH Vomiting_etiology_MeSH S_therapy_MeSH Vomiting_therapy_MeSH 
****** 14583369
----K I
----T Comparison of effectiveness of carvedilol versus bisoprolol for maintenance of sinus rhythm after cardioversion of persistent atrial fibrillation.
----A Ninety patients who underwent cardioversion of persistent atrial fibrillation (AF) were randomized to bisoprolol 5 to 10 mg once daily or carvedilol 12.5 to 25 mg twice daily. Using intention-to-treat analysis, 23 patients (46%) in the bisoprolol group and 17 patients (32%) in the carvedilol group relapsed into AF during the 1 year of total follow-up (p = 0.486). Patients treated with carvedilol had a 14% (hazard ratio 0.86) lower risk of relapse of AF compared with patients in the bisoprolol group, although results were statistically insignificant (p = 0.661) after controlling for patient age, gender, baseline heart rate, and left atrial diameter.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Atrial_Fibrillation_MeSH S_prevention_&_control_MeSH Atrial_Fibrillation_prevention_&_control_MeSH M_Bisoprolol_MeSH S_therapeutic_use_MeSH Bisoprolol_therapeutic_use_MeSH M_Carbazoles_MeSH S_therapeutic_use_MeSH Carbazoles_therapeutic_use_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH P_Electric_Countershock_MeSH M_Female_MeSH M_Follow-Up_Studies_MeSH M_Human_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Propanolamines_MeSH S_therapeutic_use_MeSH Propanolamines_therapeutic_use_MeSH M_Recurrence_MeSH S_prevention_&_control_MeSH Recurrence_prevention_&_control_MeSH M_Time_Factors_MeSH M_Treatment_Outcome_MeSH 
****** 14601714
----K 5
----T Common cardiovascular issues encountered in geriatric critical care.
----A The incidence and prevalence of CV disease is high in the growing US elderly population. It is common for CV disease to be either the primary or secondary problem for elderly patients receiving critical care. The therapeutic options for CV problems experienced in the critical care setting range from medical management with the goal of symptom relief and comfort care to invasive therapies such as PCI, intraaortic balloon pump therapy, invasive monitoring, and cardiac surgery. Age alone is not a contraindication for any of the invasive therapies. Instead, a careful risk-benefit analysis should be performed for each individual patient, taking into consideration physiologic age, comorbid conditions, other disabilities, and an assessment of quality of life. Additionally, the goals (symptom relief, improvement of quality of life, survival benefit) of any therapy should be clearly established for individual patients. End-of-life issues, cardiovascular surgery, and the disabling of ICDs deserve special consideration in the elderly, as these are often challenging issues that will likely be more frequently encountered in critical care settings as science and technology advance.
----P Journal_Article 
----M M_Aged_MeSH M_Cardiovascular_Diseases_MeSH S_epidemiology_MeSH Cardiovascular_Diseases_epidemiology_MeSH P_Critical_Care_MeSH P_Health_Services_for_the_Aged_MeSH M_Human_MeSH M_Incidence_MeSH M_Prevalence_MeSH M_Treatment_Outcome_MeSH M_United_States_MeSH S_epidemiology_MeSH United_States_epidemiology_MeSH 
****** 14615493
----K 5
----T What is the role of beta-adrenergic signaling in heart failure?
----A This review addresses open questions about the role of beta-adrenergic receptors in cardiac function and failure. Cardiomyocytes express all three beta-adrenergic receptor subtypes-beta1, beta2, and, at least in some species, beta3. The beta1 subtype is the most prominent one and is mainly responsible for positive chronotropic and inotropic effects of catecholamines. The beta2 subtype also increases cardiac function, but its ability to activate nonclassical signaling pathways suggests a function distinct from the beta1 subtype. In heart failure, the sympathetic system is activated, cardiac beta-receptor number and function are decreased, and downstream mechanisms are altered. However, in spite of a wealth of data, we still do not know whether and to what extent these alterations are adaptive/protective or detrimental, or both. Clinically, beta-adrenergic antagonists represent the most important advance in heart failure therapy, but it is still debated whether they act by blocking or by resensitizing the beta-adrenergic receptor system. Newer experimental therapeutic strategies aim at the receptor desensitization machinery and at downstream signaling steps.
----P Journal_Article Review Review__Tutorial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Animals_MeSH M_Cyclic_AMP-Dependent_Protein_Kinases_MeSH S_metabolism_MeSH Cyclic_AMP-Dependent_Protein_Kinases_metabolism_MeSH M_Disease_Models__Animal_MeSH M_GTP-Binding_Proteins_MeSH S_metabolism_MeSH GTP-Binding_Proteins_metabolism_MeSH M_Heart_Failure__Congestive_MeSH S_drug_therapy_MeSH Heart_Failure__Congestive_drug_therapy_MeSH S_physiopathology_MeSH Heart_Failure__Congestive_physiopathology_MeSH M_Human_MeSH M_Mice_MeSH M_Mice__Transgenic_MeSH M_Myocardium_MeSH S_metabolism_MeSH Myocardium_metabolism_MeSH M_Receptors__Adrenergic__beta_MeSH S_genetics_MeSH Receptors__Adrenergic__beta_genetics_MeSH S_metabolism_MeSH Receptors__Adrenergic__beta_metabolism_MeSH P_Signal_Transduction_MeSH 
****** 14626470
----K 5
----T Changing medication use in managed care: a critical review of the available evidence.
----A OBJECTIVE: To review the effectiveness of strategies to improve the quality and efficiency of medication use in managed care organizations (MCOs). STUDY DESIGN: Systematic review of published intervention studies. METHODS: Studies were identified by using computerized and manual literature searches and personal contacts, and were categorized by intervention type and adequacy of research design according to commonly accepted criteria. Reported significance and magnitude of the changes in key outcomes were used to summarize the effects of studies with adequate research designs. RESULTS: The searches identified 105 studies, 70 of which were reported since 1996. Overall, 46% of the studies met the minimum criteria for methodologic adequacy (n = 48). Consistently effective interventions included dissemination of educational materials with drug samples, participatory clinical guideline development, group or one-to-one educational outreach, and enhanced patient-specific feedback. Disease management (primarily for depression and diabetes) showed promise in improving short-term outcomes. Dissemination of educational materials and aggregated feedback alone were ineffective. Interventions in staff-model health maintenance organizations were more effective than those conducted in group-model health maintenance organizations. CONCLUSION: High-quality studies of interventions to improve drug use in MCOs are increasing in frequency. There is evidence for the effectiveness of several strategies to change drug use, but little is known about longer-term clinical outcomes. Few well-designed, published studies have assessed the efficacy or safety of financial incentives for physicians, tiered copayments for patients, or formularies--despite their widespread use.
----P Journal_Article Review Review__Academic 
----M M_Disease_Management_MeSH P_Drug_Utilization_Review_MeSH M_Education__Medical__Continuing_MeSH M_Evidence-Based_Medicine_MeSH M_Human_MeSH M_Managed_Care_Programs_MeSH S_standards_MeSH Managed_Care_Programs_standards_MeSH M_Physician's_Practice_Patterns_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_United_States_MeSH 
****** 14638555
----K 5
----T Do thiazide diuretics confer specific protection against strokes?
----A Several large studies have suggested that therapy with thiazide diuretics confers a particular benefit in reducing the risk of strokes that seem to be, at least to some extent, independent of the blood pressure-lowering effect. Such a cerebroprotective effect was documented not only with monotherapy but also when diuretics were used in combination with other drugs. The cerebroprotective effect does not seem to be shared by other drug classes, such as the beta-blockers or the angiotensin-converting enzyme inhibitors, in patients without manifest cardiovascular disease. Since stroke is one of the most devastating sequelae of high blood pressure, our data strongly favor the use of low-dose diuretics either as initial therapy or in combination in all hypertensive patients at risk for cerebrovascular disease.
----P Journal_Article Review Review__Tutorial 
----M M_Antihypertensive_Agents_MeSH S_pharmacology_MeSH Antihypertensive_Agents_pharmacology_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Blood_Pressure_MeSH S_drug_effects_MeSH Blood_Pressure_drug_effects_MeSH M_Cerebrovascular_Accident_MeSH S_epidemiology_MeSH Cerebrovascular_Accident_epidemiology_MeSH S_physiopathology_MeSH Cerebrovascular_Accident_physiopathology_MeSH S_prevention_&_control_MeSH Cerebrovascular_Accident_prevention_&_control_MeSH M_Comorbidity_MeSH M_Diuretics__Thiazide_MeSH S_pharmacology_MeSH Diuretics__Thiazide_pharmacology_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Human_MeSH M_Hypertension_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH S_epidemiology_MeSH Hypertension_epidemiology_MeSH M_Renin-Angiotensin_System_MeSH S_drug_effects_MeSH Renin-Angiotensin_System_drug_effects_MeSH S_physiology_MeSH Renin-Angiotensin_System_physiology_MeSH 
****** 14644719
----K 4
----T A 3-month randomized controlled trial of bimatoprost (LUMIGAN) versus combined timolol and dorzolamide (Cosopt) in patients with glaucoma or ocular hypertension.
----A PURPOSE: To compare the efficacy and safety of topical bimatoprost (LUMIGAN; Allergan, Inc., Irvine, CA) once daily with that of topical combined timolol and dorzolamide (Cosopt; Merck and Co, Inc., Whitehouse Station, NJ) twice daily. DESIGN: Prospective, randomized, double-masked, multicenter clinical trial. PARTICIPANTS: One hundred seventy-seven patients with a diagnosis of glaucoma or ocular hypertension and inadequate control of intraocular pressure (IOP) after at least 2 weeks of topical timolol maleate 0.5% monotherapy. METHODS: Patients were randomized to receive bimatoprost 0.03% once daily (n = 90) or combined timolol 0.5% and dorzolamide 2% twice daily (n = 87) over a 3-month period. MAIN OUTCOME MEASURES: Intraocular pressure, the primary end point, was measured at 8 AM and 10 AM at baseline, week 1, and months 1, 2, and 3, and also at 4 PM and 8 PM at baseline and month 3. RESULTS: Bimatoprost provided significantly greater IOP lowering compared with combined timolol and dorzolamide. At the 8 AM measurements, bimatoprost lowered mean IOP 6.8 mmHg to 7.6 mmHg from baseline, whereas combined timolol and dorzolamide lowered mean IOP 4.4 to 5.0 mmHg from baseline (P<0.001). At the last follow-up, patients had better diurnal IOP control with bimatoprost than combined timolol and dorzolamide. At 8 AM at the 3-month visit, the percentages of patients achieving IOPs of <or =13 mmHg, < or =14 mmHg, < or =15 mmHg, or < or =16 mmHg were more than twice as high for bimatoprost than for combined timolol and dorzolamide (all P< or =0.008). Taste perversion, ocular burning, and stinging with instillation were more common with combined timolol and dorzolamide, whereas conjunctival hyperemia was more common with bimatoprost. CONCLUSIONS: In individuals with glaucoma or ocular hypertension, uncontrolled on a topical beta-blocker alone, bimatoprost lowered IOP more consistently than did combined timolol and dorzolamide.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Administration__Topical_MeSH M_Adult_MeSH M_Aged_MeSH M_Aged__80_and_over_MeSH M_Antihypertensive_Agents_MeSH S_administration_&_dosage_MeSH Antihypertensive_Agents_administration_&_dosage_MeSH M_Comparative_Study_MeSH M_Double-Blind_Method_MeSH M_Drug_Combinations_MeSH M_Female_MeSH M_Glaucoma_MeSH S_drug_therapy_MeSH Glaucoma_drug_therapy_MeSH M_Human_MeSH M_Intraocular_Pressure_MeSH S_drug_effects_MeSH Intraocular_Pressure_drug_effects_MeSH M_Lipids_MeSH S_administration_&_dosage_MeSH Lipids_administration_&_dosage_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Ocular_Hypertension_MeSH S_drug_therapy_MeSH Ocular_Hypertension_drug_therapy_MeSH M_Ophthalmic_Solutions_MeSH M_Prospective_Studies_MeSH M_Safety_MeSH M_Sulfonamides_MeSH S_administration_&_dosage_MeSH Sulfonamides_administration_&_dosage_MeSH M_Support__Non-U_S__Gov't_MeSH M_Thiophenes_MeSH S_administration_&_dosage_MeSH Thiophenes_administration_&_dosage_MeSH M_Timolol_MeSH S_administration_&_dosage_MeSH Timolol_administration_&_dosage_MeSH 
****** 14644892
----K 3
----T Albuminuria and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE study.
----A BACKGROUND: Several studies have shown that albuminuria is associated with increased risk for fatal and nonfatal cardiovascular events, independent of conventional risk factors. The partition values for urine albumin-creatinine ratio (UACR) used to identify microalbuminuria have been based on studies that predicted risk in diabetic patients. OBJECTIVE: To determine whether the relation between albuminuria and cardiovascular risk can be used to predict cardiovascular morbidity and mortality in hypertensive patients. DESIGN: Multicenter cohort study derived from a randomized, controlled trial. PATIENTS: 8206 patients with stage II or III hypertension randomly assigned to double-blind therapy with losartan or atenolol. Follow-up was 39 122 patient-years. MEASUREMENTS: Renal glomerular permeability evaluated by UACR. RESULTS: In nondiabetic hypertensive patients with left ventricular hypertrophy, the risk for the composite cardiovascular end point increased continuously as albuminuria increased (P < 0.001 for trend). There was no specific threshold for increased risk. For every 10-fold increase in UACR, hazard ratios in nondiabetic patients increased as follows: composite end point, by 57% (95% CI, 40.6% to 75.0%); cardiovascular mortality, by 97.7% (CI, 66.5% to 235%); all-cause mortality, by 75.2% (CI, 54.0% to 99.4%); stroke, by 51.0% (CI, 28.8% to 76.9%); and myocardial infarction, by 45% (CI, 19.9% to 75.4%) (P < 0.001 for all comparisons). Values were similar in diabetic patients, although for myocardial infarction the trend was weaker and not significant. CONCLUSION: Increased UACR resulted in increasing risk for cardiovascular morbidity and mortality among hypertensive patients with left ventricular hypertrophy. We found no thresholds or plateaus. Risk increases at much lower UACR values than has been reported among diabetic patients.
----P Clinical_Trial Journal_Article Randomized_Controlled_Trial 
----M M_Aged_MeSH M_Aged__80_and_over_MeSH M_Albuminuria_MeSH S_metabolism_MeSH Albuminuria_metabolism_MeSH M_Cardiovascular_Diseases_MeSH S_etiology_MeSH Cardiovascular_Diseases_etiology_MeSH S_mortality_MeSH Cardiovascular_Diseases_mortality_MeSH M_Cause_of_Death_MeSH M_Diabetes_Mellitus_MeSH S_complications_MeSH Diabetes_Mellitus_complications_MeSH M_Female_MeSH M_Human_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_urine_MeSH Hypertension_urine_MeSH M_Hypertrophy__Left_Ventricular_MeSH S_complications_MeSH Hypertrophy__Left_Ventricular_complications_MeSH S_urine_MeSH Hypertrophy__Left_Ventricular_urine_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Prospective_Studies_MeSH M_Risk_Factors_MeSH M_Support__Non-U_S__Gov't_MeSH 
****** 14657064
----K 3
----T A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease. The International Verapamil-Trandolapril Study (INVEST): a randomized controlled trial.
----A CONTEXT: Despite evidence of efficacy of antihypertensive agents in treating hypertensive patients, safety and efficacy of antihypertensive agents for coronary artery disease (CAD) have been discerned only from subgroup analyses in large trials. OBJECTIVE: To compare mortality and morbidity outcomes in patients with hypertension and CAD treated with a calcium antagonist strategy (CAS) or a non-calcium antagonist strategy (NCAS). DESIGN, SETTING, AND PARTICIPANTS: Randomized, open label, blinded end point study of 22 576 hypertensive CAD patients aged 50 years or older, which was conducted September 1997 to February 2003 at 862 sites in 14 countries. INTERVENTIONS: Patients were randomly assigned to either CAS (verapamil sustained release) or NCAS (atenolol). Strategies specified dose and additional drug regimens. Trandolapril and/or hydrochlorothiazide was administered to achieve blood pressure goals according to guidelines from the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) of less than 140 mm Hg (systolic) and less than 90 mm Hg (diastolic); and less than 130 mm Hg (systolic) and less than 85 mm Hg (diastolic) if diabetes or renal impairment was present. Trandolapril was also recommended for patients with heart failure, diabetes, or renal impairment. MAIN OUTCOME MEASURES: Primary: first occurrence of death (all cause), nonfatal myocardial infarction, or nonfatal stroke; other: cardiovascular death, angina, adverse experiences, hospitalizations, and blood pressure control at 24 months. RESULTS: At 24 months, in the CAS group, 6391 patients (81.5%) were taking verapamil sustained release; 4934 (62.9%) were taking trandolapril; and 3430 (43.7%) were taking hydrochlorothiazide. In the NCAS group, 6083 patients (77.5%) were taking atenolol; 4733 (60.3%) were taking hydrochlorothiazide; and 4113 (52.4%) were taking trandolapril. After a follow-up of 61 835 patient-years (mean, 2.7 years per patient), 2269 patients had a primary outcome event with no statistically significant difference between treatment strategies (9.93% in CAS and 10.17% in NCAS; relative risk [RR], 0.98; 95% confidence interval [CI], 0.90-1.06). Two-year blood pressure control was similar between groups. The JNC VI blood pressure goals were achieved by 65.0% (systolic) and 88.5% (diastolic) of CAS and 64.0% (systolic) and 88.1% (diastolic) of NCAS patients. A total of 71.7% of CAS and 70.7% of NCAS patients achieved a systolic blood pressure of less than 140 mm Hg and diastolic blood pressure of less than 90 mm Hg. CONCLUSION: The verapamil-trandolapril-based strategy was as clinically effective as the atenolol-hydrochlorothiazide-based strategy in hypertensive CAD patients.
----P Clinical_Trial Journal_Article Multicenter_Study Randomized_Controlled_Trial 
----M M_Adrenergic_beta-Antagonists_MeSH S_therapeutic_use_MeSH Adrenergic_beta-Antagonists_therapeutic_use_MeSH M_Aged_MeSH M_Angiotensin-Converting_Enzyme_Inhibitors_MeSH S_therapeutic_use_MeSH Angiotensin-Converting_Enzyme_Inhibitors_therapeutic_use_MeSH M_Antihypertensive_Agents_MeSH S_adverse_effects_MeSH Antihypertensive_Agents_adverse_effects_MeSH S_therapeutic_use_MeSH Antihypertensive_Agents_therapeutic_use_MeSH M_Atenolol_MeSH S_therapeutic_use_MeSH Atenolol_therapeutic_use_MeSH M_Blood_Pressure_MeSH M_Calcium_Channel_Blockers_MeSH S_therapeutic_use_MeSH Calcium_Channel_Blockers_therapeutic_use_MeSH M_Coronary_Arteriosclerosis_MeSH S_complications_MeSH Coronary_Arteriosclerosis_complications_MeSH S_drug_therapy_MeSH Coronary_Arteriosclerosis_drug_therapy_MeSH M_Diuretics__Thiazide_MeSH S_therapeutic_use_MeSH Diuretics__Thiazide_therapeutic_use_MeSH M_Drug_Therapy__Combination_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Hydrochlorothiazide_MeSH S_therapeutic_use_MeSH Hydrochlorothiazide_therapeutic_use_MeSH M_Hypertension_MeSH S_complications_MeSH Hypertension_complications_MeSH S_drug_therapy_MeSH Hypertension_drug_therapy_MeSH M_Indoles_MeSH S_therapeutic_use_MeSH Indoles_therapeutic_use_MeSH M_Male_MeSH M_Middle_Aged_MeSH M_Support__Non-U_S__Gov't_MeSH M_Support__U_S__Gov't__P_H_S__MeSH M_Treatment_Outcome_MeSH M_Verapamil_MeSH S_therapeutic_use_MeSH Verapamil_therapeutic_use_MeSH 
****** 14678921
----K 5
----T Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians.
----A The Joint Panel of the American Academy of Family Physicians and the American College of Physicians, in collaboration with the Johns Hopkins Evidence-based Practice Center, systematically reviewed the available evidence on the management of newly detected atrial fibrillation and developed recommendations for adult patients with first-detected atrial fibrillation. The recommendations do not apply to patients with postoperative or post-myocardial infarction atrial fibrillation, patients with class IV heart failure, patients already taking antiarrhythmic drugs, or patients with valvular disease. The target physician audience is internists and family physicians dedicated to primary care. The recommendations are as follows: RECOMMENDATION 1: Rate control with chronic anticoagulation is the recommended strategy for the majority of patients with atrial fibrillation. Rhythm control has not been shown to be superior to rate control (with chronic anticoagulation) in reducing morbidity and mortality and may be inferior in some patient subgroups to rate control. Rhythm control is appropriate when based on other special considerations, such as patient symptoms, exercise tolerance, and patient preference. Grade: 2A. RECOMMENDATION 2: Patients with atrial fibrillation should receive chronic anticoagulation with adjusted-dose warfarin, unless they are at low risk of stroke or have a specific contraindication to the use of warfarin (thrombocytopenia, recent trauma or surgery, alcoholism). Grade: 1A. RECOMMENDATION 3: For patients with atrial fibrillation, the following drugs are recommended for their demonstrated efficacy in rate control during exercise and while at rest: atenolol, metoprolol, diltiazem, and verapamil (drugs listed alphabetically by class). Digoxin is only effective for rate control at rest and therefore should only be used as a second-line agent for rate control in atrial fibrillation. Grade: 1B. RECOMMENDATION 4: For those patients who elect to undergo acute cardioversion to achieve sinus rhythm in atrial fibrillation, both direct-current cardioversion (Grade: 1C+) and pharmacological conversion (Grade: 2A) are appropriate options. RECOMMENDATION 5: Both transesophageal echocardiography with short-term prior anticoagulation followed by early acute cardioversion (in the absence of intracardiac thrombus) with postcardioversion anticoagulation versus delayed cardioversion with pre- and postanticoagulation are appropriate management strategies for those patients who elect to undergo cardioversion. Grade: 2A. RECOMMENDATION 6: Most patients converted to sinus rhythm from atrial fibrillation should not be placed on rhythm maintenance therapy since the risks outweigh the benefits. In a selected group of patients whose quality of life is compromised by atrial fibrillation, the recommended pharmacologic agents for rhythm maintenance are amiodarone, disopyramide, propafenone, and sotalol (drugs listed in alphabetical order). The choice of agent predominantly depends on specific risk of side effects based on patient characteristics. Grade: 2A.
----P Guideline Journal_Article Practice_Guideline 
----M M_Adult_MeSH M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_diagnosis_MeSH Atrial_Fibrillation_diagnosis_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH S_ultrasonography_MeSH Atrial_Fibrillation_ultrasonography_MeSH M_Echocardiography__Transesophageal_MeSH M_Electric_Countershock_MeSH M_Female_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Male_MeSH M_Support__Non-U_S__Gov't_MeSH 
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----K 5
----T Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography.
----A PURPOSE: This review summarizes the available evidence regarding the efficacy of medications used for ventricular rate control, stroke prevention, acute conversion, and maintenance of sinus rhythm, as well as the efficacy of electrical cardioversion and the use of echocardiography in patients with atrial fibrillation. DATA SOURCES: The Cochrane Collaboration's database of controlled clinical trials and MEDLINE. STUDY SELECTION: Primarily randomized, controlled trials of medications. DATA EXTRACTION: Paired reviewers obtained data on efficacy and safety. Strength of evidence was assessed. DATA SYNTHESIS: Recent clinical trial results showed that most patients with atrial fibrillation have similar outcomes with strategies for controlling ventricular rate compared with strategies for restoring sinus rhythm. For efficacy of primary stroke prevention, compared with placebo, evidence was strong for warfarin and suggestive for aspirin. The evidence for an increased risk for major bleeding was suggestive for warfarin and inconclusive for aspirin. For ventricular rate control, verapamil, diltiazem, atenolol, and metoprolol were qualitatively superior to digoxin and placebo, particularly during exercise. For efficacy of acute conversion, compared with placebo, evidence was strong for ibutilide, flecainide, dofetilide, propafenone, amiodarone, and quinidine. For efficacy of maintenance of sinus rhythm after conversion from atrial fibrillation, evidence was strong for amiodarone, propafenone, disopyramide, and sotalol. Echocardiography was found to be useful in estimating risk for thromboembolism and potentially useful in estimating likelihood of successful cardioversion and maintenance. CONCLUSIONS: For several key questions in the pharmacologic management of atrial fibrillation, strong evidence exists to support 1 or more treatment options.
----P Journal_Article Review Review__Academic 
----M M_Anti-Arrhythmia_Agents_MeSH S_therapeutic_use_MeSH Anti-Arrhythmia_Agents_therapeutic_use_MeSH M_Anticoagulants_MeSH S_therapeutic_use_MeSH Anticoagulants_therapeutic_use_MeSH M_Atrial_Fibrillation_MeSH S_diagnosis_MeSH Atrial_Fibrillation_diagnosis_MeSH S_therapy_MeSH Atrial_Fibrillation_therapy_MeSH S_ultrasonography_MeSH Atrial_Fibrillation_ultrasonography_MeSH M_Echocardiography__Transesophageal_MeSH M_Electric_Countershock_MeSH M_Evidence-Based_Medicine_MeSH M_Heart_Rate_MeSH M_Human_MeSH M_Support__U_S__Gov't__P_H_S__MeSH