BACKGROUND AND PURPOSE:beta-Blockers prevent vascular events in patients after myocardial infarction and lower blood pressure, the main risk factor for stroke. Hence, we assessed the effects of atenolol on the occurrence of death from vascular causes, stroke, or myocardial infarction and on blood pressure in patients after a transient ischemic attack or nondisabling ischemic stroke. METHODS: In a double-blind, placebo-controlled randomized clinical trial we studied the occurrence of the outcome event death from vascular causes, nonfatal stroke, or nonfatal myocardial infarction and the outcome event fatal or nonfatal stroke as well as blood pressure on follow-up. A total of 1,473 aspirin-treated patients with transient ischemic attack or nondisabling ischemic stroke were randomized to 50 mg atenolol daily or placebo. The mean follow-up was 2.6 years. RESULTS: Patients on atenolol had a risk of 97/732 (13.3%) for the combined outcome event versus a risk of 95/741 (12.8%) for those on placebo (adjusted hazard ratio, 1.00; 95% confidence interval, 0.76-1.33). The adjusted hazard ratio for fatal or nonfatal stroke was 0.82 (95% confidence interval, 0.57-1.19). More patients on beta-blocker (153) reported adverse effects than on placebo (103). At the first follow-up visit after randomization (median at 4 months) systolic blood pressure in the atenolol group had dropped by 8.0 mm Hg compared with 2.2 mm Hg in the placebo group (difference, 5.8 mm Hg; 95% confidence interval, 2.9-8.6 mm Hg). For diastolic blood pressure this difference was 2.9 mm Hg (95% confidence interval, 1.5-4.4 mm Hg). CONCLUSIONS: Our data neither confirm nor rule out that atenolol prevents important vascular events in patients after transient ischemic attack or nondisabling ischemic stroke, given the modest effect on blood pressure, the restrictions in patient selection, and the limited number of patient-years.
RCT Entities:
BACKGROUND AND PURPOSE: beta-Blockers prevent vascular events in patients after myocardial infarction and lower blood pressure, the main risk factor for stroke. Hence, we assessed the effects of atenolol on the occurrence of death from vascular causes, stroke, or myocardial infarction and on blood pressure in patients after a transient ischemic attack or nondisabling ischemic stroke. METHODS: In a double-blind, placebo-controlled randomized clinical trial we studied the occurrence of the outcome event death from vascular causes, nonfatal stroke, or nonfatal myocardial infarction and the outcome event fatal or nonfatal stroke as well as blood pressure on follow-up. A total of 1,473 aspirin-treated patients with transient ischemic attack or nondisabling ischemic stroke were randomized to 50 mg atenolol daily or placebo. The mean follow-up was 2.6 years. RESULTS:Patients on atenolol had a risk of 97/732 (13.3%) for the combined outcome event versus a risk of 95/741 (12.8%) for those on placebo (adjusted hazard ratio, 1.00; 95% confidence interval, 0.76-1.33). The adjusted hazard ratio for fatal or nonfatal stroke was 0.82 (95% confidence interval, 0.57-1.19). More patients on beta-blocker (153) reported adverse effects than on placebo (103). At the first follow-up visit after randomization (median at 4 months) systolic blood pressure in the atenolol group had dropped by 8.0 mm Hg compared with 2.2 mm Hg in the placebo group (difference, 5.8 mm Hg; 95% confidence interval, 2.9-8.6 mm Hg). For diastolic blood pressure this difference was 2.9 mm Hg (95% confidence interval, 1.5-4.4 mm Hg). CONCLUSIONS: Our data neither confirm nor rule out that atenolol prevents important vascular events in patients after transient ischemic attack or nondisabling ischemic stroke, given the modest effect on blood pressure, the restrictions in patient selection, and the limited number of patient-years.