Abstract
Compared with placebo, adding betaxolol 20 mg every day to nifedipine (up to 60 mg/day in divided doses) or diltiazem (up to 360 mg/day in divided doses) for a 3-week treatment period in 135 patients with stable angina pectoris significantly (p < 0.05) lengthened the time to onset of moderate angina during exercise tolerance tests at all treatment time points. The median increases in the time to onset of moderate angina at the final exercise tolerance test (end point) compared with baseline were 1.08 and 0.53 minutes for betaxolol and placebo groups, respectively (p = 0.002, betaxolol vs placebo). The time to onset of 1 mm ST-segment depression increased significantly (p < 0.05) with betaxolol compared with placebo at all but 1 treatment time point (median increase [p = 0.001] 1.77 and 0.37 minutes, respectively, at end point). Duration of exercise also was increased significantly (p < 0.05) after the third week of treatment and at end point (median 0.62 and 0.50 minutes, respectively; p = 0.03). Generally comparable results were found within the diltiazem (n = 128) and nifedipine (n = 25) subgroups, although the nifedipine group was too small to detect statistically significant differences between betaxolol and placebo treatment. Resting systolic blood pressure, heart rate and the rate-pressure product, measured both when angina occurred and at the end of exercise, also were influenced significantly (p < 0.05) by the betaxolol addition. The only serious adverse effect associated with betaxolol treatment was syncope, seen in 2 patients.
Original language | English (US) |
---|---|
Pages (from-to) | 213-218 |
Number of pages | 6 |
Journal | The American Journal of Cardiology |
Volume | 73 |
Issue number | 4 |
DOIs | |
State | Published - Feb 1 1994 |
Bibliographical note
Funding Information:From the Cardiovascular Unit for Research and Education, University of South Florida Health Sciences Center, Tampa, Florida; Center for Stress Studies of San Diego, San Diego, California; Edmonton Cardiac Fitness Institute, Edmonton, Alberta, Canada; Arizona Heart Institute Foundation, Phoenix, Arizona; and the Veterans Administration Medical Center and University of Minnesota, Minneapolis, Minnesota. This study was supported by a grant from Lorex Pharmaceuticals, Skokie, Illinois. Manuscript received February 11, 1993; revised manuscript received July 29, 1993, and accepted August 3.