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Although all beta blockers have been found to be effective in the symptomatic relief of angina pectoris, the importance of intrinsic sympathomimetic activity (ISA) has not been studied extensively. In a randomized, double-blind study, we administered equipotent doses of propranolol (10, 20, and 40 mg four times a day) and pindolol (2.5, 5, and 10 mg four times a day), a beta blocker with significant ISA, to 52 patients with angina. Both agents were found to be effective in the treatment of angina. At peak dose, propranolol reduced the number of angina attacks per 2 weeks from 29.29 +/- 4.79 to 18.0 +/- 4.4 (p = 0.021) (a 39% reduction) and increased the exercise tolerance on the treadmill from 7.55 +/- 0.67 METS to 9.36 +/- 0.58 (p = 0.002). Pindolol decreased the number of anginal attacks per 2 weeks from 16.48 +/- 2.63 to 8.65 +/- 2.46 (p = 0.0027) (a 48% reduction) and increased exercise tolerance from 7.95 +/- 0.56 METS to 9.40 +/- 0.57 (p = 0.0245). At the end of the maximum tolerated exercise, propranolol decreased the heart rate from 110.00 +/- 3.41 to 99.71 +/- 3.74 (p = 0.0015). Pindolol also decreased the heart rate at the maximum tolerated exercise from 113.59 +/- 3.24 to 108.12 +/- 3.16 (p = 0.0102). At rest, however, propranolol induced a more pronounced (p = 0.0066) decrease in heart rate (from 69.00 +/- 1.85 to 61.50 +/- 1.99; p = 0.0018), whereas pindolol did not significantly affect the resting heart rate (65.37 +/- 1.47 to 65.5 +/- 1.44; p = 0.9392). In addition propranolol decreased echocardiographically determined ejection fraction from 0.57 +/- 0.02 to 0.15 +/- 0.01 (p = 0.04) and increased the left ventricular end-diastolic volume from 71.8 +/- 3.2 to 92.2 +/- 1.9 ml (p = 0.003), whereas pindolol did not affect the ejection fraction and caused a less pronounced (p = 0.03) increase in end-diastolic volume (from 70.8 +/- 1.8 to 80.2 +/- 2.8; p = 0.02). The data indicate that both propranolol and pindolol are effective in the treatment of angina pectoris and that pindolol decreases the resting heart rate and ejection fraction and increases the left ventricular end-diastolic volume to a lesser extent than propranolol.
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1985,
American family physician,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
September 1978,
La Nouvelle presse medicale,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1976,
Bibliotheca cardiologica,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1983,
Journal of cardiovascular pharmacology,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
April 1982,
MMW, Munchener medizinische Wochenschrift,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
September 1990,
The American journal of cardiology,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1982,
British journal of clinical pharmacology,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1988,
Acta medica Scandinavica,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
June 1992,
Srpski arhiv za celokupno lekarstvo,
J B Kostis, and
W Frishman, and
M H Hosler, and
N L Thorsen, and
L Gonasun, and
J Weinstein
January 1975,
Naunyn-Schmiedeberg's archives of pharmacology,
