Carvedilol is a nonselective beta-blocker with alpha-mediated vasodilating properties that has been shown to be effective in systemic hypertension, stable angina, and congestive heart failure (CHF). In this study, we studied the effects of carvedilol on premature ventricular contractions (PVCs) in 65 patients undergoing treatment with carvedilol (12.5-50 mg b.i.d.) for 4-8 weeks. Twelve patients had hypertension, 41 had stable angina, and 12 had CHF. Holter monitoring for 24 h was performed before and after active carvedilol therapy. Median PVCs per 24 h decreased from 25.5 to 6.0 (p less than 0.001, n = 52). Reduction in PVC activity occurred in 77% of patients, and 23% of patients with multifocal PVCs changed their morphology to unifocal. Nonsustained ventricular tachycardia was present in four patients before treatment; this was abolished in all patients. R-on-T PVC was present in six patients; it decreased in five and increased in one. New ventricular tachycardia (less than 8 beats) occurred in two patients, but QT prolongation was not noted in these patients. An improvement in Lown's classification occurred in 50% of patients. However, in the CHF group, the improvement in Lown's criteria was observed in 73% of patients. Carvedilol does not appear to possess proarrhythmic effects, and chronic therapy reduces PVC activity in a wide range of patients. This property of carvedilol is complementary to its hypotensive and anti-ischemic effects. In the CHF group, the beneficial effects of carvedilol on left ventricular function and hemodynamics may combine with the improvement in PVC activity to produce a significant improvement in mortality.