The beginning of thought about a discrete Class III antiarrhythmic action stemmed from the observation that sotalol produced a very marked increase in the time course of repolarization with little or no change in conduction velocity in cardiac muscle. It is known that in patients with hypothyroidism or hypocalcemia, both of which are associated with a marked lengthening of the cardiac action potential, arrhythmias are exceedingly rare. The acetyl metabolite of procainamide also produces, as its sole action, a marked increase in the action-potential duration, and it has antiarrhythmic activity. It is clear that lengthening the action-potential duration is antiarrhythmic. Sotalol is a unique beta blocker in not only antagonizing sympathetic stimulation competitively, but also in exerting a potent antiarrhythmic effect by prolonging repolarization. Because of the augmented tension that is associated with the increase in action-potential duration, sotalol produces a less negative inotropic effect than that seen with other beta blockers. Sotalol is a potent broad-spectrum antiarrhythmic agent because of its Class III properties, resulting from an increase in the length of cardiac repolarization, a property that is modulated by its beta-adrenergic blocking actions.