Electrophysiologic basis for the antiarrhythmic actions of sotalol and comparison with other agents

Abstract

Although synthesized as a nonselective beta-adrenergic blocking compound, sotalol has emerged as the prototype of the so-called class III antiarrhythmic compounds. It delays cardiac repolarization by inhibiting the delayed rectifier potassium current, having a lesser effect on the inward rectifying potassium current with little or no effect on the inward calcium or sodium currents. This property of prolonging repolarization with an accompanying increase in the effective refractory period is not due to blockade of the beta-adrenergic receptors. The major electrophysiologic profile of sotalol constitutes the summed effects of beta blockade and prolonged repolarization. Sotalol exerts a potent antifibrillatory action modulated by its antiadrenergic effects. It suppresses premature ventricular contractions and nonsustained ventricular tachycardia while preventing inducible ventricular tachycardia and fibrillation in patients with advanced structural heart disease. The compound is therefore likely to exert a broad spectrum of antiarrhythmic actions in ventricular arrhythmias.