Basic and clinical cardiac electrophysiology of encainide

Abstract

Encainide is a potent sodium channel antagonist. It dissociates slowly from blocked, repolarized channels (time constant of recovery greater than 20 seconds). It markedly slows myocardial and His Purkinje conduction in vitro, in animal models and in humans. In vitro the parent compound and its major metabolites, O-demethyl and 3-methoxy-O-demethyl encainide, have variable effects on action potential duration and refractoriness. In man the parent compound has relatively little effect on refractoriness and QT interval, but its metabolites may increase refractoriness moderately. Encainide has no significant effect on the normal sinoatrial node, and only its metabolites significantly depress atrioventricular nodal conduction and refractoriness. In models of ischemia, all of encainide's actions are more pronounced in ischemic than in normal tissue. Encainide is similar in its basic and clinical electrophysiologic profile to flecainide and lorcainide although its constellation of electrophysiologic properties is unique. It differs from quinidine, procainamide and disopyramide by slowing conduction more and affecting refractoriness less, and by absence of anticholinergic side effects.