Abstract
In recent years, data has become available to support the concept that a selective lengthening of the cardiac action potential (a Class III antiarrhythmic action) by whatever mechanism with an attendant increase in the effective refractory period constitutes a distinct antiarrhythmic mechanism. Such an action is exemplified clinically by hypocalemia and hypothyroidism and pharmacologically by amiodarone, sotalol and bretylium, all of which have other associated features. The N-acetylation of procainamide leads to the pharmacologically active compound, N-acetylprocainamide (NAPA). The loss of propensity to block depolarization with the preservation of the effect on repolarization in the case of NAPA makes the compound a class III antiarrhythmic agent. The process of N-acetylation has also led to longer elimination half-life and predominantly renal excretion with linear kinetics but with the preservation of the antiarrhythmic properties of the parent compound. The electrophysiologic data are consistent with the results of studies which have demonstrated that NAPA has the potential to suppress premature ventricular contractions and prevent spontaneously occurring as well inducible ventricular tachycardia in patients with heart disease. The effects on atria indicate that the drug has the potential to electively reverse atrial flutter and fibrillation to normal rhythm and maintain stability of sinus rhythm. The overall experimental and clinical data warrant further evaluation of NAPA as an antiarrhythmic agent.