Electrophysiologic effects and efficacy of recainam for sustained ventricular tachycardia

Abstract

Recainam is an investigational antiarrhythmic drug recently introduced into clinical testing. It is a phenylalkyl urea derivative that produces a concentrationdependent decrease in membrane responsiveness and maximal upstroke velocity.1 The reduction in maximal upstroke velocity displays use-dependence,1 similar to the class 1A drugs. However, unlike class 1A drugs, but similar to class 1B agents, recainam does not prolong action potential duration.1 Other studies demonstrated that recainam slows conduction with minimal effect on ventricular refractoriness,2 effects consistent with a class 1C antiarrhythmic action. Thus, these preliminary investigations suggested that recainam possesses a unique electrophysiologic profile with properties of each of the 3 class 1 subclasses. Other preclinical studies have demonstrated recainam's efficacy in suppressing ventricular arrhythmias in the postinfarction dog model3 and initial clinical studies have demonstrated that it is highly effective in suppressing ventricular premature complexes.4-6 However, no studies to date have reported the electrophysiologic effects of recainam in patients with sustained ventricular tachycardia (VT). Such is the purpose of this report.