Cardiac electrophysiologic effects of etafenone hydrochloride (Dialicor), a new antiarrhythmic agent.

The electrophysiologic effects of etafenone hydrochloride (Dialicor) were studied in isolated rabbit hearts and canine or rabbit cardiac tissues with intracellular microelectrode techniques. The concentration range used was 0.25-10 mg/L, except in experiments with direct addition of etafenone into the tissue bath. Etafenone depressed automaticity in the sinus node, atrioventricular junction and Purkinje fibers at concentrations not affecting the action potential contour. In both atrial and ventricular fibers, etafenone prolonged the action potential duration and total refractory period. The action potential upstroke was slowed and conduction time increased. Higher concentrations reduced the resting potential, causing incomplete depolarization. Atrial action potentials were affected at lower concentrations than ventricular and Purkinje action potentials. Occasi-nally, etafenone produced localized conduction block within the atria, usually sparing internodal conduction. In electrically driven hearts, direct recording of His bundle potential as well as surface electrograms revealed marked prolongation of intraatrial and intranodal conduction times, with some increase in His-Purkinje and ventricular conduction times. Depression of atrioventricular conduction was insignificant under sinus rhythm. Possible therapeutic implications of these electrophysiologic effects are discussed.