Suppression of longitudinal versus transverse conduction by sodium channel block: Effects of sodium bolus

Abstract

Background. Arrhythmias resulting from treatment with sodium channel-blocking antiarrhythmic drugs have been successfully treated with sodium infusion, although the mechanism underlying this effect is uncertain. Methods and Results. In this study, we used a multielectrode array to examine the effects of O-desmethyl encainide (ODE), a potent sodium channel-blocking metabolite of encainide, on conduction in canine ventricle. ODE depressed both longitudinal and transverse conduction velocities in a plasma concentration-related fashion (r=-0.74, -0.60; p<0.001). At ODE concentrations ≤300 ng/ml (n=34), conduction velocity was depressed to the same extent in the longitudinal (-21.9±8.4%, SD) and transverse orientations (-22.0±8.8%). However, at concentrations >300 ng/ml (n=17), conduction was significantly more impaired longitudinally than transversely (-44.5±11.7% versus -34.4±13.7%, p<0.02). In 12 animals with high concentrations (mean, 432±32 ng/ml), a 5-meq/kg bolus of sodium chloride over 1 minute immediately increased conduction velocity; this effect was significantly greater and longer lasting in the longitudinal orientation. In two animals, conduction block in the longitudinal orientation was documented at high plasma ODE and was immediately reversed by sodium bolus. Conclusions. We conclude that the major effect of sodium in animals with excess sodium channel block is improvement of longitudinal propagation; this effect may underlie the antiarrhythmic action of sodium in the analogous clinical setting.