Abstract 1360: Low Electroporation Threshold, Conduction Block, Focal Activity and Reentrant Arrhythmia in the Rabbit Atria: Possible Mechanisms of Stunning and Defibrillation Failure
Electric shock is an effective therapy against atrial and ventricular fibrillation. However, shock may induce electroporation. We hypothesized that electroporation can lead to arrhythmia due to conduction block and abnormal focal activity in the intact heart. We investigated the effect of electroporation on atrial and ventricular electrical activity using optical mapping from a 10×10mm field of view containing an area 6 mm in diameter subjected to 10 ms shocks. Electroporation was produced in the epicardium of Langendorff-perfused rabbit hearts (n=8) by shocks applied during the plateau phase of the action potential (AP). Electroporation was centered at the electrode and was evident from transient diastolic depolarization, and reduction of AP amplitude and upstroke derivative. Conduction slowing and block was observed in this region. Electroporation was voltage and polarity dependent and significantly more pronounced in the atria versus ventricles (p<0.01), with thresholds of 78±20 and 70±19 mA/cm2 versus 258±47 and 182±19 mA/cm2, for anodal and cathodal stimuli, respectively. In atria, shocks of both polarities (312±60 mA/cm2) transiently induced full conduction block, which lead to reentry (n=5) around the inexcitable area (see figure⇓). Our observations are consistent with electroporation-induced ectopic activity as a possible trigger for reentry. We showed that the atria are more vulnerable to electroporation than the ventricles, which may explain atrial predisposition to stunning after defibrillation. Moreover, our results demonstrate a possible mechanism of defibrillation failure by electroporation-induced conduction block and focal activity.