INTRODUCTION: Epicardial point stimulation produces nonuniform changes in the transmembrane voltage of surrounding cells with simultaneous occurrence of areas of transient positive and negative polarization. This is the phenomenon of virtual electrode. We sought to characterize the responses of epicardial ventricular tissue to the application of monophasic electric shocks from an internal transvenous implantable cardioverter defibrillator (ICD) lead. METHODS AND RESULTS: Langendorff-perfused rabbit hearts (n = 12) were stained with di-4-ANEPPS. A 9-mm-long distal electrode was placed in the right ventricle. A 6-cm proximal electrode was positioned horizontally 3 cm posteriorly and 1 cm superiorly with respect to the heart. Monophasic anodal and cathodal pulses were produced by discharging a 150-microF capacitor. Shocks were applied either during the plateau phase of an action potential (AP) or during ventricular fibrillation. Leading-edge voltage of the pulse was 50 to 150 V, and the pulse duration was 10 msec. Transmembrane voltage was optically recorded during application of the shock, simultaneously from 256 sites on a 11 x 11 mm area of the anterior right ventricular epicardium directly transmural to the distal electrode. The shock effect was evaluated by determining the difference between the AP affected by the shock and the normal AP. During cathodal stimulation an area of depolarization near the electrode was observed, surrounded by areas of hyperpolarization. The amplitude of polarization gradually decreased in areas far from the electrode. Inverting shock polarity reversed this effect. CONCLUSION: ICD monophasic defibrillation shocks create large dynamically interacting areas of both negative and positive polarization.
INTRODUCTION: Epicardial point stimulation produces nonuniform changes in the transmembrane voltage of surrounding cells with simultaneous occurrence of areas of transient positive and negative polarization. This is the phenomenon of virtual electrode. We sought to characterize the responses of epicardial ventricular tissue to the application of monophasic electric shocks from an internal transvenous implantable cardioverter defibrillator (ICD) lead. METHODS AND RESULTS: Langendorff-perfused rabbit hearts (n = 12) were stained with di-4-ANEPPS. A 9-mm-long distal electrode was placed in the right ventricle. A 6-cm proximal electrode was positioned horizontally 3 cm posteriorly and 1 cm superiorly with respect to the heart. Monophasic anodal and cathodal pulses were produced by discharging a 150-microF capacitor. Shocks were applied either during the plateau phase of an action potential (AP) or during ventricular fibrillation. Leading-edge voltage of the pulse was 50 to 150 V, and the pulse duration was 10 msec. Transmembrane voltage was optically recorded during application of the shock, simultaneously from 256 sites on a 11 x 11 mm area of the anterior right ventricular epicardium directly transmural to the distal electrode. The shock effect was evaluated by determining the difference between the AP affected by the shock and the normal AP. During cathodal stimulation an area of depolarization near the electrode was observed, surrounded by areas of hyperpolarization. The amplitude of polarization gradually decreased in areas far from the electrode. Inverting shock polarity reversed this effect. CONCLUSION:ICD monophasic defibrillation shocks create large dynamically interacting areas of both negative and positive polarization.