Virtual electrode effects in transvenous defibrillation-modulation by structure and interface: evidence from bidomain simulations and optical mapping.

INTRODUCTION Our goal in this combined modeling and experimental study was to gain insight into the transmembrane potential changes in defibrillation conditions, namely, when shocks are delivered by an implantable cardioverter defibrillator (ICD). Two hypotheses concerning the presence and characteristics of virtual electrode effects (VEE) during an ICD shock were tested numerically and experimentally: (H1) anisotropy-dependent VEE are induced over a considerable portion of the "bulk" myocardium; and (H2) surface (epicardial and endocardial) VEE are generated under special tissue bath conditions and are not fully anisotropy determined. METHODS AND RESULTS Optical mapping was performed on Langendorff-perfused rabbit hearts (n = 4) stained with di-4-ANEPPS. Monophasic shocks were applied during the plateau phase of an action potential through a 9-mm long distal electrode in the right or left ventricle and a 6-cm proximal electrode positioned 3 cm posteriorly to the heart. We modeled the experiment using an ellipsoidal bidomain heart with transmural fiber rotation, placed in a perfusing bath, and subjected to defibrillation shocks delivered by an electrode configuration as described. Our numerical simulations demonstrated VEE occupying a significant portion of the myocardium in the conditions of unequal anisotropy ratios for the intra- and extracellular domains. Statistically significant differences in epicardial polarization patterns were predicted numerically and confirmed experimentally when the interface conditions varied. CONCLUSION The present study concludes that VEE are present in transvenous defibrillation. They are shaped by the combined effect of cardiac tissue characteristics and interface conditions. Because of their size, VEE might contribute significantly to defibrillation outcome.