Virtual electrode-induced phase singularity in a rabbit model of chronic myocardial infarction

Shock-induced vulnerability and defibrillation have been mostly studied in a structurally normal heart, rarely the case in clinical settings. Increased vulnerability has been reported during ischemia, which is likely to contribute to defibrillation failure. The purpose of this study is to examine the mechanism of increased vulnerability after myocardial infarction (MI). Ligation of the marginal branch of the left circumflex artery in rabbits was done 1-6 weeks before acute experiments. Epicardial electrical activity of Langendorff-perfused hearts (n=4) was optically mapped before, during and after 8-ms monophasic shocks (150 microF) applied during T-wave from a right ventricular lead. Histology revealed that ligation consistently resulted in a discrete left ventricular apical infarction with a border zone (BZ) characterized by action potential shortening. Cathodal shocks produced the virtual electrode polarization pattern with an area of positive polarization near the shock lead and an adjacent area of negative polarization (de-excitation area). Maximum transmembrane voltage gradient was located in the BZ. The resulting postshock break-excitation wavefronts consistently originated at this gradient and propagated toward the base, forming a sustained reentrant arrhythmia. It was concluded that regional MI provides the substrate for increased vulnerability via virtual electrode-induced phase singularity, which originates in the BZ. This may contribute to defibrillation failure.