Abstract 2829: Degeneration of Ventricular Tachycardia Into Ventricular Fibrillation Following Right Ventricular Dilation
Studies showed that hemodynamics changes during arrhythmias lead to rapid dilation of right ventricle (RV). RV dilation results in a gradient of refractoriness between left ventricle (LV) and RV through mechano-electric feedback (MEF). We hypothesize that the gradient of refractoriness between LV and RV caused by MEF in the dilated RV is responsible for the degradation of ventricular tachycardia (VT) to ventricular fibrillation (VF). We employed a 3D model of rabbit ventricular electromechanics that incorporated a non-selective cationic stretch-activated channel (SAC). To simulate isovolumic ventricular contraction during VT and VF, a heuristic model of calcium dynamics of the cardiac myofilament with accurate force-rate dependence was included. The conductivity of the SAC depended on the magnitude of the local strain. Two different reversal potentials (−60, −10mV) were tested in the model. VT was induced by S1-S2 pacing. RV was dilated to twice its initial volume over a period of 0.5s following S2. Cases without and with RV dilation were compared. S1-S2 pacing resulted in two stable spiral waves, one on the posterior wall and another on the anterior. Breakup of spiral waves occurred only in the case of RV dilation with SAC of −10mV reversal potential. The wave breakup was due to inactivation of Na channels at elevated resting potential mediated by the stretch-induced current. 2s after the onset of arrhythmia, the patterns of VF were organized into a single stable spiral wave in LV lateral wall and multiple reentrant circuits in RV free wall (Fig 1⇓). RV dilation establishes a gradient of refractoriness between RV and LV with the recruitment of SAC, which causes degeneration of VT into VF.