Publications (2)3.2 Total impact
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ABSTRACT: Although the majority of patients undergoing defibrillation suffer from coronary heart disease, little is known about defibrillation in the setting of ischemic disease. The goal of this study is to aid understanding of defibrillation failure in ischemic hearts by studying changes in cardiac vulnerability to electric shocks the first 10 min following LAD occlusion. To do so, a 3D anatomically-accurate electrophysiologically-detailed bidomain model of the regionally ischemic ventricles following LAD occlusion was developed based on experimental data. The ventricles were paced at the apex and truncated exponential monophasic shocks were applied over a range of coupling intervals to determine the upper limit of vulnerability (ULV) and the vulnerable window (VW) in normoxia and 10 min post-occlusion. Simulation results demonstrate that, despite the profound electrophysiological changes in the ischemic region, the ULV remains unchanged 10 min post-occlusion because following high shock strengths gesULV virtual electrode polarization and postshock behavior remain unaffected by ischemia. However, the range of coupling intervals comprising the VW increases from spanning 60 ms in normoxia to 90 ms at 10 min post-occlusion. The increased in vulnerability in regional ischemia stems from the fact that slow conduction and increased dispersion of refractoriness in the ischemic region increase the likelihood of the establishment of a reentrant circuit following shocks of strength<ULV.Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 02/2006; 1:2280-3.
Article: The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks.[show abstract] [hide abstract]
ABSTRACT: Transmural electrophysiological heterogeneities have been shown to contribute to arrhythmia induction in the heart; however, their role in defibrillation failure has never been examined. The goal of this study is to investigate how transmural heterogeneities in ionic currents and gap-junctional coupling contribute to arrhythmia generation following defibrillation strength shocks. This study used a 3D anatomically realistic bidomain model of the rabbit ventricles. Transmural heterogeneity in ionic currents and reduced sub-epicardial intercellular coupling were incorporated based on experimental data. The ventricles were paced apically, and truncated-exponential monophasic shocks of varying strength and timing were applied via large external electrodes. Simulations demonstrate that inclusion of transmural heterogeneity in ionic currents results in an increase in vulnerability to shocks, reflected in the increased upper limit of vulnerability, ULV, and the enlarged vulnerable window, VW. These changes in vulnerability stem from increased post-shock dispersion in repolarisation as it increases the likelihood of establishment of re-entrant circuits. In contrast, reduced sub-epicardial coupling results in decrease in both ULV and VW. This decrease is caused by altered virtual electrode polarisation around the region of sub-epicardal uncoupling, and specifically, by the increase in (1) the amount of positively polarised myocardium at shock-end and (2) the spatial extent of post-shock wavefronts.Progress in Biophysics and Molecular Biology 96(1-3):321-38. · 3.20 Impact Factor