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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.

Type

Journal article

Journal

Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference

Publication Date

01/12/2006

Pages

2280 - 2283