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TITLE Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia
AUTHORS Blanca Rodríguez, Brock Tice, James Eason, Felipe Aguel, and Natalia Trayanova
ABSTRACT Objective: The goal of this study is to characterize the changes in vulnerability to electric shocks during phase 1A of global ischemia in the rabbit ventricles and to provide understanding of the mechanisms responsible for these changes.
Background: Mechanisms responsible for the changes in cardiac vulnerability over the course of ischemia phase 1A remain poorly understood. This is due to the rapid ischemic change in cardiac electrophysiological properties, which renders experimental evaluation of vulnerability difficult.
Methods: To examine dynamic changes in vulnerability to electric shocks over the course of acute global ischemia phase 1A, this study uses a three-dimensional anatomically-accurate bidomain model of ischemic rabbit ventricles. Monophasic shocks are applied at various coupling intervals to construct vulnerability grids in normoxia and at various stages of ischemia phase 1A.
Results: Our simulations demonstrate that 2-3min after the onset of ischemia, the upper limit of vulnerability remains at its normoxic value, 12.75 V/cm, however, arrhythmias are induced at shorter coupling intervals. As ischemia progresses, the upper limit of vulnerability decreases, reaching 6.4 V/cm in the advanced stage of ischemia phase 1A, and the vulnerable window shifts towards longer coupling intervals.
Conclusions: Changes in the upper limit of vulnerability are due to an increase in the spatial extent of the shock-end excitation wavefronts and the slower recovery from shock-induced positive polarization. Shifts in the vulnerable window stem from decreases in local repolarization times and the occurrence of post-shock conduction failure caused by prolonged post-repolarization refractoriness.
FIGURES

© CCEL 2005
Johns Hopkins University

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Vulnerability grids for normoxia and ischemia. Dark and light gray areas represent episodes of sustained and unsustained reentries, respectively.
MOVIES

© CCEL 2005
Johns Hopkins University

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Postshock electrical activity in normoxia and intermediate and advanced ischemia following a shock of strength 6.4, 9.6 and 6.4 V/cm respectively applied at CIULV.