Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia.
OBJECTIVE
The purpose 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 determine 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. The lack of understanding results from the rapid ischemic change in cardiac electrophysiologic 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 used 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 to 3 minutes 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 result from 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 postshock conduction failure caused by prolonged postrepolarization refractoriness.
Rodríguez
Blanca
B
Tulane University, New Orleans, Louisiana 70118, USA. blanca@tulane.edu
Tice
Brock M
BM
Eason
James C
JC
Aguel
Felipe
F
Trayanova
Natalia
N
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D003198:Computer Simulation; D004554:Electric Countershock; D006329:Heart Conduction System / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology*; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011817:Rabbits