Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia. Export

@article{citeulike:363075, abstract = {OBJECTIVES: 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.}, address = {Tulane University, New Orleans, Louisiana 70118, USA. blanca@tulane.edu}, author = {Rodr\'{\i}guez, B. and Tice, B. M. and Eason, J. C. and Aguel, F. and Trayanova, N.}, citeulike-article-id = {363075}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.hrthm.2004.08.018}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15851241}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15851241}, doi = {10.1016/j.hrthm.2004.08.018}, issn = {1547-5271}, journal = {Heart Rhythm}, keywords = {blanca, cardiac, defibrillation, ischemia, mine, vulnerability}, month = {December}, number = {6}, pages = {695--703}, posted-at = {2005-10-23 15:48:32}, priority = {0}, title = {Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia.}, url = {http://dx.doi.org/10.1016/j.hrthm.2004.08.018}, volume = {1}, year = {2004} }

TY - JOUR ID - citeulike:363075 L3 - citeulike-article-id:363075 N2 - OBJECTIVES: 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. IS - 6 JF - Heart Rhythm SN - 1547-5271 AD - Tulane University, New Orleans, Louisiana 70118, USA. blanca@tulane.edu EP - 703 TI - Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia. VL - 1 SP - 695 KW - blanca KW - cardiac KW - defibrillation KW - ischemia KW - mine KW - vulnerability AU - Rodríguez, B AU - Tice, BM AU - Eason, JC AU - Aguel, F AU - Trayanova, N PY - 2004/12// UR - http://dx.doi.org/10.1016/j.hrthm.2004.08.018 ER -