AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (August 15, 2008). doi:10.1152/ajpheart.00706.2008
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Submitted on July 9, 2008
Revised on July 25, 2008
Accepted on August 11, 2008

Polarity reversal lowers activation time during diastolic field stimulation of the rabbit ventricles: Insights into mechanisms

Mary M Maleckar1, Marcella C. Woods2, Veniamin Y. Sidorov2, Mark R. Holcomb2, David N. Mashburn2, John P Wikswo2, and Natalia A Trayanova1*

1 Johns Hopkins University
2 Vanderbilt University

* To whom correspondence should be addressed. E-mail: ntrayanova{at}jhu.edu.

To fully characterize the mechanisms of defibrillation, it is necessary to understand the response, within the 3D volume of the ventricles, to shocks given in diastole. Studies that have examined diastolic responses conducted measurements on the epicardium or on a transmural surface of the LV wall only. The goal of this study was to use optical imaging experiments and 3D bidomain simulations, including a model of optical mapping, to ascertain the shock-induced virtual electrode and activation patterns throughout the rabbit ventricles following diastolic shocks. We tested the hypothesis that the locations of shock-induced regions of hyperpolarization govern the different diastolic activation patterns for shocks of reversed polarity. In model and experiment, uniform-field monophasic shocks of reversed polarities (cathode over the right ventricle is RV-, reverse polarity is LV-) were applied to the ventricles in diastole. Experiments and simulations revealed that RV- shocks resulted in longer activation times as compared to LV- shocks of the same strength. 3D simulations demonstrated that RV- shocks induced a greater volume of hyperpolarization at shock-end as compared to LV- shocks; most of these hyperpolarized regions were located in the LV. The results of this study indicate that ventricular geometry plays an important role in both the location and size of the shock-induced virtual anodes that determine activation delay during the shock and subsequently affect shock-induced propagation. If regions of hyperpolarization that develop during the shock are sufficiently large, activation delay may persist until shock end.







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