HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/6/H2078    most recent 01175.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Rodríguez, B. Articles by Trayanova, N. Search for Related Content PubMed PubMed Citation Articles by Rodríguez, B. Articles by Trayanova, N.

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study

¹Tulane University, New Orleans, Louisiana 70118; ²Washington and Lee University, Lexington, Virginia 24450; ³Johns Hopkins University, Baltimore, Maryland 21218; and ⁴Universidad Politécnica de Valencia, 46022 Valencia, Spain

Submitted 11 December 2003 ; accepted in final form 11 December 2004

The goal of this modeling research is to provide mechanistic insight into the effect of altered membrane kinetics associated with 5–12 min of acute global ischemia on the upper limit of cardiac vulnerability (ULV) to electric shocks. We simulate electrical activity in a finite-element bidomain model of a 4-mm-thick slice through the canine ventricles that incorporates realistic geometry and fiber architecture. Global acute ischemia is represented by changes in membrane dynamics due to hyperkalemia, acidosis, and hypoxia. Two stages of acute ischemia are simulated corresponding to 5–7 min (stage 1) and 10–12 min (stage 2) after the onset of ischemia. Monophasic shocks are delivered in normoxia and ischemia over a range of coupling intervals, and their outcomes are examined to determine the highest shock strength that resulted in induction of reentrant arrhythmia. Our results demonstrate that acute ischemia stage 1 results in ULV reduction to 0.8A from its normoxic value of 1.4A. In contrast, no arrhythmia is induced regardless of shock strength in acute ischemia stage 2. An investigation of mechanisms underlying this behavior revealed that decreased postshock refractoriness resulting mainly from 1) ischemic electrophysiological substrate and 2) decrease in the extent of areas positively-polarized by the shock is responsible for the change in ULV during stage 1. In contrast, conduction failure is the main cause for the lack of vulnerability in acute ischemia stage 2. The insight provided by this study furthers our understanding of mechanisms by which acute ischemia-induced changes at the ionic level modulate cardiac vulnerability to electric shocks.

ionic channels; computer simulations; arrhythmias

This article has been cited by other articles:

				B. M. Tice, B. Rodriguez, J. Eason, and N. Trayanova Mechanistic investigation into the arrhythmogenic role of transmural heterogeneities in regional ischaemia phase 1A Europace, November 1, 2007; 9(suppl_6): vi46 - vi58. [Abstract] [Full Text] [PDF]

				N. Trayanova Defibrillation of the heart: insights into mechanisms from modelling studies Exp Physiol, March 1, 2006; 91(2): 323 - 337. [Abstract] [Full Text] [PDF]