Postshock Arrhythmogenesis in a Slice of the Canine Heart

Hillebrenner, Matthew G.; Eason, James; Campbell, Craig; Trayanova, Natalia A.

doi:10.1046/j.1540.8167.90317.x

Cited by 7 publications

(6 citation statements)

References 32 publications

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“…Finally, the electrode configuration was not changed in this study. On the basis of the study by Hillebrenner et al (16), alternate electrode configuration is expected to only affect the value of the ULV and not the mechanisms underlying it. Despite these limitations, this study provides a wealth of information regarding the mechanisms that underlie the changes in electrical vulnerability during acute myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

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

Rodríguez

Tice²,

Eason³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Effect of acute global ischemia on the upper limit of vulnerability: a simulation study. Am J Physiol Heart Circ Physiol 286: H2078 -H2088, 2004. First published January 29, 2004 10.1152/ajpheart.01175.2003The 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 finiteelement 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 ELECTRICAL DEFIBRILLATION is recognized as the most effective therapy against the malignant arrhythmias that lead to sudden cardiac death. However, although the majority of the patients that undergo defibrillation typically suffer from some form of coronary disease, little is known about the effect of acute ischemia on defibrillation efficacy. Experimental studies provide conflicting evidence: some report an increase in defibrillation threshold (DFT) (3,29,38,43), whereas others find no change (5,20,22,32) or even a decrease (2) in DFT during acute ischemia.Numerous studies (5,7,18) have demonstrated that the DFT is strongly linked to the upper limit of vulnerability (ULV) of cardiac tissue to electric shocks. Much research has focused on investigating the mechanisms of cardiac vulnerability in an attempt to better understand how failed defibrillation shocks reinitiate cardiac arrhythmias. During the past decade, experiments using optical mapping techniques (8,12,13,46) and computer simulation studies (25,30,37,41) have significantly improved the understanding of the mechanisms of shockinduced arrhythmogenesis, cul...

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Section: Discussionmentioning

confidence: 99%

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

Rodríguez

Tice²,

Eason³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Tachyarrhythmias were considered sustained if shock-induced reentry lasted for at least 800 ms. Rotor frequencies were determined by taking the inverse of the average cycle length measured over six successive depolarizations at points chosen near, but not in, the rotor core. Phase singularities were detected using the method described by Hillebrenner et al,22 which allowed for analysis of filaments with respect to the PS.…”

Section: Methodsmentioning

confidence: 99%

“…C: Early-stage breakthroughs (0–600 ms) for different PS penetration depths (one-third, as in the rest of this study, compared with full-wall penetration, with endpoints located subepicardially). D: Breakthroughs observed after failed 4 V/cm defibrillation shocks (0–400 ms) with22 and without the PS. Error bars indicate maximum deviation.…”

Section: Figurementioning

confidence: 99%

Arrhythmogenic mechanisms of the Purkinje system during electric shocks: A modeling study

et al. 2009

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Background-The function of the Purkinje system (PS) is to ensure fast and uniform activation of the heart. Although this vital role during sinus rhythm is well understood, this is not the case when shocks are applied to the heart, especially in the case of failed defibrillation. The PS activates differently from the myocardium, has different electrophysiological properties, and provides alternate propagation pathways; thus, there are many ways in which it can contribute to postshock behavior.

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“…Increasing shock strength results in higher voltage gradients across borders between regions of opposite polarity, leading to more break excitations 35 which then traverse the post-shock excitable gap earlier 37 and at a faster velocity, 35 as well as extend the refractoriness of the tissue surrounding the excitable gap to a larger degree, 38 ultimately resulting in termination of all post-shock wavefronts. Finally, modelling studies 39,40 have also demonstrated that the complexity of pre-shock activity is an important factor in the outcome of the defibrillation shock. To ascertain the predictive capabilities of the modelling studies described above, simulation results of defibrillation have been compared with optimal mapping results; to do so, the process of optical mapping was successfully modelled.…”

Section: Computer Modelling Of the High-voltage Defibrillation Procesmentioning

confidence: 99%

New insights into defibrillation of the heart from realistic simulation studies

Trayanova

Rantner

2014

Europace

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Cardiac defibrillation, as accomplished nowadays by automatic, implantable devices, constitutes the most important means of combating sudden cardiac death. Advancing our understanding towards a full appreciation of the mechanisms by which a shock interacts with the heart, particularly under diseased conditions, is a promising approach to achieve an optimal therapy. The aim of this article is to assess the current state-of-the-art in whole-heart defibrillation modelling, focusing on major insights that have been obtained using defibrillation models, primarily those of realistic heart geometry and disease remodelling. The article showcases the contributions that modelling and simulation have made to our understanding of the defibrillation process. The review thus provides an example of biophysically based computational modelling of the heart (i.e. cardiac defibrillation) that has advanced the understanding of cardiac electrophysiological interaction at the organ level, and has the potential to contribute to the betterment of the clinical practice of defibrillation.

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Postshock Arrhythmogenesis in a Slice of the Canine Heart

Abstract: These results present new evidence regarding the mechanisms underlying failure of defibrillation shocks.

Cited by 7 publications

References 32 publications

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

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

Arrhythmogenic mechanisms of the Purkinje system during electric shocks: A modeling study

New insights into defibrillation of the heart from realistic simulation studies

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