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James C Eason

Publications and source records attributed to James C Eason.

5 recordsLinked to original sources
PubMed2004

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

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.

Action Potentials↗
PubMed2003

Mechanistic inquiry into decrease in probability of defibrillation success with increase in complexity of preshock reentrant activity.

Energy requirements for successful antiarrhythmia shocks are arrhythmia specific. However, it remains unclear why the probability of shock success decreases with increasing arrhythmia complexity. The goal of this research was to determine whether a diminished probability of shock success results from an increased number of functional reentrant circuits in the myocardium, and if so, to identify the responsible mechanisms. To achieve this goal, we assessed shock efficacy in a bidomain defibrillation model of a 4-mm-thick slice of canine ventricles. Shocks were applied between a right ventricular cathode and a distant anode to terminate either a single scroll wave (SSW) or multiple scroll waves (MSWs). From the 160 simulations conducted, dose-response curves were constructed for shocks given to SSWs and MSWs. The shock strength that yielded a 50% probability of success (ED(50)) for SSWs was found to be 13% less than that for MSWs, which indicates that a larger number of functional reentries results in an increased defibrillation threshold. The results also demonstrate that an isoelectric window exists after both failed and successful shocks; however, shocks of strength near the ED(50) value that were given to SSWs resulted in 16.3% longer isoelectric window durations than the same shocks delivered to MSWs. Mechanistic inquiry into these findings reveals that the two main factors underlying the observed relationships are 1) smaller virtual electrode polarizations in the tissue depth, and 2) differences in preshock tissue state. As a result of these factors, intramural excitable pathways leading to delayed breakthrough on the surface were formed earlier after shocks given to MSWs compared with SSWs and thus resulted in a lower defibrillation threshold for shocks given to SSWs.

Animals↗
PubMed2003

Postshock arrhythmogenesis in a slice of the canine heart.

INTRODUCTION: Recent evidence has demonstrated that defibrillation shocks terminate or reset reentrant activity in the myocardium through the generation of virtual electrode polarization (VEP). Previous research has revealed that the shock establishes phase singularities (PSs) in the tissue via the VEP mechanism. The aim of this study was to examine, as a function of shock strength and electrode configuration, the relationship between end-shock PSs and the reentrant circuits established after failed defibrillation attempts. METHODS AND RESULTS: The study uses a complex three-dimensional finite-element bidomain model of a slice of the canine heart characterized by realistic geometry and fiber architecture and undergoing a single scroll wave. Defibrillation shocks of increasing strength are delivered through three different electrode configurations. The results demonstrated that >98% of all PSs have a lifetime of half a reentrant cycle or less. Stronger shocks result in a faster rate of annihilation of postshock PSs. For failed shocks, the surviving PSs underlie the activity of one or more scroll waves, which remain stationary in the slice. For all electrode configurations tested, the increase in shock strength leads to a rapid initial increase in the number of postshock reentries followed by a slower decrease; similar behavior is observed with regard to end-shock PSs. CONCLUSION: These results present new evidence regarding the mechanisms underlying failure of defibrillation shocks.

Animals↗
PubMed2002

Termination of reentry by a long-lasting AC shock in a slice of canine heart: a computational study.

INTRODUCTION: A heart in fibrillation can be entrained by long-lasting alternating current (AC) stimuli, leading to defibrillation. To investigate the role entrainment plays in defibrillation, computer simulations of AC cardioversion in a three-dimensional slice of the canine heart were performed. METHODS AND RESULTS: A bidomain finite element model of a 1-mm thick slice across the ventricles of a canine heart was used to simulate termination of transmural reentry with AC shocks. Cardioversion defibrillation thresholds (DFTs) were determined for 200-msec (L) AC shocks at varying frequencies. At the DFT, the entire tissue is entrained by the AC shock. DFT decreases as the frequency of the long-lasting AC shock increases. We hypothesize that this decrease is due to the short period of the high-frequency AC waveform, leaving strong virtual electrode polarization (VEP) after the shock ends. To test this hypothesis, the end-shock VEP were compared for different frequencies, demonstrating stronger polarization as frequency increased. To examine whether entrainment by the long-lasting AC shock contributes to the VEP at the end of the shock, additional simulations were conducted using single-period (Z) AC waveforms. Z waveform DFTs were higher than L waveform DFTs; the Z waveform VEP was weaker than the L waveform VEP at the same frequency. This indicates that entrainment contributes to the development of stronger VEP and, thus, to lower DFT at high frequencies. CONCLUSION: This study offers for the first time a mechanistic insight into cardioversion with long-lasting AC shocks.

Animals↗