Short-term cardiac memory and mother rotor fibrillation

University of California, Los Angeles (UCLA) Cardiovascular Research Laboratory, Departments of Medicine (Cardiology), Physiology, and Physiological Sciences, David Geffen School of Medicine at UCLA, Los Angeles, California Submitted 2 September 2005 ; accepted in final form 18 June 2006 Short-term...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2007-01, Vol.292 (1), p.H180-H189
Hauptverfasser: Baher, Ali, Qu, Zhilin, Hayatdavoudi, Ashkan, Lamp, Scott T, Yang, Ming-Jim, Xie, Fagen, Turner, Stephen, Garfinkel, Alan, Weiss, James N
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container_issue 1
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container_title American journal of physiology. Heart and circulatory physiology
container_volume 292
creator Baher, Ali
Qu, Zhilin
Hayatdavoudi, Ashkan
Lamp, Scott T
Yang, Ming-Jim
Xie, Fagen
Turner, Stephen
Garfinkel, Alan
Weiss, James N
description University of California, Los Angeles (UCLA) Cardiovascular Research Laboratory, Departments of Medicine (Cardiology), Physiology, and Physiological Sciences, David Geffen School of Medicine at UCLA, Los Angeles, California Submitted 2 September 2005 ; accepted in final form 18 June 2006 Short-term cardiac memory refers to the effects of pacing history on action potential duration (APD). Although the ionic mechanisms for short-term memory occurring over many heartbeats (also called APD accommodation) are poorly understood, they may have important effects on reentry and fibrillation. To explore this issue, we incorporated a generic memory current into the Phase I Luo and Rudy action potential model, which lacks short-term memory. The properties of this current were matched to simulate quantitatively human ventricular monophasic action potential accommodation. We show that, theoretically, short-term memory can resolve the paradox of how mother rotor fibrillation is initiated in heterogeneous tissue by physiological pacing. In simulated heterogeneous two-dimensional tissue and three-dimensional ventricles containing an inward rectifier K + current gradient, short-term memory could spontaneously convert multiple wavelet fibrillation to mother rotor fibrillation or to a mixture of both fibrillation types. This was due to progressive acceleration and stabilization of rotors as accumulation of memory shortened APD and flattened APD restitution slope nonuniformly throughout the tissue. ventricular fibrillation; mathematical modeling; electrical restitution; action potential accommodation Address for reprint requests and other correspondence: J. N. Weiss, David Geffen School of Medicine at UCLA, Division of Cardiology, 47-123 CHS, 10833 LeConte Ave., Los Angeles, CA 90095-1679 (e-mail: jweiss{at}mednet.ucla.edu )
doi_str_mv 10.1152/ajpheart.00944.2005
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Although the ionic mechanisms for short-term memory occurring over many heartbeats (also called APD accommodation) are poorly understood, they may have important effects on reentry and fibrillation. To explore this issue, we incorporated a generic memory current into the Phase I Luo and Rudy action potential model, which lacks short-term memory. The properties of this current were matched to simulate quantitatively human ventricular monophasic action potential accommodation. We show that, theoretically, short-term memory can resolve the paradox of how mother rotor fibrillation is initiated in heterogeneous tissue by physiological pacing. In simulated heterogeneous two-dimensional tissue and three-dimensional ventricles containing an inward rectifier K + current gradient, short-term memory could spontaneously convert multiple wavelet fibrillation to mother rotor fibrillation or to a mixture of both fibrillation types. This was due to progressive acceleration and stabilization of rotors as accumulation of memory shortened APD and flattened APD restitution slope nonuniformly throughout the tissue. ventricular fibrillation; mathematical modeling; electrical restitution; action potential accommodation Address for reprint requests and other correspondence: J. N. 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To explore this issue, we incorporated a generic memory current into the Phase I Luo and Rudy action potential model, which lacks short-term memory. The properties of this current were matched to simulate quantitatively human ventricular monophasic action potential accommodation. We show that, theoretically, short-term memory can resolve the paradox of how mother rotor fibrillation is initiated in heterogeneous tissue by physiological pacing. In simulated heterogeneous two-dimensional tissue and three-dimensional ventricles containing an inward rectifier K + current gradient, short-term memory could spontaneously convert multiple wavelet fibrillation to mother rotor fibrillation or to a mixture of both fibrillation types. 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subjects Action Potentials
Adaptation, Physiological
Animals
Cardiac arrhythmia
Cardiology
Cardiovascular system
Computer Simulation
Heart
Heart Conduction System - physiopathology
Models, Cardiovascular
Rabbits
Ventricular Fibrillation - physiopathology
title Short-term cardiac memory and mother rotor fibrillation
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