Abstract
Mechano-electric feedback affects the electrophysiological and mechanical function of the heart and the cellular, tissue, and organ properties. To determine the main factors that contribute to this effect, this study investigated the changes in the action potential characteristics of the ventricle during contraction. A model of stretch-activated channels was incorporated into a three-dimensional multiscale model of the contracting ventricle to assess the effect of different preload lengths on the electrophysiological behavior. The model describes the initiation and propagation of the electrical impulse, as well as the passive (stretch) and active (contraction) changes in the cardiac mechanics. Simulations were performed to quantify the relationship between the cellular activation and recovery patterns as well as the action potential durations at different preload lengths in normal and heart failure pathological conditions. The simulation results showed that heart failure significantly affected the excitation propagation parameters compared to normal condition. The results showed that the mechano-electrical feedback effects appear to be most important in failing hearts with low ejection fraction.
Highlights
Investigating the effects of intracellular electromechanical coupling and mechano-electric feedback (MEF) on myocardial function and its contribution to arrhythmogenesis is of great importance
The results showed that the mechano-electrical feedback effects appear to be most important in failing hearts with low ejection fraction
We investigated the effects of mechano-electric coupling in the heart at the system level using a previously developed 3D multiscale model of the contracting ventricle [14]
Summary
Investigating the effects of intracellular electromechanical coupling and mechano-electric feedback (MEF) on myocardial function and its contribution to arrhythmogenesis is of great importance. Changes in the electrophysiological behavior explained by stretch-activated channels (SACs) were observed experimentally [1,2,3]. Several strongly coupled electromechanical models of the ventricles described mechanical deformation triggered by electrical activation with consideration of the MEF [8,9,10,11]. Such studies typically demonstrate the effect of mechano-electric coupling via the SACs in terms of arrhythmogenesis without taking into account load induced electrophysiological changes. The alterations of ventricular loading conditions may provide a basis for initiation of arrhythmia as observed in experimental studies [12,13]
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