Why the study?
Mechanoelectrical feedback via stretch-activated channels is generally proarrhythmic at high pacing rates, but more studies are needed to elucidate the underlying mechanism.
Does mechanoelectrical feedback modulate cardiac alternans and arrhythmogenesis in a computational model of cardiac tissue?
Does mechanoelectrical feedback modulate cardiac alternans and arrhythmogenesis in a computational model of cardiac tissue?
Mechanoelectrical feedback can promote arrhythmogenesis by inducing spatially discordant alternans and conduction block in a computational model of cardiac tissue.
MEF may promote alternans-related arrhythmias at high rates; leaves open clinical relevance pending experimental validation.
The deformation of the heart tissue due to the contraction can modulate the excitation, a phenomenon referred to as mechanoelectrical feedback (MEF), via stretch-activated channels. The effects of MEF on the electrophysiology at high pacing rates are shown to be proarrhythmic in general. However, more studies need to be done to elucidate the underlying mechanism. In this work, we investigate the effects of MEF on cardiac alternans, which is an alternation in the width of the action potential that typically occurs when the heart is paced at high rates, using a biophysically detailed electromechanical model of cardiac tissue. We observe that the transition from spatially concordant alternans to spatially discordant alternans, which is more arrhythmogenic than concordant alternans, may occur in the presence of MEF and when its strength is sufficiently large. We show that this transition is due to the increase of the dispersion of conduction velocity. In addition, our results also show that the MEF effects, depending on the stretch-activated channels' conductances and reversal potentials, can result in blocking action potential propagation.
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Hazim et al. (2020) studied this question.
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