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Heterogeneous mechanical dyskinesis during acute myocardial ischaemia isthought to contribute to arrhythmogenic alterations to cardiacelectrophysiology. Various forms of mechano-electric coupling (MEC) mechanismshave been suggested to contribute to these changes, with two primary mechanismsbeing: (1) myofilament-dependent calcium release events, and (2) the activationof stretch-activated currents (SACs). In this computational investigation, weassessed the collective impact of these processes on mechanically-inducedalternans that create an arrhythmogenic substrate during acute ischaemia. Toappraise the potential involvement of MEC in ischaemia-induced arrhythmias, wedeveloped a coupled model of ventricular myocyte electrophysiology andcontraction including SACs and stretch-dependent calcium buffering and release.The model, reflecting observed electrophysiological changes during ischaemia,was exposed to a series of stretch protocols that replicated both physiologicaland pathological mechanical conditions. Pathologically realistic myofiberstretch variations revealed calcium sensitivity changes dependent onmyofilament, leading to alterations in cytosolic calcium concentrations. Undercalcium overload conditions, these changes resulted in electrical alternans.The study implies that strain impacts cellular electrophysiology throughmyofilament calcium release and SAC opening in ventricular mechano-electricalmodels, parameterised to available data. This supports experimental evidencesuggesting that both calcium-driven instability via MEC and SAC-induced effectscontribute to electrical alternans in acute ischaemia.

An In-Silico Study on Integrated Mechanisms of Mechano-Electric Coupling in Ischaemic Arrhythmogenesis