Mechano-electric feedback significantly reduces the occurrence of delayed afterdepolarization-driven focal activity, affecting premature ventricular contractions.
Computational modeling demonstrates that mechano-electric feedback plays a critical role in reducing the occurrence of delayed-afterdepolarization-driven premature ventricular contractions.
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Delayed afterdepolarizations (DADs), which occur during the diastolic phase of a cardiomyocyte action potential (AP), are frequently observed under specific pathophysiological conditions. The synchronization of DAD-capable myocytes can effectively overcome the inherent source-sink mismatch with adjacent normal myocytes, so it is an important mechanism for the genesis of premature ventricular contractions (PVCs). Our study elucidates the role of mechano-electrical feedback in modulating this critical source-sink requirement and its interplay with diffusional anisotropy in cardiac tissue. We combine the ten Tusscher-Panfilov 06 (TP06) electrophysiological model for human ventricular myocytes with cardiac-tissue-mechanics models and account for spontaneous calcium releases (SCRs) and the randomness associated with these and with the disordered arrangement of DAD myocytes in a clump. Our work leads to a quantification of the time dependence of the intracellular cytosolic calcium transient Ca
Roshan et al. (Tue,) reported a other. Mechano-electric feedback significantly reduces the occurrence of delayed afterdepolarization-driven focal activity, affecting premature ventricular contractions.