Computational models of human ventricular cells demonstrated that ectopic excitation can be triggered by after-depolarizations and up/down regulation of specific membrane conductance systems.
Computational modeling provides insights into the cellular and tissue-level requirements for the initiation and propagation of ventricular ectopic beats.
Cardiac ventricular cells and tissues are normally excitable, and are activated by propagating waves of excitation that are initiated in the specialized pacemaking region of the heart. However, isolated or repetitive activity can be initiated at abnormal (ectopic) sites in the ventricles. To trigger an endogenous ectopic beat, there must be a compact focus of cells with changed membrane excitation parameters and kinetics, which initiate activity by after-depolarizations triggered by propagating activity, or that have bifurcated into autorhythmicity. This ectopic focus needs to be large enough, and adequately coupled, to drive the surrounding tissue. We investigate the initiation of ectopic excitation in computational models of human ventricular cells triggered by after-depolarizations and by up/down regulation of specific membrane conductance systems, and the propagation and evolution of ectopic activity in homogeneous or heterogeneous and isotropic, anisotropic, or orthotropic tissues.
Benson et al. (Thu,) conducted a other in Ectopic activation of the ventricles. Computational models of human ventricular cells was evaluated on Initiation, propagation, and evolution of ectopic excitation. Computational models of human ventricular cells demonstrated that ectopic excitation can be triggered by after-depolarizations and up/down regulation of specific membrane conductance systems.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: