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Delayed ventricular arrhythmias during acute myocardial ischemia phase 1B are related to a rise in tissue impedance and are most likely sustained in a thin layer of subepicardium. It has been hypothesized that coupling of depressed midmyocardial tissue to the surviving subepicardial layer sets the conditions for reentrant arrhythmias. This hypothesis was verified by means of bidomain simulations on a 3D slab consisting of a normal subepicardial layer coupled to a depressed depolarized midmyocardial layer. The heterogeneity in the coupling was defined by varying the transmural conductivities between the two layers in a circular centrally-located region. The resulting dispersion of effective refractory period in the subepicardium allows for reentry to occur. As uncoupling increases within the circular island, the vulnerability to reentry increases. A higher degree of depolarization in the midmyocardium inhibits the induction of reentry.

Original publication




Conference paper

Publication Date





2272 - 2275


Action Potentials, Animals, Arrhythmias, Cardiac, Computer Simulation, Heart Conduction System, Humans, Models, Cardiovascular, Myocardial Ischemia, Myocytes, Cardiac