Interplay between ephaptic coupling and complex geometry of border zone during acute myocardial ischemia: Effect on arrhythmogeneity

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Abstract

Acute myocardial ischemia is an imbalance between myocardial blood supply and demand, which is caused by the cessation of blood flow within the heart resulting from an obstruction in one of the major coronary arteries. A severe blockage may result in a region of nonperfused tissue known as ischemic core (IC). As a result, a border zone (BZ) between perfused and nonperfused regions is created due to differences in blood and oxygen supplies. Recent experimental findings reveal a complex "finger-like" geometry in BZ; however, its effect on arrhythmogenicity is not clear. Ephaptic coupling, which relies on the intercalated disk between cell ends, has been suggested to play an active role in mediating intercellular electrical communication when gap junctions are impaired. In this paper, we explored the interplay between ephaptic coupling and the geometry of BZ on action potential propagation across the ischemic region. Our study shows that ephaptic coupling can greatly suppress the occurrence of a conduction block, which points to its beneficial effect. The beneficial effect of ephaptic coupling is more evident in BZ with the "finger-like" geometry. In addition, the complex geometry of BZ, i.e., more frequent, deeper, and wider "fingers," promotes the conduction through the ischemic region. In contrast, the larger size of IC impedes the cardiac conduction across the ischemic region. Our results also show that ephaptic coupling promotes the impact of the complex geometry of BZ on signal propagation; however, it inhibits the impact of IC size.

Original languageEnglish (US)
Article number033111
JournalChaos
Volume30
Issue number3
DOIs
StatePublished - Mar 1 2020

Bibliographical note

Funding Information:
This study was funded by the National Science Foundation (NSF) (No. DCSD 1662250) (E.G.T.) and the Institute for Engineering and Medicine at the University of Minnesota grants (E.G.T.).

Publisher Copyright:
© 2020 Author(s).

Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.

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