Cardiac cells communicate electrically to coordinate heart contractions and pump blood. Gap junctions in the intercalated discs (ID) between myocytes form low-resistance pathways that facilitate electrical propagation. Traditionally, gap junctional coupling is considered the primary mechanism for cell communication, but experimental studies show that conduction can persist even with impaired gap junctions. For example, in gap junction-deficient rats, the heart still shows slow, discontinuous signal propagation, suggesting the existence of other communication mechanisms. One such mechanism is ephaptic coupling (EpC), an electrical field effect in the ID that maintains conduction even in the absence of gap junctions. EpC has been explored experimentally and numerically, especially in altered ID under normal and diseased conditions. However, a lack of direct evidence emphasizes the need to study its physiological role in the heart. Some research indicates that EpC can increase conduction velocity (CV) and reduce conduction failure, but its effects on cardiac arrhythmias are not well understood. Our study focuses on reentry arrhythmia, where rapid, irregular heartbeats can lead to cardiac arrest. Previous modeling work suggests that strong EpC can terminate reentry in ischemic hearts, though the mechanism remains unclear. We aim to investigate the mechanisms underlying reentry termination across different levels of EpC and gap junctional coupling using a two-dimensional discrete bidomain model with EpC. Our results identify two mechanisms: (1) Strong EpC terminates reentry through self-attenuation, driven by inactivation of fast sodium currents and (2) moderate EpC terminates reentry through self-collision, influenced by increased CV and anisotropy. A boundary where termination does not occur is also observed.
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