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SUMMARY:Colloquium: Ning Wei
DESCRIPTION:The Impact of Ephaptic Coupling and Ionic Electrodiffusion on Arrhythmogenesis in the Heart\nNing Wei\nAssistant Professor\nPurdue University \nCardiac myocytes synchronize through electrical signaling to contract heart muscles\, facilitated by gap junctions (GJs) in the intercalated disc (ID). GJs provide low-resistance pathways for electrical impulse propagation between myocytes\, serving as the primary mechanism for electrical communication in the heart. However\, research indicates that conduction can persist without GJs. For instance\, GJ knockout mice still exhibit slow\, discontinuous electrical propagation\, suggesting alternative communication mechanisms. Ephaptic coupling (EpC) serves as an alternative way for cell communication\, relying on electrical fields within narrow clefts between neighboring myocytes. Studies show that EpC can enhance conduction velocity (CV) and reduce conduction block (CB)\, especially when GJs are compromised.  Reduced GJs and significant electrochemical gradients are prevalent in various heart diseases. However\, existing models often fail to capture their combined influence on cardiac conduction\, which limits our understanding of both the physiological and pathological aspects of the heart.  Our study aims to address this gap by developing a two-dimensional (2D) multidomain electrodiffusion model that incorporates EpC. This is the first model to capture the dynamics of all ions across multiple domains\, enabling us to reveal the impact of EpC in the heart. In particular\, we investigated the interplay between ionic electrodiffusion and EpC on action potential propagation\, morphology\, electrochemical properties and arrhythmogenesis in both healthy and ischemic hearts. Our findings indicate that ionic electrodiffusion enhances CV and reduces CB under strong EpC. Specifically\, the electrodiffusion of Ca2+ and K+ intensifies the effects of EpC on action potential morphology\, whereas Na+ diffusion mitigates these effects. Ionic electrodiffusion also facilitates action potential propagation into ischemic regions when EpC is substantial. Moreover\, strong EpC can effectively terminate reentry\, prevent its initiation\, and lower the maximum dominant frequency (max DF)\, irrespective of GJ functionality. However\, weak EpC may help counteract proarrhythmic effects when GJ coupling is slightly to moderately reduced\, contributing to the stabilization of conduction patterns.  Additionally\, strong EpC  notably alters ionic concentrations in the cleft\, significantly increasing [K+] and nearly depleting [Ca2+]\, while causing moderate changes in [Na+]. This multidomain electrodiffusion model sheds light on the mechanisms of EpC in the heart. 
URL:/math/event/colloquium-ning-wei/
LOCATION:EMS Building\, E495\, 3200 N Cramer St\, Milwaukee\, WI\, United States
CATEGORIES:Colloquia
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