Decreased ephaptic coupling depresses cardiac excitability and slows conduction

Excitability in cardiomyocytes is dependent on the subthreshold current required to raise transmembrane potential to the activation threshold and subsequent recruitment of voltage gated sodium channels to trigger an action potential. Conduction in cardiomyocytes is dependent on the robustness and speed of action potential propagating through tissue. Both are equally important for normal heart function. Cardiac sodium channels are densely expressed in the intercalated disc within the perinexal nanodomain, which is two orders of magnitude narrower than bulk extracellular interstitium.