Abstract
The accurate propagation of action potentials is indispensable for normal contractile function of the heart. The underlying mechanism of action potential propagation under physiological conditions has been explained by the gap junction responsible for electrical interaction between cardiomyocytes. However, many phenomena under pathological conditions cannot be explained by the gap junctional mechanism. Therefore, the presence of an alternative mechanism besides the gap junctional mechanism has been suggested. In this review, we introduce simulations of action potential propagation in a myofiber model incorporating a novel mechanism resulting from the morphology of cardiomyocytes and the subcellular distributions of functional proteins such as ion channels and transporters, in addition to the conventional gap junctional mechanism. It is possible that the novel conduction mechanism incorporating subcellular distributions of functional proteins plays an important role in homeostasis of excitation propagation in the diseased heart.
