Automaticity in ventricular myocyte cell pairs with ephaptic and gap junction coupling.

Spontaneous electrical activity, or automaticity, in the heart is required for normal physiological function. However, irregular automaticity, in particular, originating from the ventricles, can trigger life-threatening cardiac arrhythmias. Thus, understanding mechanisms of automaticity and synchronization is critical. Recent work has proposed that excitable cells coupled via a shared narrow extracellular cleft can mediate coupling, i.e., ephaptic coupling, that promotes automaticity in cell pairs. However, the dynamics of these coupled cells incorporating both ephaptic and gap junction coupling has not been explored. Here, we show that automaticity and synchronization robustly emerges via a Hopf bifurcation from either (i) increasing the fraction of inward rectifying potassium channels (carrying the IK1 current) at the junctional membrane or (ii) by decreasing the cleft volume. Furthermore, we explore how heterogeneity in the fraction of potassium channels between coupled cells can produce automaticity of both cells or neither cell, or more rarely in only one cell (i.e., automaticity without synchronization). Interestingly, gap junction coupling generally has minor effects, with only slight changes in regions of parameter space of automaticity. This work provides insight into potentially new mechanisms that promote spontaneous activity and, thus, triggers for arrhythmias in ventricular tissue.