Roles of line stimulation-induced virtual electrodes and action potential prolongation in arrhythmic propagation

Line stimulation across fibers generates a virtual electrode (VE) pattern that consists of adjacent +Vm and -Vm regions. In this study, we evaluated Vm at the break of line stimulation pulses to determine where arrhythmias arise and their propagation direction relative to +Vm and -Vm regions.

We optically mapped the anterior left ventricular epicardium of isolated rabbit hearts (n = 9). Monophasic line stimuli were applied across fibers at various coupling intervals. In 18 of 24 break arrhythmias, i.e., arrhythmias in which propagation occurred after the break but < or = 30 msec postshock, excitation propagated from the border between +Vm and -Vm regions toward the -Vm region (P < 0.05) for either shock polarity, even though locations of positive and negative Vm changed with shock polarity. In 13 of 18 make arrhythmias, i.e., arrhythmias in which propagation occurred before the break, the excitation propagated from the center of the +Vm region toward the -Vm regions (P < 0.05). For late arrhythmias, i.e., arrhythmias in which propagation was found >30 msec postshock, propagation was reversed, i.e., toward the +Vm region (P < 0.01), which was where the positive VE produced action potential prolongation.

The propagation of break, make, and late arrhythmias is spatially related to VEs. The different direction of propagation of late arrhythmias relative to the VEs is explained by the delayed recovery of Vm due to VE-induced action potential prolongation.