RATE-DEPENDENT ANISOTROPIC CONDUCTION PROPERTY IN THE EPICARDIAL BORDER ZONE OF CANINE MYOCARDIAL INFARCTS AND ITS MODIFICATION BY MORICIZINE

We evaluated anisotropic conduction properties, different conduction v elocities depending on fiber orientation, in normal and infarcted myoc ardium and the effects of moricizine on anisotropic conduction. Variou s cycle lengths of stimulation were applied to 15 mongrel dogs, and ep icardial mapping was performed using a 96-channel mapping electrode. M oricizine was then administered to seven dogs and the same procedure w as performed. Conduction velocities were calculated from these maps. P rogrammed electrical stimulations were performed before and after mori cizine administration to induce ventricular arrhythmias. Before morici zine administration, a rate-dependent decrease in longitudinal conduct ion velocity was observed in the infarcted zone. Moricizine suppressed longitudinal conduction in the normal zone significantly at 300 msec pacing, but not at slower rates. Moricizine at a dose of 4 mg/kg, on t he other hand, suppressed longitudinal conduction in the infarcted zon e significantly at all pacing cycle lengths. The effect of moricizine on transverse conduction was inconsistent. In three dogs, sustained ve ntricular tachycardia (VT) was induced either before or after moricizi ne administration. The mean cycle length of sustained VT was prolonged from 202 msec to 291 msec after 4 mg/kg of moricizine. Thus, the chan ges in cycle length of ventricular tachycardia observed were most like ly the result of slowing of conduction velocity, especially in the lon gitudinal direction, in the infarcted myocardium. We conclude that the electrophysiologic nature of the subacute ischemic model was modified by moricizine, leading to depression of the conduction velocity of lo ngitudinal conduction and the inducibility of ventricular arrhythmias.