Supraventricular arrhythmias in experimental myocardial infarction

The electrophysiological mechanisms underlying supraventricular dysrhythmias that accompany acute myocardial infarction were studied in rabbits subjected to ligation of right coronary artery. In vivo, sinus bradycardia, atrioventricular block and rapid atrial arrhythmias were observed 2 to 5 hours after coronary occlusion; evidence of ventricular arrhythmias was absent. The bradyarrhythmias were markedly improved after iv administration of atropine. The infarcted hearts were then removed and the isolated sinoatrial (SA) node, right atrium and atrioventricular (AV) node were studied with intracellular microelectrodes in vitro. Rapid, repetitive atrial depolarizations occurring spontaneously or initiated by premature atrial stimulation were observed only in preparations obtained from infarcted hearts. In disseminated areas localized within the SA node and the atrium, the subendocardial fibers had a reduced action potential amplitude but showed also normal potentials in other regions as compared with noninfarcted preparations. Sinus rate, poststimulatory sinus-node recovery time, intraatrial conduction and the parameters of AV nodal function including action potential amplitude and conduction were not significantly different in preparations isolated from infarcted and noninfarcted hearts. The results suggest that the observed bradyarrhythmias accompanying acute myocardial infarction may be partly due to a vagomimetic reflex whereas the supraventricular tachycardias seem to result from direct cellular damage.