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Accelerated atrioventricular conduction appearing during acute myocardial infarction.

Fourteen out of 976 patients (1.4 percent) developed accelerated atrioventricular conduction during the course of acute myocardial infarction. Seven (50 percent) had an anterior myocardial infarction, six (42.8 percent) had an inferior myocardial infarction, and one (7.1 percent) had combined anterior and inferior myocardial infarctions. In 85.7 percent, the short PR developed within the first 48 hours that followed the onset of symptoms of acute infarction. One patient (7.1 percent) died during hospitalization, and the other 13 patients were alive at follow-up. In 58.3 percent, the abbreviated PR segment persisted. At follow-up, one patient had multiple ventricular premature beats, but none had supraventricular arrhythmias. Possible mechanisms responsible for accelerated atrioventricular conduction in this setting are discussed. In 41.7 percent of our cases in whom the PR reverted to normal, it is suggested that the causative mechanism was transient, namely ischemia or autonomic imbalance, related to the acute illness. In seven patients (58.3 percent) in whom the short PR persisted without increase in the incidence of supraventricular tachycardias, we postulate that the abbreviated PR is consequent to partial infarction of the atrioventricular node reducing the available tissue responsible for the normal nodal delay. The appearance of a short PR in the course of acute myocardial infarction had no undesirable hemodynamic or arrhythmic consequences, and the short-term and long-term prognoses were unaffected in this series.