Arrhythmias in the first hours of acute myocardial infarction

Abstract

R EPORTS of arrhythmias complicating myocardial infarction usually concern those observed in the Coronary Care Unit (CCU). However, the median time between the onset of symptoms and admission to a CCU may be more than 8 hr.’ In an endeavor to document the incidence of arrhythmia in the acute phase of infarction and to obtain information about their etiology, a prospective study was made of 294 patients who were observed and monitored within 1 hr after the onset of chest pain. A high incidence of arrhythmias was observed among the 294 patients (Table 1). Bradyarrhythmia within the first hour occurred in 34% and was most frequent among patients with posterior infarction (Table 2). When atrioventricular block developed in patients with posterior infarction, it was apparent within the first hour. Ventricular ectopic beats occurred in 93% of patients within 4 hr. Ventricular tachycardia and supraventricular tachycardia were comparatively uncommon during the acute phase. The incidence of ventricular fibrillation among 294 patients observed within 1 hr of the onset of infarction was 19%. Among the 55 who developed ventricular fibrillation, 41 (75%) did so within 2 hr and 46 (84%) within 4 hr of the onset of chest pain (Fig. 1). Those who developed ventricular fibrillation often did so without warning ventricular ectopic activity or despite apparently adequate antiarrhythmic therapy. Others workers have also questioned the value of warning ventricular ectopic activity in predicting ventricular fibrillation. Prophylactic antiarrhythmic agents appeared less successful in the acute phase of myocardial infarction than when given later. Assessment of the autonomic nervous system at the onset of infarction was attempted, since it was postulated that a relationship might exist between ventricular arrhythmias and autonomic dysfunction. Assessment was impossible in those patients who presented with ventricular fibrillation, ventricular tachycardia, or supraventricular tachycardia and in those who have been on digitalis or beta-blocking drugs prior to the onset of acute infarction. Patients with a history of hypertension and those with left bundle branch block or combined anterior and posterior infarction were also excluded. Analysis of autonomic status was therefore limited to 240 of the 294 patients and was based on analysis of blood pressure and heart rate data. Patients with sinus tachycardia at the initial examination were considered to have sympathetic overactivity. Transient hypertension (blood pressure 160/l 00 mm Hg or greater) in the absence of sinus tachycardia was also regarded as evidence of sympathetic overactivity, as a sympathetic pressor response with minimal alteration in heart rate has been described.2.3 Patients with sinus bradycardia or atrioventricular block (second degree or complete) were considered to show parasympathetic overactivity. Transient hypotension (systolic blood pressure 100 mm Hg or less) in the absence of bradycardia was also regarded as evidence of parasympathetic overactivity. Eighty-nine of the 240 patients were seen within 30 min. Only 15 (I 7%) of the 89 had a normal heart rate and a normal blood pressure when first seen (Fig. 2). Over one-third showed evidence of sympathetic overactivity. Parasympathetic overactivity was present in almost half the patients. The systolic blood pressure at the initial examination was not greater than 80 mm Hg in nearly one-quarter of the patients. Forty seven percent of the patients with bradyarrhythmia had a systolic blood pressure not greater than 80 mm Hg. Eight percent of all patients seen within 30 min had complete atrioventricular block; none of these had a systolic blood pressure greater than 80 mm Hg. The mean heart rates and blood pressures are shown in Table 3. The incidence of autonomic disturbance was related to the site of infarction (Fig. 3). Para-