Cardiac Arrhythmias During Myocardial Infarction

Abstract

A 58-year-old man, who had used cocaine and other illicit drugs in the past, had mild, intermittent exertional chest discomfort for 2 weeks followed by severe, prolonged chest pain, which began while he was dancing and was unrelieved by rest. An electrocardiogram recorded on arrival at the emergency department (Figure 1) showed acute inferoposterior myocardial infarction with some features of right coronary arterial occlusion, i.e., ST elevation lead III > lead II and ST depression in lead I, and some features of left circumflex occlusion, i.e., ST depression in leads V1, V2, and aVR (1). Right-sided chest leads showed no significant ST elevation. The cardiac rhythm was marked sinus arrhythmia that did not meet criteria for type I or type II sinoatrial block. The P-R intervals were at the upper limit of normal (0.18 to 0.22 seconds). Over the next several hours, there was minimal sinus arrhythmia. The PR interval varied from 0.42 to 0.18 seconds, and there was further evolution of the changes of inferoposterior myocardial infarction. Figure 1. Electrocardiogram at the time of presentation to the hospital. See text for explication. Twelve hours after the first electrocardiogram, the tracing changed dramatically (Figure 2). Marked sinus arrhythmia was completely dissociated from a regular accelerated idioventricular rhythm, so-called block-acceleration dissociation, i.e., the presence of some degree of atrioventricular block with the atrioventricular dissociation probably being accentuated by the accelerated idioventricular rate (2). Accelerated idioventricular rhythm is common in acute myocardial infarction and, unlike ventricular tachycardia, does not worsen prognosis (3). Figure 2. Electrocardiogram 12 hours after arrival at the hospital. See text for explication. Although the electrocardiogram has features of both right and left circumflex coronary arterial occlusion, two facts suggest the right as the culprit. First, the right is the culprit four times as often as the left circumflex in patients with acute inferior myocardial infarction (1). Second, the artery to the atrioventricular node arises from the right coronary 90% of the time, and any degree of new atrioventricular block suggests the right as the culprit; a caveat here is that inferior myocardial infarction, especially early in its course, often is accompanied by an increase in vagal tone that could be responsible, at least in part, for the atrioventricular block, as well as the marked sinus arrhythmia. Coronary arteriography revealed total occlusion of the right coronary in its mid portion and 90% narrowing of the left circumflex beyond a large first obtuse marginal branch. A bare metal stent was placed in the right coronary artery, and the patient had an uneventful postprocedural course with no further arrhythmia.