Atropine and Acute Myocardial Infarction

To the Editor: In a recent paper by Epstein et al.,' a comparison was made between our study2' 3 and that of Scherlag et al.4 on the relationship between heart rate and the likelihood of ventricular ectopic activity during coronary occlusion in dogs. The paper indicated that, in contrast to our results, Scherlag et al. found that increasing heart rate during coronary occlusion provoked ventricular arrhythmias and fibrillation, and vagal stimulation often reduced ventricular ectopic activity. I would like to point out that these two studies are markedly different in experimental design and, therefore, are not comparable. We observed the incidence of ventricular premature beats within 5 min of the start of coronary occlusion at various heart rates between 75 and 150/min. In most instances the duration of occlusion was 1-3 min since the arterial clamp was removed immediately with the appearance of ventricular premature beats. In the study of Scherlag et al., ventricular tachycardia or fibrillation was provoked by increasing heart rate to 200/min by atrial pacing during coronary occlusion of longer durations lasting up to 20 min. As previously observed by US,5-7 the effects of coronary occlusion on electrophysiologic properties of the ventricular myocardium are variable depending on the time of observation relative to the start of occlusion. Coronary occlusion produces an initial decrease in diastolic threshold, refractory period, and conduction time in the affected area within 2-3 min after the start of occlusion, followed by a marked increase in these parameters with the continuation of occlusion. It is possible that excitability and conductivity are initially increased because of moderate myocardial ischemia, but they are subsequently depressed when the myocardium becomes severely ischemic. Our observations2' 3 on the relationship between heart rate and the incidence of ventricular premature beats were made during this initial phase of increased excitability and conductivity, when the ectopic beats are more likely to be due to the discharge of automatic Purkinje fibers. The increased excitability is also expected to facilitate focal reexcitation resulting from increased asynchrony of repolarization at the boundary between the normal myocardium and the moderately ischemic myocardium with accelerated repolarization process. The observed increase in the incidence of premature beats at slower heart rates may, then, be due to an increase in the degree of asynchrony of repolarization between the normal and moderately ischemic areas. It has been shown that, during constriction (partial occlusion) of a coronary