Deleterious effects of increased heart rate on infarct size in the conscious dog

This study was designed to determine whether augmentation of heart rate influences infarct size after coronary occlusion in unanesthetized dogs, some of which had experimentally induced atrioventricular (A-V) block. Coronary occlusion was produced in 27 conscious dogs by constriction of an externalized coronary arterial snare placed 3 to 5 days earlier. Heart rate was augmented at selected intervals after coronary occlusion by ventricular pacing or administration of isoproterenol or atropine, and left atrial pressure was monitored in selected animals in each group. Infarct size was determined from analysis of serial serum creatine phosphokinase (CPK) changes and verified by myocardial CPK analysis. After coronary occlusion alone, release of CPK from myocardial tissue ceased within approximately 14 hours, and calculated infarct size therefore became constant. Augmentation of heart rate at that time by ventricular pacing or administration of isoproterenol or atropine led to extension of infarction with additional myocardial necrosis averaging 40, 72 and 40 percent, respectively, of the initial infarct size in the 3 groups. Stepwise increments of heart rate led to progressively smaller increments in infarct size, and even modest increases in heart rate (from 60 to 90 beats/min) in dogs with A-V block led to marked increases in infarct size averaging 73 percent ± 17 (SE, no. = 4). Augmentation of heart rate with isoproterenol as late as 72 hours after coronary occlusion led to marked extension of infarction. Thus, acceleration of heart rate after coronary occlusion consistently and markedly increased the extent of myocardial necrosis.