Experimental coronary arterial occlusion and release: Effects on enzymes,electrocardiograms, myocardial contractility and reactive hyperemia

After less than 1 hour of coronary arterial occlusion, the myocardium suffers irreversible changes as revealed by electron microscopy. Yet, the earliest clinical laboratory indexes of myocardlal infarction—elevated serum enzyme levels and significant Q waves on the electrocardiogram—are not detected until at least 6 hours after coronary occlusion. To study the early period after coronary occlusion in the dog, occlusion of the left anterior descending coronary artery for 1 to 3 hours was followed by release, and coronary sinus and venous enzyme levels, the electrocardiogram and myocardial contractility from the infarcted area, and reactive hyperemia were monitored. Coronary sinus enzyme levels rose within 15 minutes after release of occlusion in half of the experiments with $\text{1}\text{to}\text{1}\text{1}\text{2}$ hours and in all of those with 2 to 3 hours of occlusion, and this rise preceded the rise in venous levels by only 10 to 20 minutes. Significant Q waves appeared 15 to 30 minutes after release of occlusion as the serum enzymes were increasing. Thus, clinically, the delayed appearance of increased serum enzymes and significant electrocardiographic Q waves is probably largely due to a lack of circulation in the infarcted area rather than to prolonged survival time. Also, the venous enzyme level reflects the coronary sinus level minutes later. The presence of viable myocardium in the infarcted area was suggested by elevation of the S-T segment upon reclamping, and by residual myocardial contractility and retained capacity for reactive hyperemia. These findings occurred in some experiments even In the presence of a significant Q wave.