PROGRESSION OF MYOCARDIAL DAMAGE FOLLOWING CORONARY MICROEMBOLIZATION IN DOGS

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Abstract
Whether induction of ischemic heart failure by microembolization leads to only a single episode of myocardial injury or whether it sets up a vicious cycle of progressive myocardial damage was studied. Acute left ventricular (LV) failure was produced in 15 closed-chest anesthetized dogs by injection of 50 .mu.m plastic microspheres into the left main coronary artery. The dogs showed signs of severely depressed LV function; there was a marked increase in LV end-diastolic pressure and a marked decrease in stroke volume. Myocardial lactate uptake decreased or reversed to production. Six dogs with very high LV end-diastolic pressure died during the subsequent 3 days and autopsy revealed pulmonary edema. The LV function was re-examined in 4 dogs at 2 and 4 wk after embolization. Except for a modest elevation of LV end-diastolic pressure, there were no hemodynamic or metabolic signs of myocardial dysfunction. Gross and light microscopic examination of the heart in dogs 8 h-6 wk following microsphere injections, revealed numerous small infarcts or focal areas of granulation or scar tissue throughout the entire left ventricle. At 1-6 wk close to the infarcts there were scattered myocytes with strong eosinophilia and pyknosis or loss of nuclei, interpreted as myocytolysis. In 2 dogs killed at 6 wk after the embolization there were areas of granulation tissue, similar to a recent infarction .apprx. 1 wk old. Thus, in spite of apparent functional restoration there were morphological signs of repeated and progressive myocardial injury several weeks after coronary embolization.