Ischemia-Activated Platelets in Normal and in Naturally Occurring Hypertrophied Myocardium

Substantial myocardial platelet aggregations in the coronary microvascula ture of normal and of naturally occurring hypertrophied myocardia have been documented after ischemia and reperfusion. Eleven normal canine (group I) hearts underwent an isolated cardiac bypass preparation and were compared with 5 myocardia (Group II) hypertrophied by congenital aortic stenosis. All 16 hearts experienced transient ischemia during the isolated cardiac bypass and produced platelet aggregations (111 In tagged: P \u3c 0.05). Hypothermic (25°C) potassium crystalloid cardioplegia did not wash out these depositions, and with the onset of reperfusion, both platelet and erythrocyte (99mTc tagged) radioactiv ity profoundly increased (p=0.0101). These increases progressed during the hour of reperfusion (p = 0.0369) and, specifically, in the endocardium. In summary, intracoronary platelets are activated after transient ischemic episodes, in particular the vulnerable hypertrophied myocardium in naturally occurring aortic stenotic hearts. These ischemia-activated platelet aggregations persist despite the application of hypothermic crystalloid cardioplegia. These depositions, in turn, allowed an ongoing pattern of platelet and erythrocyte aggregations during the reperfusion period. These data have important clinical implications for myocardial protection and reperfusion during acute myocar dial ischemia and infarction for the normal and hypertrophied myocardium