Intracoronary platelet aggregation: Pattern of deposition after ischemia, cardioplegia, and reperfusion

Abstract

Platelet deposition in the coronary microvasculature has not been completely defined in the temporal relationship to acute myocardial ischemia, the application of crystalloid cardioplegia, and during reperfusion on heart bypass. Twenty-two canine hearts were serially biopsied for the analysis of radioactively tagged platelets. Eleven hearts underwent an isolated heart support preparation with seven followed by potassium cardioplegic arrest and reperfusion while the remaining 4 were maintained on continuous bypass. All 11 hearts undergoing bypass experienced transient (<90 sec) ischemia during bypass preparation and produced platelet aggregation in the myocardium (51.12 ± 24.0 as compared to nonischemic control group 12.3 ± 4.7; P = 0.005). Potassium cardioplegia did not completely wash out these platelets to the nonischemic control levels (27.8 ± 14.9; P = 0.04). With the onset of reperfusion after 1 hr of cardioplegic arrest, platelet radioactivity profoundly increased (133.3 ± 72.8; P = 0.0101) and remained high throughout the hour of reperfusion (324.7 ± 269.3; P = 0.0369). In summary, intracoronary platelets are activated after transient ischemic episodes during initiation of heart bypass. These ischemia-activated platelet aggregations persist despite the application of cardioplegia during the arrest period. This deposition, in turn, allowed an ongoing pattern of platelet aggregation during the early and subsequent reperfusion. This pattern of ischemia-activated platelet aggregations probably accounts for the progressive reperfusion injury and support of an antiplatelet treatment for coronary microvasculature protection.