Mild myocardial stunning affects platelet aggregation and certain hemostatic factors in swine

Myocardial stunning is characterized by transient contractile dysfunction o ccurring subsequent to an episode of ischemia followed by reperfusion. Plat elet activation and hemostatic abnormalities have been described in patient s with unstable angina and acute myocardial infarction, however, their role in the pathogenesis of myocardial stunning is unknown. The purpose of this study was to determine if platelet aggregation and certain hemostatic fact ors change during myocardial stunning following brief coronary arterial occ lusion. Nine Yorkshire swine underwent left anterior descending coronary ar tery occlusion for 8 minutes followed by 90 minutes of reperfusion. Blood s amples were obtained at baseline, at 4 and 8 minutes of occlusion, and at 6 0 and 90 minutes of reperfusion. Platelet aggregability and concentrations of antithrombin III, protein C, protein S, fibronectin, endothelin I, and t he stable metabolites of thromboxane (TxB(2)) and prostacyclin (6-keto-PGF( 1a)) were measured in systemic circulation. The occlusion phase was associa ted with a decline of endothelin 1 (-13.6%), and TxB(2) (-19.6%), and eleva tion of antithrombin III (+40.2%) and protein C (+22.9%). Mild myocardial s tunning was associated with a significant increase in platelet aggregation (+33.7%), endothelin-1 (+24.7%), 6-keto-PGF(1a) (+41.5%), TxB(2) (+11.9%), and protein C (+42.3%) during the reperfusion phase. There were no changes in plasma fibronectin and total protein S. Thus, mild myocardial stunning f ollowing brief coronary artery occlusion is associated with substantial dyn amic changes in platelet aggregability and certain hemostatic factors. Thes e results may be relevant to understanding the mechanisms determining myoca rdial stunning and coronary arterial patency following reperfusion.