Mild Myocardial Stunning Affects Platelet Aggregation and Certain Hemostatic Factors in Swine

Abstract

Myocardial stunning is characterized by transient contractile dysfunction occurring subsequent to an episode of ischemia followed by reperfusion. Platelet activation and hemostatic abnormalities have been described in patients 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 factors change during myocardial stunning following brief coronary arterial occlusion. Nine Yorkshire swine underwent left anterior descending coronary artery occlusion for 8 minutes followed by 90 minutes of reperfusion. Blood samples were obtained at baseline, at 4 and 8 minutes of occlusion, and at 60 and 90 minutes of reperfusion. Platelet aggregability and concentrations of antithrombin III, protein C, protein S, fibronectin, endothelin 1, and the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1a) were measured in systemic circulation. The occlusion phase was associated with a decline of endothelin 1 (-13.6%), and TxB2 (-19.6%), and elevation of antithrombin III (+40.2%) and protein C (+22.9%). Mild myocardial stunning was associated with a significant increase in platelet aggregation (+33.7%), endothelin-1 (+24.7%), 6-keto-PGF1a (+41.5%), TxB2 (+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 following brief coronary artery occlusion is associated with substantial dynamic changes in platelet aggregability and certain hemostatic factors. These results may be relevant to understanding the mechanisms determining myocardial stunning and coronary arterial patency following reperfusion.

Activated platelets contribute importantly to myocardial reperfusion injury

“…The magnitude of these changes has been consistently found to correlate with the severity of the clinical manifestation of the acute coronary syndrome (1,10). Although limited, several animal experiments have shown that myocardial stunning after brief coronary occlusion is associated with substantial dynamic changes in platelet aggregability and other hemostatic factors (37). For example, inhibiting the activity of platelets, but not of neutrophils, improves contractile recovery from myocardial stunning (14).…”

Platelet Glycoprotein IIb/IIIa Inhibitor Tirofiban Ameliorates Cardiac Reperfusion Injury

“…17) Serebruany, et al also reported that myocardial stunning after coronary ligation is associated with substantial dynamic changes in platelet aggregation and other haemostatic factors. 18) Moreover, many studies have illustrated that the addition of platelets to the perfusate impairs coronary blood flow, 19) decreases ventricular and postischemic contractile recovery, 20,21) and promotes the occurrence of life-threatening cardiac arrhythmia 22) in numerous models of myocardial RI.…”