Mild myocardial stunning affects platelet aggregation and hemostasis in swine

Published

Journal Article

The key role of platelet activation and hemostatic disorders have been increasingly recognized in patients with unstable angina and acute myocardial infarction. However, the dynamics of the hemostatic profile during brief ischemia-reperfusion are poorly understood and may contribute to the pathogenesis of myocardial stunning (MS). The purpose of current study was to investigate the serial changes of platelet aggregation and hemostatic profile during occlusion and reperfusion of mild MS using an in vivo animal model. Nine open-chested Yorkshire swine underwent coronary artery occlusion for 8 minutes followed by 90 minutes of reperfusion. Blood samples were obtained at baseline, at 4 and at B minutes of occlusion, and at 60 and 90 minutes of reperfusion. Platelet aggregability and concentrations of antithrombin-lll (AT-III), Protein C, Protein S, ftoronectin, endothelin-1 (ET-1), as well as the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto- PGF1a), were measured in the systemic circulation. The occlusion phase of MS was associated with a decline of ET-1 (-13.6%), TxB2 (-19.6%); and elevation of AT-III (+40.2%) and Prolein C (+22.9%). Short-term ischemia-reperfusion resulted in significant increase of platelet aggregation (+33.7%), ET-1 (+24.7%), 6-keto-PGFia (+41.5%), TxB2 (+11.9%) and Protein C (+42.3%) during the reperfusion phase. There were no significant changes in fibronectin and total Protein S levels. We conclude that mild MS is associated with substantial dynamic changes in platelet aggregability and the hemostatic profile. This data provides support for the involvement of cellular mechanisms and endothelial dysfunction in the pathogenesis of MS. Further investigation is warranted.

Duke Authors

Cited Authors

  • Serebruany, VL; Herzog, WR; Gurbel, PA

Published Date

  • December 1, 1996

Published In

Volume / Issue

  • 10 / 3

International Standard Serial Number (ISSN)

  • 0892-6638

Citation Source

  • Scopus