Plasma von Willebrand Factor in Patients with Acute Myocardial Infarction

  • SAKAI Hiroyuki
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • GOTO Shinya
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • AOKI Naoto
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • FUSEGAWA Yuichi
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • GOTO Mami
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • ONO Miyuki
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,
  • HANDA Shunnosuke
    Division of Cardiology, Department of Medicine Tokai University School of Medicine,

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  • 急性心筋梗塞急性期の血漿von Willebrand Factorの検討

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Abstract

Acute myocardial infarction is known to be caused by thrombotic occlusion of coronary arteries. Although several investigators have suggested the abnormalities of plasma hemostatic parameters in patients with myocardial infarction, the relationship between these events and the onset of coronary thrombosis is still unclear. Recent in vitro investigations suggest the importance of the interaction between plasma ligand protein, von Willebrand factor (vWF), and platelet glycoproteins in the onset of arterial thrombosis, which occurs under the high shear stress of blood flow. In the present study, we investigated hemostatic abnormalities in patients with acute myocardial infarction by measuring plasma indicators including thrombin antithrombin III complex (TAT), plasminogen activator inhibitor 1 (PAI-1), the antigen level and ristocetin cofactor activities of vWF, and multimer analysis of vWF. In addition to hypercoagulabilities and increased antithrombolytic activities, a significant increase in antigen level or ristocetin cofactor activity of vWF was observed in patients with acute myocardial infarction. Although further study is needed, the increased levels of vWF in acute myocardial infarction may contribute to the re-occlusion of coronary artery after reperfusion treatment.

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