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  • Title: Enhanced shear-induced von Willebrand factor binding to platelets in acute myocardial infarction.
    Author: Li M, Goto S, Sakai H, Kim JY, Ichikawa N, Yoshida M, Ikeda Y, Handa S.
    Journal: Thromb Res; 2000 Nov 15; 100(4):251-61. PubMed ID: 11113268.
    Abstract:
    Recent investigations have suggested that von Willebrand factor (vWF) plays a crucial role in platelet thrombosis under flow conditions. The effects of plasma obtained from 15 patients with acute myocardial infarction and 10 patients with the chest pain syndrome as controls, on shear-induced vWF binding to platelets and subsequent platelet activation, as evidenced by microparticle release, were investigated by quantitative flow cytometry. Platelet-rich plasma was obtained from a 38-year-old healthy male volunteer with blood type O. Stored plasma from either the acute myocardial infarction or control patients was then added to the freshly prepared platelet-rich plasma in equal volumes. The mixtures were then exposed to specific shear rates in an optically modified cone-plate viscometer. The number of vWF molecules bound to the platelet surface and the number of microparticles released from the platelets were then measured by quantitative flow cytometry using an FITC-conjugated anti-vWF monoclonal antibody. The shear-induced increase in vWF binding to the platelet surface was enhanced in the presence of plasma from patients with acute myocardial infarction (acute myocardial infarction plasma). The shear-induced release of microparticles from platelets was enhanced from 889+/-134 in the presence of control plasma to 1045+/-222 in the presence of the acute myocardial infarction plasma (p<0.05). Acute myocardial infarction plasma also reduced the shear rate threshold required to induce measurable shear-induced vWF binding from 10800 s(-1) to 9000 s(-1). We conclude that the plasma of acute myocardial infarction patients contains factors that enhance shear-induced vWF binding and vWF-mediated platelet activation, which may contribute to thrombotic re-occlusions of the coronary arteries in patients who have received reperfusion treatments.
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