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Thrombosis Journal 2005
Elevated levels of procoagulant microparticles in a patient with myocardial infarction, antiphospholipid antibodies and multifocal cardiac thrombosisKeywords: endothelium, acute coronary syndrome Abstract: In primary anti-phospholipid syndrome (APS), arterial or venous thrombosis and recurrent pregnancy loss are common thrombotic manifestations associated with anti-phophospholipid antibodies (APL) [1]. A variety of cardiac affections including valvular lesions, myocardial dysfunction or infarction, early bypass graft failure, and intracardiac thrombosis have been reported [2-4]. Yet in vitro, APL inhibit phospholipid-dependent blood coagulation and bind to membrane phospholipids exposed by stimulated or apoptotic cells [5]. Furthermore, in the presence of APL, vascular cells are stimulated and acquire procoagulant, proadhesive and proinflammatory phenotypes [1,6]. Two non-exclusive hypotheses have been proposed to explain the thrombotic propensity in APS (i) APL could impede the natural anticoagulant protein C pathway, also involving anionic phospholipids (ii) APL would promote sustained cell activation through the interaction of immune complexes with vascular cells [1,7].Procoagulant microparticles (MP) are shed from the plasma membrane of any stimulated or apoptotic cells [8,9]. Under most physiopathological conditions among which acute myocardial syndrome, circulating MP, are mainly of platelet origin [10,11] and can be viewed as a "storage pool" by themselves, disseminating procoagulant activities [9,12]. In blood flow, released MP contribute to thrombotic propensity by virtue of exposed anionic phospholipids enhancing the catalytic surface available for blood coagulation. In addition, harbored membrane glycoproteins or antigens cytoadhesins, and proinflammatory lipids confer to MP the potency of cellular effectors through multiple amplification loops [13].Elevated levels of circulating MP were detected in various diseases, a proportion of them associated with thrombotic disorders [6,8,14-18]. In a particular patient with a past history of mesenteric vein thrombosis and moderate titers of anti-phospholipid antibodies referring for acute myocardial infarction, we h
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