Elevated levels of procoagulant microparticles in a patient with myocardial infarction, antiphospholipid antibodies and multifocal cardiac thrombosis

O Morel, L Jesel, J M Freyssinet, F Toti, O Morel, L Jesel, J M Freyssinet, F Toti

Abstract

Circulating procoagulant microparticles (MP) are pathogenic markers of enhanced coagulability associated to a variety of disorders and released from stimulated vascular cells. When derived from endothelial cells, MP were found characteristic of thrombotic propensity in primary antiphospholipid syndrome (APS). The prothrombotic status of a patient with antiphospholipid antibodies (APL), a past history of mesenteric vein thrombosis and presenting myocardial infarction and extensive intracardiac thrombosis was examined by measurement of circulating procoagulant MP. MP of platelet and endothelial origins were highly elevated with respect to values detectable in patients with myocardial infarction and no history of APS (6- and 3-fold elevation, respectively) or in healthy volunteers (13- and 25-fold elevation, respectively). In this particular patient, with moderate APL titer, a drastic release of procoagulant MP could have contributed to thrombus growth and the development of extensive intracardiac thrombosis.

Figures

Figure 1
Figure 1
At patient admission, left coronary angiogram revealed thrombotic obstruction of left anterior descending artery (A). Large thrombus in the right auricle emerging through tricuspid valve within right ventricle (B) and apical thrombus complicating anterior aneurysm (C) detected by computer tomography scan, performed the next day. Large thrombus emerging from superiour vena cava and prolabing in the right auricle, evidenced by Trans-oesophagial echocardiography (D). Extensive thrombus emerging from superiour vena cava within right auricle, evidenced by magnetic resonance imaging (E).

References

    1. Arnout J, Vermylen J. Current status and implications of autoimmune antiphospholipid in relation to thrombotic disease. Journal of Thrombosis and Haemostasis. 2003;1:931–942. doi: 10.1046/j.1538-7836.2003.00125.x.
    1. Harpaz D, Glikson M, Sidi Y, Hod H. Successful thrombolytic therapy for acute myocardial infarction in a patient with the antiphospholipid antibody syndrome. Am Heart J. 1991;122:1492–1495. doi: 10.1016/0002-8703(91)90604-G.
    1. Morton KE, Gavaghan TP, Krilis SA, Daggard GE, Baron DW, Hickie JB, Chesterman CN. Coronary artery bypass graft failure--an autoimmune phenomenon? Lancet 1986 Dec 13;2(8520):1353-7 Related Articles, Links. 1986;2(8520):1353–1357.
    1. Musuraca G, Imperadore F, Terraneo C, De Girolamo P, Cemin C, Bonmassari R, Vergara G. Successful treatment of post-exertion acute myocardial infarction by primary angioplasty and stenting in a patient with antiphospholipid antibody syndrome. Blood Coagul Fibrinolysis. 2004;15:95–98. doi: 10.1097/00001721-200401000-00015.
    1. Triplett DA. Antiphospholipid antibodies. Arch Pathol Lab Med. 2002;126:1424–1429.
    1. Combes V, Simon AC, Grau GE, Arnoux D, Camoin L, Sabatier F, Mutin M, Sanmarco M, Sampol J, Dignat-George F. In vitro generation of endothelial microparticles and possible prothrombotic activity in patients with lupus anticoagulant. J Clin Invest. 1999;104:93–102.
    1. Bordron A, Dueymes M, Levy Y, Jamin C, Leroy JP, Piette JC, Shoenfeld Y, Youinou PY. The binding of some human antiendothelial cell antibodies induces endothelial cell apoptosis. J Clin Invest. 1998;101:2029–2035.
    1. VanWijk MJ, VanBavel E, Sturk A, Nieuwland R. Microparticles in cardiovascular diseases. Cardiovasc Res. 2003;59:277–287. doi: 10.1016/S0008-6363(03)00367-5.
    1. Morel O, Toti F, Hugel B, Freyssinet JM. Cellular microparticles: A disseminated storage pool of bioactive vascular effectors. Curr Opin Hematol. 2004;11:156–164. doi: 10.1097/01.moh.0000131441.10020.87.
    1. Singh N, Gemmell C, Daly P, E. Y. Elevated platelet-derived microparticle levels during unstable angina. Can J Cardiol. 1995;11:1015–1021.
    1. Nomura S, Uehata S, Saito S, Osumi K, Ozeki Y, Kimura Y. Enzyme immunoassay detection of platelet-derived microparticles and RANTES in acute coronary syndrome. Thromb Haemost. 2003;89:506–512.
    1. Muller I, Klocke A, Alex M, Kotzsch M, Luther T, Morgenstern E, Zieseniss S, Zahler S, Preissner K, Engelmann B. Intravascular tissue factor initiates coagulation via circulating microvesicles and platelets. Faseb J. 2003;17:476–478.
    1. Freyssinet JM. Cellular microparticles: what are they bad or good for? J Thromb Haemost. 2003;1:1655–1662. doi: 10.1046/j.1538-7836.2003.00309.x.
    1. Hugel B, Martinez C, Kunzelmann C, Freyssinet JM. Membane microparticles: two sides of the coin. Physiology. 2005;20:22–27. doi: 10.1152/physiol.00029.2004.
    1. Dignat-George F, Camoin-Jau L, Sabatier F, Arnoux D, Anfosso F, Bardin N, Veit V, Combes V, Gentile S, Moal V, Sanmarco M, Sampol J. Endothelial microparticles: a potential contribution to the thrombotic complications of the antiphospholipid syndrome. Thromb Haemost. 2004;91:667–673.
    1. Mallat Z, Benamer H, Hugel B, Benessiano J, Steg PG, Freyssinet JM, Tedgui A. Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes. Circulation. 2000;101:841–843.
    1. Hugel B, Socie G, Vu T, Toti F, Gluckman E, Freyssinet JM, Scrobohaci ML. Elevated levels of circulating procoagulant microparticles in patients with paroxysmal nocturnal hemoglobinuria and aplastic anemia. Blood. 1999;93:3451–3456.
    1. Aupeix K, Hugel B, Martin T, Bischoff P, Lill H, Pasquali JL, Freyssinet JM. The significance of shed membrane particles during programmed cell death in vitro, and in vivo, in HIV-1 infection. J Clin Invest. 1997;99:1546–1554.
    1. Hugel B, Zobairi F, Freyssinet JM. Measuring circulating-cell derived microparticles. J Thromb Haemost. 2004;2:1846–1847. doi: 10.1111/j.1538-7836.2004.00939.x.
    1. Bernal-Mizrachi L, Jy W, Jimenez JJ, Pastor J, Mauro LM, Horstman LL, de Marchena E, Ahn YS. High levels of circulating endothelial microparticles in patients with acute coronary syndromes. Am Heart J. 2003;145:962–970. doi: 10.1016/S0002-8703(03)00103-0.
    1. Morel O, Jesel L, Hugel B, Douchet MP, Zupan M, Chauvin M, Freyssinet JM, Toti F. Protective effects of vitamin C on endothelium damage and platelet activation during myocardial infarction in patients with sustained generation of circulating microparticles. J Thromb Haemost. 2003;1:171–177. doi: 10.1046/j.1538-7836.2003.00010.x.
    1. Gawaz M, Neumann FJ, Ott I, Schiessler A, Schomig A. Platelet function in acute myocardial infarction treated with direct angioplasty. Circulation. 1996;93:229–237.
    1. Goto S, Tamura N, Li M, Handa M, Ikeda Y, Handa S, Ruggeri ZM. Differents effects of various anti-GPIIb-IIIa agents on shear induced platelet activation and expression of procoagulant activity. J Thromb Haemost. 2003;1:2022–2030. doi: 10.1046/j.1538-7836.2003.00349.x.
    1. Morel O, Hugel B, Jesel L, Mallat Z, Lanza F, Douchet MP, Zupan M, Chauvin M, Cazenave JP, Tedgui A, Freyssinet JM, Toti F. Circulating procoagulant microparticles and soluble GPV in myocardial infarction treated by primary percutaneous transluminal coronary angioplasty. A possible role for GPIIb-IIIa antagonists. J Thromb Haemost. 2004;2:1118–1126. doi: 10.1111/j.1538-7836.2004.00805.x.
    1. Serebruany VL, Malinin AI, Jerome SD, Lowry DR, Morgan AW, Sane DC, Tanguay JF, Steinhubl SR, O'Connor C M. Effects of clopidogrel and aspirin combination versus aspirin alone on platelet aggregation and major receptor expression in patients with heart failure: the Plavix Use for Treatment Of Congestive Heart Failure (PLUTO-CHF) trial. Am Heart J. 2003;146:713–720. doi: 10.1016/S0002-8703(03)00260-6.

Source: PubMed

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