title: Increased levels of procoagulant tissue factor-bearing microparticles within the occluded coronary artery of patients with ST-segment elevation myocardial infarction: role of endothelial damage and leukocyte activation.
abstract: OBJECTIVE
  During myocardial infarction, platelet activation and endothelial apoptosis are responsible for the release of procoagulant membrane-derived microparticles (MPs) in the bloodstream. Few data are available on the potential role played by MPs in coronary atherothrombosis. In the present study, we investigated the levels and cellular origins of MPs within the occluded coronary artery of patients with ST-segment elevation myocardial infarction (STEMI) treated by primary angioplasty (PCI).
  
  
  METHODS
  A total of 12 patients with STEMI treated by primary PCI within 24h of symptom onset were included in this study. MPs procoagulant activity and cellular origin were characterized within the occluded coronary artery before PCI (C(0)), after restoration of the epicardial blood flow (C(1)), and in blood collected from the femoral artery (F).
  
  
  RESULTS
  Levels of leukocyte-derived CD11a(+) MPs, endothelial-derived CD105(+) MPs, and tissue factor (TF)-bearing MPs were significantly higher within the occluded coronary artery than in peripheral blood samples. Restoration of the epicardial blood flow led to a significant reduction of procoagulant CD11a(+) and CD105(+) MPs by 30% and 42%, respectively (p<0.05).
  
  
  CONCLUSIONS
  Elevation of procoagulant MPs within the occluded coronary artery of patients with STEMI suggests their pathophysiological role in coronary atherothrombosis.
authors.affiliation: Pôle d'activité médico-chirurgicale, Cardiovasculaire des Hôpitaux, Universitaires de Strasbourg, Nouvel Hôpital Civil, place de l'Hôpital, 67098 Strasbourg Cedex, France. olivier.morel@chru-strasbourg.fr
authors.forename: Olivier
authors.initials: O
authors.lastname: Morel
authors.forename: Bruno
authors.initials: B
authors.lastname: Pereira
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Averous
authors.forename: Antoine
authors.initials: A
authors.lastname: Faure
authors.forename: Laurence
authors.initials: L
authors.lastname: Jesel
authors.forename: Philippe
authors.initials: P
authors.lastname: Germain
authors.forename: Lelia
authors.initials: L
authors.lastname: Grunebaum
authors.forename: Patrick
authors.initials: P
authors.lastname: Ohlmann
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Freyssinet
authors.forename: Pierre
authors.initials: P
authors.lastname: Bareiss
authors.forename: Florence
authors.initials: F
authors.lastname: Toti
mesh_terms: D000328:Adult; D015906:Angioplasty, Balloon, Coronary; D015703:Antigens, CD / Q000032:analysis; D017209:Apoptosis; D040881:CD11a Antigen / Q000032:analysis; D055252:Cell-Derived Microparticles / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D003326:Coronary Circulation; D054059:Coronary Occlusion / Q000097:blood* / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000628:therapy; D003328:Coronary Thrombosis / Q000097:blood* / Q000150:complications / Q000276:immunology / Q000473:pathology / Q000628:therapy; D000071063:Endoglin; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000628:therapy; D011956:Receptors, Cell Surface / Q000032:analysis; D013925:Thromboplastin / Q000276:immunology / Q000378:metabolism*; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: D015703:Antigens, CD; D040881:CD11a Antigen; C064206:ENG protein, human; D000071063:Endoglin; D011956:Receptors, Cell Surface; D013925:Thromboplastin