title: Elevated levels of shed membrane microparticles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes.
abstract: BACKGROUND
  Apoptotic microparticles are responsible for almost all tissue factor activity of the plaque lipid core. We hypothesized that elevated levels of procoagulant microparticles could also circulate in the peripheral blood of patients with recent clinical signs of plaque disruption and thrombosis.
  
  
  RESULTS
  We studied 39 patients with coronary heart disease, including 12 patients with stable angina and 27 patients with acute coronary syndromes (ACS), and 12 patients with noncoronary heart disease. We isolated the circulating microparticles by capture with annexin V and determined their procoagulant potential with a prothrombinase assay. The cell origins of microparticles were determined in an additional 22 patients by antigenic capture with specific antibodies. The level of procoagulant microparticles did not differ between stable angina patients and noncoronary patients (10.1+/-1.6 nmol/L phosphatidylserine [PS] equivalent versus 9.9+/-1.6 nmol/L PS equivalent, respectively). However, procoagulant microparticles were significantly elevated in patients with ACS (22.2+/-2.7 nmol/L PS equivalent) compared with other coronary (P<0.01) or noncoronary (P<0.01) patients. Microparticles of endothelial origin were significantly elevated in patients with ACS (P<0.01), which suggests an important role for endothelial injury in inducing the procoagulant potential.
  
  
  CONCLUSIONS
  High levels of procoagulant endothelial microparticles are present in the circulating blood of patients with ACS and may contribute to the generation and perpetuation of intracoronary thrombi.
authors.affiliation: Institut National de la Santé et la Recherche Médicale, INSERM U141, IFR Circulation, Hôpital Lariboisière, Paris, France.
authors.forename: Z
authors.initials: Z
authors.lastname: Mallat
authors.forename: H
authors.initials: H
authors.lastname: Benamer
authors.forename: B
authors.initials: B
authors.lastname: Hugel
authors.forename: J
authors.initials: J
authors.lastname: Benessiano
authors.forename: P G
authors.initials: PG
authors.lastname: Steg
authors.forename: J M
authors.initials: JM
authors.lastname: Freyssinet
authors.forename: A
authors.initials: A
authors.lastname: Tedgui
mesh_terms: D000208:Acute Disease; D000787:Angina Pectoris / Q000097:blood*; D015703:Antigens, CD; D017209:Apoptosis; D051929:CD146 Antigen; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications*; D003328:Coronary Thrombosis / Q000097:blood* / Q000209:etiology; D004730:Endothelium, Vascular / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins; D008875:Middle Aged; D019006:Neural Cell Adhesion Molecules; D010718:Phosphatidylserines / Q000097:blood; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D011446:Prospective Studies; D011956:Receptors, Cell Surface / Q000032:analysis; D019851:Thrombophilia / Q000097:blood / Q000209:etiology*; D013925:Thromboplastin / Q000032:analysis*
chemical_list: D015703:Antigens, CD; D051929:CD146 Antigen; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules; D010718:Phosphatidylserines; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011956:Receptors, Cell Surface; C053675:endothelial cell procoagulant activity; D013925:Thromboplastin