title: Circulating endothelial microparticles correlate inversely with endothelial function in patients with ischemic left ventricular dysfunction.
abstract: BACKGROUND
  Bone-marrow derived endothelial progenitor cells (CD34+ and VEGFR2+ KDR+ EPC) and endothelial-derived microparticles (CD 31+Annexin V+, EMP; indicator for endothelial apoptosis) were examined in the peripheral blood of 35 male, clinically stable patients with 3-vessel coronary artery disease (CAD). The patients were divided in 2 groups, those with preserved or normal function (n = 17; EF 65 +/- 6%) and those with reduced left ventricular (LV) function (n = 18; EF 36 +/- 11%).
  
  
  RESULTS
  The number of circulating EPCs was decreased by 25% (P = .07) and the number of EMPs was increased by 109 % (P < .05) in patients with LV dysfunction compared with those with normal or preserved LV function. EPCs were positively correlated (r = 0.24 for patients with LV dysfunction and r = 0.28 for patients with preserved LV function) with endothelial function as assessed by flow-mediated vasodilatation. In contrast, EMPs were inversely correlated (r = -0.42 for patients with LV dysfunction and r = -0.49 for patients with preserved LV function).
  
  
  CONCLUSIONS
  CAD patients with significant LV dysfunction show an increased index of endothelial cell damage. This decrease (or lack of compensatory elevation) of EPCs may result in a reduced potential for repair and thus contribute at least in part to the pathogenesis of endothelial dysfunction.
authors.affiliation: Herzzentrum der Kliniken der Ruhr-Universität Bochum, Standort St. Josef-Hospital, Gudrunstrasse 56, 44791 Bochum, Germany.
authors.forename: Daniel
authors.initials: D
authors.lastname: Bulut
authors.forename: Karin
authors.initials: K
authors.lastname: Maier
authors.forename: Nadine
authors.initials: N
authors.lastname: Bulut-Streich
authors.forename: Jan
authors.initials: J
authors.lastname: Börgel
authors.forename: Christoph
authors.initials: C
authors.lastname: Hanefeld
authors.forename: Andreas
authors.initials: A
authors.lastname: Mügge
mesh_terms: D000368:Aged; D017304:Annexin A5 / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood / Q000503:physiopathology; D042783:Endothelial Cells; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000503:physiopathology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000097:blood*; D012307:Risk Factors; D013234:Stem Cells; D013318:Stroke Volume; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*
chemical_list: D017304:Annexin A5; D019408:Platelet Endothelial Cell Adhesion Molecule-1