title: CD31+/Annexin V+ microparticles in healthy offsprings of patients with coronary artery disease.
abstract: BACKGROUND
  First-degree relatives of patients with premature coronary artery disease (CAD) develop endothelial dysfunction even in the case they are apparently healthy. In this study we wanted to clarify whether reduced blood levels of circulating endothelial progenitor cells (EPCs), an endogenous repair mechanism to replace dysfunctional endothelium, or elevated endothelial-derived microparticles (EMPs), an indicator and a mediator of increased endothelial cell damage/apoptosis, are an initial step in the pathogenesis of endothelial dysfunction in genetically predisposed subjects.
  
  
  METHODS
  Fifty-six healthy young men (aged 23 to 31 years) from a fire brigade were enrolled, of which 20 subjects had a positive family history (FH) for premature CAD. Subjects with or without a positive FH did not differ with respect to age, body mass index, risk factors and C-reactive protein. Endothelial function was assessed by hyperaemia-mediated relaxation of the brachial artery, blood levels of EPCs (VEGFR2(+)CD34(+) cells) and number of EMPs (CD31(+(bright))/Annexin V(+) particles) were analysed by flow cytometry.
  
  
  RESULTS
  Hyperaemia-mediated relaxation of the brachial artery was similar in both groups, and the blood levels of EPCs were comparable. However, the number of EMPs were significantly increased in subjects with a positive FH compared to those with a negative FH (neg. FH: 55.31 +/- 4.88 vs. pos. FH: 70.37 +/- 6.32 particles microL(-1 )platelet poor plasma; P < 0.05). Number of EMPs correlate inversely with the FMD response.
  
  
  CONCLUSIONS
  These results suggest that increased plasma levels of EMPs may be an initial step in the development of endothelial dysfunction in genetically predisposed subjects.
authors.affiliation: Heart & Vascular Center of the Ruhr-University, Clinic of Cardiology & Angiology, St. Josef-Hospital, Bochum, Germany. daniel.bulut@rub.de
authors.forename: D
authors.initials: D
authors.lastname: Bulut
authors.forename: H
authors.initials: H
authors.lastname: Tüns
authors.forename: A
authors.initials: A
authors.lastname: Mügge
mesh_terms: D000328:Adult; D017304:Annexin A5 / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000503:physiopathology*; D042783:Endothelial Cells / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D011237:Predictive Value of Tests; D055815:Young Adult
chemical_list: D017304:Annexin A5; D002097:C-Reactive Protein