title: Increased circulating endothelial cells in acute heart failure: comparison with von Willebrand factor and soluble E-selectin.
abstract: BACKGROUND
  Circulating endothelial cells (CECs) in the peripheral blood, probably representing the most direct evidence of endothelial cell damage, are increased in myocardial infarction, unstable angina and critical limb ischaemia. As chronic heart failure is also associated with endothelial abnormalities, we hypothesised that CECs are raised in acute heart failure and that they would correlate with plasma indices of endothelial perturbation, that is, von Willebrand factor (vWf) and soluble E-selectin.
  
  
  METHODS
  We studied 30 patients with acute heart failure (venesected within 24 h of emergency hospital admission), 30 patients with chronic stable heart failure (venesected as out-patients, all patients in sinus rhythm with ejection fraction < or = 40%) and 20 healthy controls. CECs were quantified using epifluorescence microscopy after CD146-immunomagnetic separation and phenotyped by streptavidin/biotin immunocytochemistry. Citrated plasma was analysed for soluble E-selectin and vWf by ELISA.
  
  
  RESULTS
  Levels of CECs, vWf and soluble E-selectin were significantly higher (all p<0.01) in patients with heart failure compared to controls, with no significant differences between acute and chronic heart failure. CECs correlated with plasma vWf (p<0.0001) and soluble E-selectin (p = 0.022) but not ejection fraction or NYHA class. In multiple regression analysis, heart failure was the only independent predictor of raised CECs (p<0.0001). Immunoperoxidase-defined surface expression of CD34, CD45 and CD36 by CECs was <2%, 0% and 8%, respectively.
  
  
  CONCLUSIONS
  CECs, a possibly heterologous population, may be used as a novel measure of endothelial damage in acute heart failure and may have implications for the thrombotic risk associated with acute and chronic heart failure and prognosis in this condition.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, United Kingdom.
authors.forename: Aun Yeong
authors.initials: AY
authors.lastname: Chong
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
authors.forename: Bethan
authors.initials: B
authors.lastname: Freestone
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
mesh_terms: D000208:Acute Disease; D000368:Aged; D018952:Antigens, CD34 / Q000378:metabolism; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D019040:E-Selectin / Q000097:blood*; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D004727:Endothelium / Q000378:metabolism / Q000473:pathology; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D017493:Leukocyte Common Antigens / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D014841:von Willebrand Factor / Q000378:metabolism*
chemical_list: D018952:Antigens, CD34; D019040:E-Selectin; D014841:von Willebrand Factor; D017493:Leukocyte Common Antigens