title: Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary intervention.
abstract: OBJECTIVE
  Endothelial progenitor cells (EPCs) are circulating mononuclear cells with the capacity to mature into endothelial cells and contribute to vascular repair. We assessed the effect of local vascular injury during percutaneous coronary intervention (PCI) on circulating EPCs in patients with coronary artery disease.
  
  
  METHODS
  Prospective case-control study in a university teaching hospital.
  
  
  METHODS
  54 patients undergoing elective coronary angiography.
  
  
  METHODS
  EPCs were quantified by flow cytometry (CD34(+)KDR(+) phenotype) complemented by real-time polymerase chain reaction (PCR), and the colony forming unit (CFU-EC) functional assay, before and during the first 24 hours after diagnostic angiography (n = 27) or PCI (n = 27).
  
  
  RESULTS
  Coronary intervention, but not diagnostic angiography, resulted in an increase in blood neutrophil count (p<0.001) and C-reactive protein concentrations (p = 0.001) in the absence of significant myocardial necrosis. Twenty-four hours after PCI, CFU-ECs increased threefold (median [IQR], 4.4 [1.3-13.8] vs 16.0 [2.1-35.0], p = 0.01), although circulating CD34(+)KDR(+) cells (0.019% (SEM 0.004%) vs 0.016% (0.003%) of leucocytes, p = 0.62) and leucocyte CD34 mRNA (relative quantity 2.3 (0.5) vs 2.1 (0.4), p = 0.21) did not. There was no correlation between CFU-ECs and CD34(+)KDR(+) cells.
  
  
  CONCLUSIONS
  Local vascular injury following PCI results in a systemic inflammatory response and increases functional CFU-ECs. This increase was not associated with an early mobilisation of CD34(+)KDR(+) cells, suggesting these cells are not the primary source of EPCs involved in the immediate response to vascular injury.
authors.affiliation: Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, Edinburgh, EH16 4SU, UK. nick.mills@ed.ac.uk
authors.forename: N L
authors.initials: NL
authors.lastname: Mills
authors.forename: O
authors.initials: O
authors.lastname: Tura
authors.forename: G J
authors.initials: GJ
authors.lastname: Padfield
authors.forename: C
authors.initials: C
authors.lastname: Millar
authors.forename: N N
authors.initials: NN
authors.lastname: Lang
authors.forename: D
authors.initials: D
authors.lastname: Stirling
authors.forename: C
authors.initials: C
authors.lastname: Ludlam
authors.forename: M L
authors.initials: ML
authors.lastname: Turner
authors.forename: G R
authors.initials: GR
authors.lastname: Barclay
authors.forename: D E
authors.initials: DE
authors.lastname: Newby
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003327:Coronary Disease / Q000628:therapy*; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology*; D005260:Female; D006335:Heart Injuries / Q000473:pathology*; D006801:Humans; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology; D009205:Myocarditis / Q000209:etiology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology; D010641:Phenotype; D011446:Prospective Studies; D013234:Stem Cells / Q000166:cytology / Q000502:physiology*
chemical_list: D002097:C-Reactive Protein