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Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary intervention.

TitleDissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary intervention.
Publication TypeJournal Article
Year of Publication2009
AuthorsMills NL, Tura O, Padfield GJ, Millar C, Lang NN, Stirling D, Ludlam C, Turner ML, Barclay GR, Newby DE
JournalHeart
Volume95
Issue24
Pagination2003-8
Date Published2009 Dec
ISSN1468-201X
KeywordsAngioplasty, Balloon, Coronary, C-Reactive Protein, Case-Control Studies, Coronary Disease, Endothelial Cells, Female, Heart Injuries, Humans, Leukocyte Count, Leukocytes, Mononuclear, Male, Middle Aged, Myocardial Infarction, Myocarditis, Myocytes, Cardiac, Phenotype, Prospective Studies, Stem Cells
Abstract

OBJECTIVES: 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.

DESIGN AND SETTING: Prospective case-control study in a university teaching hospital.

PATIENTS: 54 patients undergoing elective coronary angiography. Interventions and

MAIN OUTCOME MEASURES: 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

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.

DOI10.1136/hrt.2008.163162
Alternate JournalHeart
PubMed ID19482845