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

Mills, N.L., Tura, O., Padfield, G.J., Millar, C., Lang, N.N. , Stirling, D., Ludlam, C., Turner, M.L., Barclay, G.R. and Newby, D.E. (2009) Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary intervention. Heart, 95(24), pp. 2003-2008. (doi: 10.1136/hrt.2008.163162) (PMID:19482845)

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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<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.

Item Type:Articles
Additional Information:Funding: Michael Davies British Cardiovascular Society Research Fellowship (NM); British Heart Foundation Project Grant (PG/07/017/22405); National Health Service Research and Development Fund (SPG2005/27).
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Newby, Professor David and Lang, Dr Ninian
Authors: Mills, N.L., Tura, O., Padfield, G.J., Millar, C., Lang, N.N., Stirling, D., Ludlam, C., Turner, M.L., Barclay, G.R., and Newby, D.E.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Heart
Publisher:BMJ Publishing Group
ISSN:1355-6037
ISSN (Online):1468-201X
Published Online:27 November 2009

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