Dissociation of Phenotypic and Functional Endothelial Progenitor Cells in Patients Undergoing Percutaneous Coronary Intervention

Nicholas L Mills ^1*, Olga Tura ¹, Gareth J Padfield ¹, Christopher Millar ¹, Ninian N Lang ¹, David Stirling ², Christopher Ludlam ², Marc Turner ¹, G Robin Barclay ¹ and David E Newby ¹

¹ The University of Edinburgh, United Kingdom
² Royal Infirmary of Edinburgh, United Kingdom

^* To whom correspondence should be addressed. E-mail: nick.mills{at}ed.ac.uk.

Accepted 21 April 2009

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: Fifty-four patients undergoing elective coronary angiography.

Interventions and main outcome measures: EPCs were quantified by flow cytometry (CD34⁺KDR⁺ phenotype) complemented by real-time 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 3-fold (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±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.