Endothelial progenitor cells (EPCs) are bone marrow-derived undifferentiated cells that are rapidly mobilized in response to tissue ischemia and incorporated into sites of neovascularization. EPCs co-express surface CD34, CD133 and vascular endothelial growth factor receptor-2 (VEGFR-2) antigens and develop an endothelial phenotype in culture. In animal models of tissue ischemia EPCs were shown to participate in angiogenesis and vasculogenesis. We sought to determine whether circulating EPCs level correlate with collateral formation following a non-ST segment elevation myocardial infarction (NSTEMI). In addition, we sought to evaluate the effect of percutaneous coronary intervention (PCI) on the levels of circulating EPCs. Twenty patients who underwent PCI within a week of NSTEMI were divided into two groups: patients without collaterals [coll(−), n=10] and patients with Rentrop grade 3–4 collaterals [coll(+), n=10]. Two blood samples were drawn from all patients: before PCI and 24±2 hours after PCI. Using flow cytometry the percentage of cells co-expressing VEGFR-2 and CD133 was determined. In addition, EPC colonies were grown from peripheral blood mononuclear cells, characterized, and counted after 7 days of culture. The clinical characteristics of the two groups were similar. The coll(+) group had a higher degree of culprit vessel stenosis and lower initial TIMI flow grade. The relative number of EPCs (co-expressing VEGFR-2 and CD133) before PCI was significantly higher in the coll(+) group than in the coll(−) group (1.49±0.9% vs. 0.77±0.4%, P=0.045). There were no significant inter-group differences in the number of EPC colony-forming cells. The number of EPC colonies increased significantly in the coll(−) group following PCI (from 9.5±4.8 to 14.0±5.9 per 106 cultured cells, P=0.01). This study supports an association between circulating EPC levels and collateral formation in patients with a NSTEMI. Furthermore, these findings suggest that vascular injury during PCI triggers mobilization of EPCs to the peripheral blood, especially in patients without coronary collaterals. Our data suggest that patients with high levels of circulating EPCs are more likely to form coronary artery collaterals and that vascular injury induces EPC recruitment.

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