Endothelial progenitor cell mobilization after percutaneous coronary intervention

Background In animal models, circulating endothelial progenitor cells (EPC) have been shown to participate in repair of damaged or degenerating vascular surfaces. In humans, reduced EPC counts correlate with cardiovascular risk and disease outcome; yet it has been difficult to establish that EPC are in fact mobilized in response to vascular injury as a physiologic response. We therefore studied early (<12 h) mobilization of EPCs into the peripheral circulation after a defined vascular manipulation, percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) and non-ACS patients. Methods and results CD34/CD31 positive EPC colony forming units (EPC-CFU) were quantified by a blinded observer in peripheral blood samples from eight control patients with angiographically normal coronary arteries, and in 30 patients with coronary artery lesions before and 12 h after PCI. All patients (n = 38) had one or more CV risk factors. Ten patients presented with acute coronary syndrome (PCIACS), and the rest (n = 20) underwent elective PCI (PCIElect). Despite the presence of an acute coronary syndrome, patients in the PCIACS group did not present with increased EPC-CFU compared with either the PCIElect or control groups (P > 0.05). In addition, EPC-CFU (colonies/ml blood) increased significantly in the PCIElect group after stent placement (11.8 + 1.6 before versus 16.5 + 1.9 after, P = 0.0009), while in contrast, PCI did not stimulate EPC mobilization in patients in the PCIACSgroup (9.6 + 3.2 before versus 6.5 + 1.8, P = 0.20). We found a higher presenting vascular endothelial growth factor (VEGF) level in the PCIElect group compared to PCIACS (78.7 + 25.2 versus 15.3 + 7.9 pg/ml blood, P = 0.02). However, VEGF levels increased after PCI only in the PCIACS group (15.3 + 7.9 to 133.3 + 27.5 pg/ml, P = 0.003) and not in the PCIElect group (78.7 + 25.2 to 79.7 + 12.2 pg/ml, P = 0.97). Conclusion Our findings suggest that focal coronary endothelial injury as a result of PCI triggers early mobilization of EPC into the peripheral circulation in patients presenting for an elective PCI, without a corresponding rise in VEGF levels. In contrast, patients with an acute coronary syndrome fail to respond to PCI with early EPC mobilization despite a significant rise in VEGF. The results of the present study may suggest a novel mechanism for early EPC augmentation after PCI.