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 (<12h) 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.


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 12h after PCI. All patients (n=38) had one or more CV risk factors. Ten patients presented with acute coronary syndrome (PCI(ACS)), and the rest (n=20) underwent elective PCI (PCI(Elect)). Despite the presence of an acute coronary syndrome, patients in the PCI(ACS) group did not present with increased EPC-CFU compared with either the PCI(Elect) or control groups (P>0.05). In addition, EPC-CFU (colonies/ml blood) increased significantly in the PCI(Elect) 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 PCI(ACS) group (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 PCI(Elect) group compared to PCI(ACS) (78.7+25.2 versus 15.3+7.9 pg/ml blood, P=0.02). However, VEGF levels increased after PCI only in the PCI(ACS) group (15.3+7.9 to 133.3+27.5 pg/ml, P=0.003) and not in the PCI(Elect) group (78.7+25.2 to 79.7+12.2 pg/ml, P=0.97).


CONCLUSIONS
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.
Banerjee
Subhash
S
University of Texas Southwestern Medical Center, Dallas, TX, USA. mdcare@aol.com
Brilakis
Emmanouil
E
Zhang
Shuqi
S
Roesle
Michele
M
Lindsey
Jason
J
Philips
Binu
B
Blewett
Christopher G
CG
Terada
Lance S
LS
D015906:Angioplasty, Balloon, Coronary; D018952:Antigens, CD34 / Q000276:immunology; D002478:Cells, Cultured; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000473:pathology / Q000628:therapy*; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology*; D005260:Female; D019650:Hematopoietic Stem Cell Mobilization; D006801:Humans; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000276:immunology; D011379:Prognosis; D013234:Stem Cells / Q000276:immunology / Q000473:pathology*
D018952:Antigens, CD34; D019408:Platelet Endothelial Cell Adhesion Molecule-1