Mobilization of CD34+KDR+ endothelial progenitor cells predicts target lesion revascularization
Version of Record online: 4 SEP 2012
© 2012 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 10, Issue 9, pages 1906–1913, September 2012
How to Cite
BONELLO, L., HARHOURI, K., BAUMSTARCK, K., ARNAUD, L., LESAVRE, N., PIOT, C., PAGANELLI, F., DIGNAT-GEORGE, F. and SABATIER, F. (2012), Mobilization of CD34+KDR+ endothelial progenitor cells predicts target lesion revascularization. Journal of Thrombosis and Haemostasis, 10: 1906–1913. doi: 10.1111/j.1538-7836.2012.04854.x
- Issue online: 4 SEP 2012
- Version of Record online: 4 SEP 2012
- Accepted manuscript online: 16 JUL 2012 12:44PM EST
- Received 12 April 2012, accepted 10 July 2012
- bare metal stent;
- coronary artery disease;
- endothelial progenitor cell;
- in-stent restenosis;
- percutaneous coronary intervention
Summary. Background: Endothelial lesion and regeneration are critical events in the process leading to in-stent restenosis (ISR) after bare metal stent (BMS) percutaneous coronary intervention (PCI).
Objectives: To prospectively investigate the relationship between biomarkers reflecting endothelial turnover and the occurrence of ISR.
Methods: We performed a multicenter prospective observational study that included 156 patients undergoing elective PCI with BMS. Endothelial lesion was assessed by the enumeration of circulating endothelial cells (CECs). Endothelial regeneration was evaluated by enumeration of circulating CD34+ progenitor cells (CD34+ PCs) and CD34+KDR+ endothelial progenitor cells (EPCs). Measurements were performed before PCI, and 6 and 24 h after PCI. Dynamic changes were evaluated by calculating the delta value of each marker. The primary and secondary endpoints of the study were clinical target lesion revascularizations (TLRs) and major adverse cardiovascular events (MACEs) after 6 months of follow-up.
Results: During follow-up, 28 MACEs were recorded, including 27 TLRs. PCI induced a significant rise in the numbers of CECs, CD34+ PCs, and CD34+KDR+ EPCs. Baseline, 6-h and 24-h levels of these markers did not differ between patients with and without TLR. The delta percentage of CD34+KDR+ EPCs was significantly reduced in patients with TLR as compared with patients without TLR (− 0.56 ± 8.1 vs. 2.91 ± 6.2; P = 0.015). In multivariate analysis, the delta percentage of CD34+KDR+ EPCs independently predicted the occurrence of TLR and MACEs (P = 0.02 and P = 0.014, respectively).
Conclusion: The endothelial regenerative response to injury induced by PCI, assessed by CD34+KDR+ EPCs mobilized among progenitor cells, determines the risk of TLR and MACEs in stable coronary artery disease patients.