Both carotid and peripheral percutaneous transluminal angioplasty mobilize progenitor cells

It is well known that circulating endothelial progenitor cells (EPC) are involved in injured endothelium repair, contributing to angiogenesis in in vitro and in vivo models. The main triggers of EPC mobilization from bone marrow to peripheral blood are ischemia and vascular trauma. Endothelial injury induced by coronary angioplasty has been recently shown as sufficient to trigger EPC mobilization in coronary artery disease (CAD) patients. Aim of our work was to evaluate the effect of internal carotid angioplasty and peripheral transluminal angioplasty on circulating progenitor cells (PC, CD34+ cells) and EPC (CD34+KDR+ cells) mobilization. Methods: 10 patients (7 males and 3 females, mean age 64.2 ± 10.3 years) undergoing elective percutaneous transluminal angioplasty (PTA) were consecutively enrolled. 5 patients underwent internal carotid angioplasty (IC-PTA) and the others peripheral transluminal angioplasty (P-PTA). Inclusion criteria were: carotid stenosis greater than 70 for IC-PTA; peripheral stenosis greater than 70 and documented peripheral arterial disease (PAD), defined by an intermittent claudication (Leriche-Fontaine stage II) for P-PTA. Patients with unstable angina, myocardial infarction or stroke within the preceding 3 months were excluded to avoid any potentially confounding effect. Peripheral blood samples were collected at the time of admission (t0), on day 1 (t1), on day 7 (t7) and on day 30 (t30). C-reactive protein (CRP), white blood cells (WBC) and VEGF were evaluated. Circulating PC and EPC were determined by flow cytometry analysis. Data are expressed as cells number per ml of blood according to the International Society of Hematotherapy and Graft Engineering protocol. Patients were treated according to the international guidelines and the angioplasty outcome was evaluated by Echo colour Doppler ultrasonography at t1, t7 and t30. Results: No significant differences were found in the prevalence of risk factors. The efficacy of PTA was confirmed in all patients, showing stent patency by Echo colour Doppler evaluation. In all patients the PC count at t7 was significantly increased compared with basal level (t0: 1694±141/mL vs. t7: 2748±375/mL, p0.024) and t1 (t1: 1413±215/mL vs. t7: 2748±375/mL, p0.002), in parallel to VEGF concentration (t0: 530±95 vs t7: 759±153 pg/mL, p0.024; t1: 555±92 vs t7: 759±153 pg/mL, p0.037). Regarding EPC levels, at t7 a trend to an increase compared to both t0 (t0: 595±72/mL vs. t7: 737±98/mL, p0.085) and t1 (t1: 529±87/mL vs. t7: 737±98/mL, p0.052) was observed, maintained up to day 30. CRP was significantly increased after angioplasty, with a peak at t1 (t0: 4.3±0.5 vs t1: 42.3±13.8 mg/L, p0.028), remaining elevated at t7 (t0: 4.3±0.5 vs t7: 26.2±4.3 mg/L, p0.001) and decreasing to baseline levels at t30. Considering IC-PTA and P-PTA separately, in the first group we observed both for PC and EPC levels a trend to increase lasting up to 30 days, while in P-PTA patients the mobilization lasted only up to 7 days. Conclusions: Our data show a transient PC and EPC mobilization together with an increase of VEGF and CRP levels following vascular injury, suggesting that it can be part of an inflammatory response PTA-induced. No relevant differences seem to exist between IC-PTA and P-PTA except for 1-month progenitor quantification. Longitudinal studies and a greater number of patients are required to determinate the role that PC mobilization PTA-induced may play as prognostic factor to identify high-risk patients for restenosis and other cardiovascular events after PTA.