Oral Session IV. Translational cardiovascular science

Abstract

O397 Balance between circulating endothelial progenitor cells (EPCs) and mature circulating endothelial cells (CECs) in relation to the severity of peripheral arterial disease FCesari, F Sofi, RCaporale, G Pratesi, R Pulli, C Pratesi, RAbbate, GFGensini University of Florence, Florence, Italy, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy Topic: Peripheral vascular disease Introduction: the maintenance of endothelial health depends, not only on the local milieu, but also on circulating endothelial progenitor cells (EPCs) derived from the bone marrow. Indeed, EPCs support the integrity of vascular endothelium and promote revascularisation of ischemic areas. On the other hand, circulating mature endothelial cells (CECs) are considered a marker of endothelial injury. Previous studies demonstrated reduced number of EPCs in peripheral arterial disease (PAD) patients, but few data are available on CECs. Aim of our study was to contemporary assess EPCs and CECs in PAD patients in relation to the severity of the disease. Methods: in 30 PAD patients [22 M/ 8 F; median age: 69 (45-86) years] we measured circulating EPCs and CECs by using flow cytometry. EPCs were defined as CD34+KDR+, CD133+KDR+ and CD34+CD133+KDR+, while CECs were defined as CD146+/CD31+/CD45-/CD61-. Results: a significant trend of decrease (p<0.05) in relation to the clinical severity of the disease, as seen by Fontaine’s stages, was observed for CD133+/KDR+ EPCs [stage IIa: 0.093 (0.060.25); stage IIb: 0.049 (0.02-0.16); stage III: 0.03 (0.02-0.05); stage IV: 0.035 (0.02-0.08) cells/ ÿ ÙL]. On the contrary, a significant (p<0.05) increase was showed by CECs [stage IIa: 0.077 (0.02-0.13); stage IIb: 0.084 (0.02-0.19); stage III: 0.15 (0.05-0.19); stage IV: 0.22 (0.08-0.33) cells/ ÿ ÙL]. In order to evaluate the balance existing between EPCs and CECs in relation to the clinical progression of the disease, we calculated the CECs/EPCs ratio. By increasing Fontaine’s stage, a progressive and significant (p<0.05) increase in ratio value was observed, indicating a prominent role of CECs with respect to EPCs number [stage IIa: 0.62 (0.2-2.30); stage IIb: 1.22 (0.23-7.67); stage III: 6.39 (1.43-7.71); stage IV: 6.14 (1-16)] Conclusions: our results demonstrate an inbalance between EPCs and CECs in PAD patients in relation to the progression of the disease, possibly indicating that the endothelial damage observed in these patients is not sufficiently repaired by a concomitant increase of the regenerative capacity of EPCs.