Abstract

Background Bone-marrow derived endothelial progenitor cells (CD34+ and VEGFR2 + KDR + EPC) and endothelial-derived microparticles (CD 31+Annexin V+, EMP; indicator for endothelial apoptosis) were examined in the peripheral blood of 35 male, clinically stable patients with 3-vessel coronary artery disease (CAD). The patients were divided in 2 groups, those with preserved or normal function (n = 17; EF 65 ± 6%) and those with reduced left ventricular (LV) function (n = 18; EF 36 ± 11%). Methods and Results The number of circulating EPCs was decreased by 25% ( P = .07) and the number of EMPs was increased by 109 % ( P < .05) in patients with LV dysfunction compared with those with normal or preserved LV function. EPCs were positively correlated ( r = 0.24 for patients with LV dysfunction and r = 0.28 for patients with preserved LV function) with endothelial function as assessed by flow-mediated vasodilatation. In contrast, EMPs were inversely correlated ( r = –0.42 for patients with LV dysfunction and r = –0.49 for patients with preserved LV function). Conclusions CAD patients with significant LV dysfunction show an increased index of endothelial cell damage. This decrease (or lack of compensatory elevation) of EPCs may result in a reduced potential for repair and thus contribute at least in part to the pathogenesis of endothelial dysfunction.

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