Bulut Daniel, Maier Karin, Bulut-Streich Nadine, Börgel Jan, Hanefeld Christoph, Mügge Andreas
Herzzentrum der Kliniken der Ruhr-Universität Bochum, Standort St. Josef-Hospital, Gudrunstrasse 56, 44791 Bochum, Germany.
J Card Fail. 2008 May;14(4):336-40. doi: 10.1016/j.cardfail.2007.11.002.
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%).
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).
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.
在35例临床病情稳定的男性三支冠状动脉疾病(CAD)患者的外周血中检测了骨髓来源的内皮祖细胞(CD34+和VEGFR2+KDR+内皮祖细胞)和内皮来源的微粒(CD 31+膜联蛋白V+,内皮微粒;内皮细胞凋亡指标)。这些患者被分为两组,即心功能保留或正常组(n = 17;射血分数65±6%)和左心室(LV)功能降低组(n = 18;射血分数36±11%)。
与左心室功能正常或保留的患者相比,左心室功能不全患者的循环内皮祖细胞数量减少了25%(P = 0.07),内皮微粒数量增加了109%(P < 0.05)。通过血流介导的血管舒张评估,内皮祖细胞与内皮功能呈正相关(左心室功能不全患者r = 0.24,左心室功能保留患者r = 0.28)。相比之下,内皮微粒与内皮功能呈负相关(左心室功能不全患者r = -0.42,左心室功能保留患者r = -0.49)。
左心室功能显著不全的CAD患者内皮细胞损伤指数增加。内皮祖细胞数量的减少(或缺乏代偿性升高)可能导致修复潜力降低,从而至少部分促成内皮功能障碍的发病机制。