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.
Subject(s)
Annexin A5/blood , Endothelial Cells , Endothelium, Vascular/physiopathology , Myocardial Ischemia/blood , Myocardial Ischemia/physiopathology , Platelet Endothelial Cell Adhesion Molecule-1/blood , Ventricular Dysfunction, Left/physiopathology , Aged , Coronary Artery Disease/blood , Coronary Artery Disease/physiopathology , Flow Cytometry , Humans , Male , Middle Aged , Risk Factors , Stem Cells , Stroke Volume , Ultrasonography , Ventricular Dysfunction, Left/blood , Ventricular Dysfunction, Left/diagnostic imagingABSTRACT
OBJECTIVE: Endothelial progenitor cells (EPCs) may have an important role in vascular homeostasis and repair. METHODS: We examined the level of circulating EPCs in pre- (n = 22; mean age 28.7 years), and postmenopausal healthy females without (n = 30; mean age 61.6 years) or under current hormone replacement therapy (HRT) (n = 19; mean age 59.8 years). RESULTS: Premenopausal females had the highest level of circulating EPCs (0.147 +/- 0.076 per thousand of polymorphnuclear cells). The level of EPCs was lowest in postmenopausal females (0.094 +/- 0.058 per thousand), and increased significantly with HRT on average by 25.5%. In addition, the proliferative capacity of circulating EPCs was assessed under cell culture conditions. This capacity was significantly increased in EPCs isolated from postmenopausal subjects under current HRT as compared to corresponding samples obtained from postmenopausal females without HRT. CONCLUSIONS: This observation is in line with the hypothesis that the hormonal status in females modulates the cardiovascular risk and that circulating EPCs could be involved in this phenomenon.
