Abstract
BackgroundChronic kidney disease (CKD) is an independent risk factor for the development and severity of coronary artery disease (CHD) and endothelial dysfunction. There is an increase in the circulating angiogenesis inhibitors endostatin (END), thrombospondin-2 (TSP), angiopoietin-2 (ANG) and the nitric oxide (NO) inhibitor asymmetric dimethyl arginine (ADMA) in CKD patients. The aim of this study was to evaluate associations of the serum level of these factors and of the related angiogenesis inhibitor, endoglin (ENG), with burden of coronary atherosclerosis.MethodsOne hundred twenty-two patients undergoing coronary angiography were recruited from the cardiac catheterization lab at a single center. The total burden of coronary plaque (mm2) and the presence of coronary collaterals were quantified using quantitative coronary angiography (QCA). Serum levels of angiogenesis inhibitors were measured by ELISA (ENG, END, and ANG), Luminex assay (TSP), or HLPC (ADMA), respectively. Associations with plaque burden and coronary collateral supply were analyzed in multi-variable linear and logistic regression models.ResultsThere was no significant association found between levels of circulating ADMA, ENG, END, ANG, or TSP and coronary plaque burden or collateral formation.ConclusionsOur findings suggest that associations of circulating END, ENG, TSP, and ANG with cardiovascular mortality are unlikely to be mediated via direct effects on coronary plaque formation or by inhibition of collateral formation. Whether associations of these factors with mortality are mediated via local concentrations, myocardial tissue, or intra-plaque expression of these factors or by an effect on plaque vulnerability merits additional investigation.
Highlights
Chronic kidney disease (CKD) is an independent risk factor for the development and severity of coronary artery disease (CHD) and endothelial dysfunction
Results were similar in analyses using the Gensini score in place of the percent area stenosis
asymmetric dimethyl arginine (ADMA) has been implicated as an independent risk factor for both all-cause mortality and cardiovascular events [20, 21], and it has been associated with the presence of atherosclerosis in some but not all studies [22, 23]
Summary
Chronic kidney disease (CKD) is an independent risk factor for the development and severity of coronary artery disease (CHD) and endothelial dysfunction. “Framingham” risk factors are well-established contributors to the pathogenesis of coronary disease, and factors beyond hyperlipidemia, diabetes, and hypertension appear to play important roles in the development and progression of atherosclerosis [2]. The vascular endothelium plays a key role in maintaining homeostasis, and it functions to promote vasodilation, inhibit luminal and vascular wall coagulation, and prevent the proliferation of smooth muscle and foam cells. These functions may be perturbed, when the bioavailability of nitric oxide (NO) is low, leading to a state favoring vasoconstriction, thrombosis, vascular smooth muscle cell proliferation, and the generation of atherosclerotic plaque [5]. The regulation of angiogenesis appears to be a key Charytan et al Fibrogenesis & Tissue Repair (2015) 8:13 factor in the propagation of coronary artery disease and rupture of atherosclerotic plaque [3]
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