Abstract

showed a lower FMD (median [interquartile range] 8.5 % [7.3–9.3] vs. 4.7 % [2.7–7.2], p<0.01), demonstrating systemic endothelial dysfunction (ED). Predictors of ED in CSX patients included hypertension, levels of C-reactive protein (CRP) and obesity (body mass index ≥30 kg/m 2 ). These results confirm previous data that in CSX the vascular abnormality may extend beyond coronary microcirculation and involve ED in peripheral arteries, and also further support the role of inflammation as a pathogenetic factor in these patients. Indeed, CRP levels were previously found increased in CSX patients, and were also shown to correlate with systemic ED and with endotheliumdependent CMVD [4–6]. Notably, in a recent study we found that CRP levels were the only independent predictor of endothelium-independent CMVD in a group of CSX patients [7]. A novel finding in the study by Ong et al. is the association of hypertension and obesity with ED in CSX. Other studies failed to show hypertension as an independent predictor of ED in these patients [7]. Thus this relation deserves further investigation in larger studies. On the other hand, no previous study assessed whether obesity can contribute to ED in CSX, although obesity was associated with ED in other clinical settings [8], and was also associated with coronary ED in a mixed group of patients with normal or mildly diseased coronary arteries [9]. ObesitycaninduceEDbyseveralmechanisms.Itisusually associated with other CVRFs, which can by themselves induce ED, but it often also results in insulin resistance, increased oxidative stress, release of pro-inflammatory and vasoactive substances (e.g., endothelin-1, angiotensin), and activation of the adrenergic system, all of which negatively affect vascular function [8, 9].

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