Delayed Flow-Mediated Vasodilation and Critical Coronary Stenosis

Abstract

Endothelial dysfunction, wall thickening and plaque are progressive manifestations of atherosclerosis. Delayed or absent brachial artery dilation after ischemic stimulus has been associated with severity of extracoronary and coronary atherosclerosis. In the current study, we aimed to verify if delayed or absent dilation associates with critical coronary stenosis. We also evaluated the association between coronary stenosis, carotid artery wall thickness and peripheral artery disease. Endothelial function was investigated by flow-mediated dilation of the brachial artery up to 3 min after ischemia, and patients classified as early, late or no dilators. Coronary angiography was performed through transradial or femoral artery approach. Computerized quantitative angiography was used to obtain percent stenosis of all lesions, while the Gensini score was used to evaluate the severity of coronary atherosclerosis. Seventy-four patients were enrolled. Carotid wall thickness and plaque, and peripheral artery disease were detected by ultrasound. Subjects with critical coronary stenosis showed a higher prevalence of delayed or absent dilation (coronary stenosis ≥70 per cent: late dilators 50 per cent, no dilators 35 per cent; coronary stenosis ≤70 per cent : late dilators 27 per cent, no dilators 6 per cent). The Gensini score was progressively higher in late dilators and no dilators compared with early dilators (early: 4.5±13.5; late 17.5±27.1; no 39.7±55.0; P<0.02). Carotid atherosclerosis and peripheral artery disease were more prevalent in subjects with critical coronary stenosis. Delayed or absent dilation associates with coronary stenosis and different degree of coronary atherosclerosis. The kinetic of arterial dilation seems to be relevant as the magnitude of dilation.

Effect of empagliflozin on brachial artery shear stress and endothelial function in subjects with type 2 diabetes: Results from an exploratory study

“…Cardiovascular risk factors, including diabetes, alter the endothelial response to SS variations, which can be assessed through flow-mediated (or SS-mediated) vasodilatation of the brachial artery. [12][13][14]17 In the present study, we hypothesized that empagliflozin might influence SS and endothelial function by influencing blood viscosity. Therefore, we accurately measured blood flow velocity, arterial diameter and blood viscosity.…”

Relationship between Flow-mediated Endothelial Vasodilation and the Pulse Wave Velocity, and Cervical Carotid Artery Stenosis

“…The PWV is associated with major cardiovascular risk factors and a predictor of the prognosis of patients with end-stage renal failure and hypertension. 7) According to Tamaki et al, 4) it is associated with carotid atherosclerosis but not with the severity of cervical carotid artery stenosis. However, it is correlated with the carotid IMT in patients with type 2 DM.…”

Initiating guideline-concordant gout treatment improves arterial endothelial function and reduces intercritical inflammation: a prospective observational study

“…The mean allopurinol and febuxostat doses at treatment target were 384 ± 131 mg and 53 ± 23 mg/day, respectively. The median [interquartile range] time from initiating ULT (visit 2) to achieving sU target (visit 3) was 21 [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] weeks for the overall group (for non-tophaceous subjects, 17 [12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] weeks; for tophaceous patients, 29 [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] weeks).…”

“…Alternatively, we recently reported that, compared to non-gout healthy controls, patients with gout have impairment of both brachial artery flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD), measurements of endothelium-dependent and endothelium-independent (smooth muscle) arterial responsiveness respectively [ 25 ]. Impaired endothelial function assessed by FMD correlates with risk for future coronary events [ 26 – 29 ], and studies both in vitro and in animal models indicate that urate may impede the ability of endothelial cells to generate nitric oxide and thus limit arterial responsiveness [ 30 , 31 ]. Therefore, both endothelial function and inflammation may be targets for lowering cardiovascular risk in patients with gout.…”