Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.
Although carotid IMT is significantly correlated with extent and severity of CAD, the relationship is weak. This relatively poor correlation (r2 < .10) should be considered in the interpretation of clinical trials that use carotid IMT as a surrogate end point for coronary atherosclerosis.
In hypercholesterolemic rabbits, oral L -arginine (the substrate for endothelium derived nitric oxide) attenuates endothelial dysfunction and atheroma formation, but the effect in hypercholesterolemic humans is unknown. Using high resolution external ultrasound, we studied arterial physiology in 27 hypercholesterolemic subjects aged 29 Ϯ 5 (19-40) years, with known endothelial dysfunction and LDL-cholesterol levels of 238 Ϯ 43 mg/dl. Each subject was studied before and after 4 wk of L -arginine (7 grams ϫ 3/ day) or placebo powder, with 4 wk washout, in a randomized double-blind crossover study. Brachial artery diameter was measured at rest, during increased flow (causing endothelium-dependent dilation, EDD) and after sublingual glyceryl trinitrate (causing endothelium-independent dilation). After oral L -arginine, plasma L -arginine levels rose from 115 Ϯ 103 to 231 Ϯ 125 mol/liter ( P Ͻ 0.001), and EDD improved from 1.7 Ϯ 1.3 to 5.6 Ϯ 3.0% ( P Ͻ 0.001). In contrast there was no significant change in response to glyceryl trinitrate. After placebo there were no changes in endothelium-dependent or independent vascular responses. Lipid levels were unchanged after L -arginine and placebo.
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