Advanced Stages Of Atherosclerosis Research Articles

Subclinical carotid atherosclerosis in patients with coronary disease

B-mode ultrasonography is a simple and valid method to evaluate subclinical atherosclerosis of the major superficial arteries. The aim of this study was toknow by this technique the prevalence of carotid atherosclerosisin patients with coronary disease and related factors. In 232patients (205 men and 27 women; age: mean [standard deviation]59 [8] years) with coronary disease, intima-media thickness (IMT),presence and number of atheroma plaques in carotid arteries wereevaluated by B-mode ultrasonography. Controls were 50 healthy subjects whose age was not different from patients. Carotid atherosclerosis was considered when IMT was higher than mean plus two standarddeviations of control values, and/or existence of atheroma plaques. Carotid IMT wasincreased in patients compared to controls 0.82 [0.22] vs 0.62[0.12] mm; p < 0.001) and there were more patients with plaques(67 vs 20%; p < 0.001). Carotid atherosclerosis was found in170 patients and 11 controls (73 vs 22%; p < 0.001). By multivariate analysis, carotid atherosclerosis was associated with age (oddsratio: 1.05; 95% confidence interval [CI], 1.01-1.09) and smoking(odds ratio, 2.11; 95% CI: 1.04-4.26). The presence of more thanone plaque was associated with levels of low-density-lipoprotein(LDL)-cholesterol (odds ratio, 1.01; 95% CI, 1.00-1.02). In the patients with coronary disease, prevalence of subclinical carotid atherosclerosisis very high (73%), and it is associated with age and smoking. The advanced stage of atherosclerosis, evaluated by the existence of more than one plaque, is correlated with LDL-cholesterol levels.

Attenuation of acetylcholine-induced vasoconstriction by L-arginine is related to the progression of atherosclerosis

To determine if L-arginine, a precursor of the endothelium-derived relaxing factor, restores endothelium-dependent dilation in human coronary arteries, we studied 21 patients in whom the lumina of the coronary arteries were angiographically smooth or slightly irregular and in whom there was a constrictor response to acetylcholine (ACh) in the left anterior descending coronary artery or the circumflex coronary artery. We examined the response to intracoronary ACh before and after infusion of L-arginine by measuring coronary diameter with quantitative angiography. Intracoronar injection of ACh produced vasoconstriction in the majority of patients with coronary risk factors. The percentage diameter change in smooth segments in patients with entirely smooth coronary arteries (group 1, n = 44) from baseline was −20.7% ± 17.4%. During systemic infusion of L-arginine, the constrictor response to ACh in these segments was significantly attenuated (−2.2% ± 15.1% from baseline, p < 0.01, ACh alone vs ACh during L-arginine infusion). In smooth segments in patients with luminal irregularities in the other coronary arteries (group 2, n = 19), ACh produced a marked constriction (−32.5% ± 22.5% from baseline, p < 0.05, group 1 vs group 2). Infusion of L-arginine also attenuated ACh-induced vasoconstriction in these segments (−9.7% ± 14.1% from baseline, p < 0.01, ACh vs ACh during L-arginine infusion). In segments with irregular lumina (group 3, n = 26), ACh produced more prominent vasoconstriction. The percentage diameter change was −40.9% ± 26.5% from baseline ( p < 0.01 vs group 1). In contrast, infusion of L-arginine did not attenuate ACh-induced vasoconstriction in these segments (−41.2% ± 26.9% from baseline). Infusion of L-arginine alone did not affect coronary diameter either in smooth or in irregular segments. L-arginine did not augment the dilator response to ACh in normal segments ( n = 7) (15.4% ± 9.7% vs 16.3% ± 10.6%, p not significant [NSJ ACh vs ACh during L-arginine infusion). The endothelium-independent vasodilation by isosorbide dinitrate was well preserved in all coronary segments examined (30.4% ± 21.2% in group I, 26.1% ± 18.1% in group 2, and 32.6% ± 20.6% in group 3; p NS). We conclude that exogenous L-arginine reverses ACh-induced vasoconstriction in human coronary arteries in the early stages of atherosclerosis, whereas L-arginine does not reverse the response in the advanced stage of atherosclerosis.