PubMed · 7246854
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R L Kinlough-Rathbone, J F Mustard. 1981. Atherosclerosis. Current Concept.. https://doi.org/10.1016/0002-9610(81)90068-4
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Within blood vessels the accumulation of monocytes/macrophages at sites of modified lipoproteins is an important feature in atherosclerosis. Recently the presence of LDL and other proteins modified by hypochlorous acid (HOCl-LDL) was demonstrated in human atherosclerotic vessels and human inflammatory kidney disease by immunohistology and protein chemistry. Chemokines contribute to a specific and directed migration of inflammatory cells. IL-8 (alpha-chemokine) attracts mainly neutrophils and distinct T-cell subsets while MCP-1 (beta-chemokine) preferentially acts on monocytes/macrophages. In the present study it was postulated that HOCl-LDL may induce and amplify inflammatory reactions by the induction of chemokine synthesis in local monocytes. After exposure of human monocytes to HOCl-LDL, it was found that mRNA and protein of the chemokine IL-8 was strongly induced, while the chemokine MCP-1 was not. HOCl-LDL itself led to a chemotactic migration of neutrophils. A chemotactic response of human monocytes toward HOCl-LDL was not detectable. We propose that HOCl-LDL may represent a form of LDL modification in the atherosclerotic process which initiates leukocyte infiltration; these mononuclear cells have been observed in the early stages of atherosclerosis.
PURPOSE: We assessed the performance of T2-weighted MR imaging in detecting atherosclerotic fibrous caps and in depicting their integrity. METHODS: Twenty atherosclerotic lesions removed by carotid endarterectomy were imaged on a 1.5-T system using T2-weighted spin-echo sequences. The MR images were reviewed independently by four blinded interpreters for fibrous caps and ruptures. The results obtained from the observers were then graded against histologic findings by using receiver-operating characteristic (ROC) curve analysis. RESULTS: The area under the ROC curve for fibrous cap detection was 0.80, indicating that T2-weighted MR imaging was a good but not definitively diagnostic test for detecting ex vivo fibrous caps. The ROC curve for fibrous cap characterization yielded an area of 0.75, indicating that T2-weighted MR imaging was a fair but not highly diagnostic test for depicting fibrous cap integrity. A definite reading for detection of fibrous caps or rupture was fairly specific (90% and 98%, respectively) but not very sensitive (37% and 12%, respectively). CONCLUSIONS: T2-weighted MR imaging of ex vivo atherosclerotic plaques aided in the detection and evaluation of fibrous caps. In both cases, MR imaging proved more useful for ruling out disease than for confirming its presence.
BACKGROUND: Recruitment of circulating leukocytes at sites of atherosclerosis is mediated through a family of adhesion molecules. The function of circulating forms of these adhesion molecules remains unknown, but their levels may serve as molecular markers of subclinical coronary heart disease (CHD). METHODS AND RESULTS: To determine the ability of circulating vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intercellular adhesion molecule-1 (ICAM-1) to serve as molecular markers of atherosclerosis and predictors of incident CHD, we studied 204 patients with incident CHD, 272 patients with carotid artery atherosclerosis (CAA), and 316 control subjects from the large, biracial Atherosclerosis Risk In Communities (ARIC) study. Levels of VCAM-1 were not significantly different among the patients with incident CHD, those with CAA, and control subjects. Higher levels of E-selectin and ICAM-1 were observed for the patients with CHD (means [ng/mL]: E-selectin, 38.4; ICAM-1, 288.7) and those with CAA (E-selectin, 41.5; ICAM-1, 283.6) compared with the control subjects (E-selectin, 32.8; ICAM-1, 244.2), but the distributions were not notably different between the patients with CHD and CAA. Results of logistic regression analyses indicated that the relationship of ICAM-1 and E-selectin with CHD and CAA was independent of other known CHD risk factors and was most pronounced in the highest quartile. The odds of CHD and CAA were 5.53 (95% CI, 2.51-12.21) and 2.64 (95% CI, 1.40-5.01), respectively, for those with levels of ICAM-1 in the highest quartile compared with those in the lowest quartile. Odds of CAA were 2.03 (95% CI, 1.14-3.62) for those with levels of E-selectin in the highest quartile compared with those in the lowest quartile. CONCLUSIONS: These data indicate that plasma levels of ICAM-1 and E-selectin may serve as molecular markers for atherosclerosis and the development of CHD.