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      Atherosclerotic Expansive Remodeled Plaques: A Wolf in Sheep’s Clothing

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          Geometric arterial remodeling is an important determinant of luminal narrowing in atherosclerotic disease. Expansive remodeling retards while constrictive remodeling accelerates luminal narrowing by plaque formation. Cross-sectional as well as follow-up studies revealed that expansive remodeling is associated with adverse cardiovascular events and a vulnerable plaque phenotype. Although the relation between expansive remodeling and plaque vulnerability is associative rather than causal, expansively remodeled plaques should be considered as a wolf in sheep’s clothes. Further understanding of the processes that regulate arterial remodeling and plaque rupture may lead to new strategies to responsibly manipulate these processes for the benefit of patient outcomes.

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          Most cited references 8

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          Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site.

          The beta2 integrin leukocyte function antigen-1 (LFA-1) has an important role in the pathophysiology of inflammatory and autoimmune diseases. Here we report that statin compounds commonly used for the treatment of hypercholesterolemia selectively blocked LFA-1-mediated adhesion and costimulation of lymphocytes. This effect was unrelated to the statins' inhibition of 3-hydroxy-3-methylglutaryl coenzyme-A reductase; instead it occurred via binding to a novel allosteric site within LFA-1. Subsequent optimization of the statins for LFA-1 binding resulted in potent, selective and orally active LFA-1 inhibitors that suppress the inflammatory response in a murine model of peritonitis. Targeting of the statin-binding site of LFA-1 could be used to treat diseases such as psoriasis, rheumatoid arthritis, ischemia/reperfusion injury and transplant rejection.
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            Morphological predictors of arterial remodeling in coronary atherosclerosis.

            Although arterial remodeling in atherosclerotic arteries affects luminal patency, the role of plaque components has not been systematically studied. Coronary segments (n=2885) were harvested from the hearts of 36 patients who died of severe coronary artery disease after perfusion fixation. Remodeling was determined by morphometric analysis of 657 sections selected as reference segments and 1318 segments with atheromatous plaques. Atherosclerotic plaques were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemorrhage with or without rupture or erosion, or total occlusion. Plaque components consisted of calcification, lipid core, macrophage burden, and fibrosis. There was no correlation between plaque area and lumen size in proximal arteries, unlike middle and distal segments, which demonstrated a significant correlation. Marked expansion of the internal elastic lamina (IEL) occurred in plaque hemorrhages with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions and total occlusions there was shrinkage of the IEL. Macrophage burden, lipid core size, calcium (in fibrous plaque and lipid core), and medial atrophy were all associated with positive remodeling; fibrous areas, however, were negatively associated with remodeling. Inflammation, calcification, and medial thinning are primary determinants of positive remodeling, which appears to be a feature of plaque instability.
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              Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: an in vivo intravascular ultrasound study.

              This intravascular ultrasound study sought to examine to what extent native coronary artery stenosis is accompanied by vessel wall thickening or inadequate compensatory enlargement (relative vessel constriction), or both. In human femoral arteries, inadequate compensatory enlargement is reported to be a paradoxic mechanism for the development of severe arterial lumen narrowing. However, it is unclear in human coronary arteries whether inadequate compensatory enlargement contributes to the development of critical arterial stenosis. Thirty-five primary coronary artery lesions from 30 patients (19 men, 11 women; mean [+/- SD] age 65 +/- 13 years) were imaged by intravascular ultrasound. The vessel cross-sectional area and lumen area were measured, and the wall area (vessel cross-sectional area minus lumen area) was calculated at the lesion site and at the proximal and distal reference sites. We defined compensatory enlargement to be present when the vessel cross-sectional area at the lesion site was larger than that at the proximal reference site, inadequate compensatory enlargement when the vessel cross-sectional area at the lesion site was smaller than that at the distal reference site and intermediate remodeling when the vessel cross-sectional area at the lesion site was intermediate between the two reference sites. Compensatory enlargement was observed in 19 (54%) of 35 lesions, inadequate compensatory enlargement in 9 (26%) of 35 and intermediate remodeling in 7 (20%) of 35. In the inadequate compensatory enlargement group, reduction of the vessel cross-sectional area contributed to 39% of lumen reduction. Compensatory enlargement commonly (54%) occurs at stenotic coronary lesions. However inadequate compensatory enlargement results in a substantial amount (39%) of the lumen area reduction in 26% of primary coronary artery lesions.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                December 2002
                17 January 2003
                : 39
                : 6
                : 514-523
                aLaboratory of Experimental Cardiology, University Medical Center and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands, and bDivision of Cardiovascular Medicine, Stanford University Medical Center, Stanford, Conn., USA
                67204 J Vasc Res 2002;39:514–523
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 3, References: 68, Pages: 10
                Research Paper


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