Acute coronary syndromes, plaque vulnerability, and carotid artery disease: The changing role ofatherosclerosis imaging* (original) (raw)
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Plaque characteristics and arterial remodeling in coronary and peripheral arterial systems
Atherosclerosis, 2012
Background: Few studies have examined plaque characteristics among multiple arterial beds in vivo. The purpose of this study was to compare the plaque morphology and arterial remodeling between coronary and peripheral arteries using gray-scale and radiofrequency intravascular ultrasound (IVUS) at clinical presentation. Methods and results: IVUS imaging was performed in 68 patients with coronary and 93 with peripheral artery lesions (29 carotid, 50 renal, and 14 iliac arteries). Plaques were classified as fibroatheroma (VH-FA) (further subclassified as thin-capped [VH-TCFA] and thick-capped [VH-ThCFA]), fibrocalcific plaque (VH-FC) and pathological intimal thickening (VH-PIT). Plaque rupture (13% of coronary, 7% of carotid, 6% of renal, and 7% of iliac arteries; P ¼ NS) and VH-TCFA (37% of coronary, 24% of carotid, 16% of renal, and 7% of iliac arteries; P ¼ 0.02) were observed in all arteries. Compared with coronary arteries, VH-FA was less frequently observed in renal (P < 0.001) and iliac arteries (P < 0.006). Lesions with positive remodeling demonstrated more characteristics of VH-FA in coronary (84% vs. 25%, P < 0.001), carotid (72% vs. 20%, P ¼ 0.001), and renal arteries (42% vs. 4%, P ¼ 0.001) compared with those with intermediate/negative remodeling. There was positive relationship between remodeling index and percent necrotic area in all four arteries. Conclusions: Atherosclerotic plaque phenotypes were heterogeneous among four different arteries; renal and iliac arteries had more stable phenotypes compared with coronary artery. In contrast, the associations of remodeling pattern with plaque phenotype and composition were similar among the various arterial beds.
Plaque burden, arterial remodeling and plaque vulnerability: determined by systemic factors?
Journal of the American College of Cardiology, 2001
This study was designed to determine whether arterial remodeling and plaque vulnerability are influenced by systemic factors. BACKGROUND Atherosclerotic luminal narrowing is caused by gradual plaque growth and arterial remodeling. In the acute phase, luminal narrowing may be accelerated by acute thrombus formation, usually precipitated by rupture of a vulnerable plaque.
Atherosclerosis of coronary blood vessels - local or systemic inflamation?
Prilozi / Makedonska akademija na naukite i umetnostite, Oddelenie za biološki i medicinski nauki = Contributions / Macedonian Academy of Sciences and Arts, Section of Biological and Medical Sciences, 2013
The presence of atherosclerotic lesions in the blood vessels is a predisposition for the development and occurrence of acute ischaemic attacks. Bigger atherosclerotic lesions in the coronary blood vessels cause lumen occlusion, which is a cause of acute myocardial infarction. Endothelial dysfunction is defined as an ability of the endothelium to produce vasorelaxing nitric oxide (NO), or deregulation of the other vasoactive substances, such as angiotensin II and endothelin . This definition describes endothelial dysfunction as an improper vasomotor constriction of the vessel, that leads to lumen occlusion of the already existing atherosclerotic lesions. According to the modern model, the development of atherosclerotic plaque and inappropriate endothelial NO production have a synergistic role in patho-physiological and molecular processes in the blood vessels . Lesions in the coronary arteries are deposits of huge quantities of foamy cells and fibrous plaques. The thin fibrous plaques are 10-20% of the total plaque population and are the cause of 80-90% of clinical cases due to their ability to rupture . According to all the results from published studies by far, it has been pointed out that the plaque stability, not the absolute size influences the rupture potential. Elucidating the risk factors that may modify in the atherogenesis and the consequent atherothrombic effect is the first step to this goal.
Arteriosclerosis, Thrombosis, and Vascular Biology, 1999
Retrospectively, plaque rupture is often colocalized with inflammation of the cap and shoulder of the atherosclerotic plaque. Local inflammation is therefore considered a potential marker for plaque vulnerability. However, high specificity of inflammation for plaque rupture is a requisite for application of inflammation markers to detect rupture-prone lesions. The objective of the present study was to investigate the prevalence and distribution (local versus general) of inflammatory cells in nonruptured atherosclerotic plaques. The cap and shoulder of the plaque were stained for the presence of macrophages and T lymphocytes in 282 and 262 cross sections obtained from 74 coronary and 50 femoral arteries, respectively. From most cases, 2 atherosclerotic arteries were studied to gain insight into the local and systemic distribution of the inflammatory process. In 45% and 41% of all cross sections, staining for macrophages was observed in the femoral and coronary arteries, respectively. Rupture of the fibrous cap was observed in 2 femoral and 3 coronary artery segments and was always colocalized with inflammatory cells. At least 1 cross section stained positively for CD68 or acid phosphatase in 84% and 71% of all femoral and coronary arteries, respectively. Only 1 femoral and 6 coronary arteries revealed a positive stain for CD68 in all investigated segments. Inflammation of the cap and shoulder of the plaque is a common feature, locally observed, in atherosclerotic femoral and coronary arteries. The high prevalence of local inflammatory responses should be considered if they are used as a diagnostic target to detect vulnerable, rupture-prone lesions. (Arterioscler Thromb Vasc Biol. 1999;19:54-58.) Key Words: atherosclerosis Ⅲ plaque vulnerability Ⅲ plaque rupture Ⅲ inflammation Ⅲ macrophages
Relationship Between Coronary Artery Remodeling and Plaque Composition in Culprit Lesions
Circulation Journal, 2007
Background-In vivo studies with intravascular ultrasound have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of marked outward remodeling. A large lipid core and a high macrophage count are recognized histological markers for plaque vulnerability. The link between plaque vulnerability in terms of these markers and remodeling in coronary arteries has not been explored. Methods and Results-In 88 male subjects who died suddenly with coronary artery disease, 108 plaques were studied. The percent remodeling was calculated. Lesions with remodeling Ն0% were considered to have positive remodeling, and those in which remodeling was Ͻ0% were considered to have negative remodeling. Percent lipid core and macrophage count at the plaque were assessed. Of 108 plaque sites, 64 (59.2%) had undergone no remodeling or positive remodeling, and 44 (40.7%) had negative remodeling (vessel shrinkage). Lesions with positive remodeling, compared with lesions with vessel shrinkage, had a larger lipid core (percent mean lipid core was 39.0Ϯ21.0% versus 22.3Ϯ23.1%, respectively; PϽ0.0001) and a higher macrophage count (mean macrophage count was 15.6Ϯ12.3 versus 8.9Ϯ11.6, respectively; Pϭ0.005). Conclusions-We have shown that coronary artery plaques with positive remodeling have a higher lipid content and macrophage count, both markers of plaque vulnerability. These results may explain why plaque rupture is often apparent at sites with only modest luminal stenoses (but marked positive remodeling). (Circulation. 2002;105:939-943.)