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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A recent anatomical study has reported a relationship between the presence of ulcerated atheromatous plaque of the aortic arch and cerebral infarction. Several studies using transoesophageal echocardiography have established that atherothrombosis of the ascending and proximal is a potential source of systemic embolism. We have shown that aortic plaques > or = 4 mm in thickness increase the risk of cerebral infarction by 9. Several studies have shown that this localisation of atherosclerosis was also a powerful marker of general vascular risk. In the multicenter FAPS (French Study of Aortic Plaque in Stroke) trial, the authors followed up 331 patients who had suffered cerebral infarction, aged over 60 years, for a mean duration of 2.4 years. The occurrence rate of cerebral infarction and the incidence of cardiovascular complications (death, myocardial infarction, cerebral infarction, systemic embolism) was respectively 11.9% and 26% per year. The presence of plaques with thickness greater or equal to 4 mm was associated with an adjusted relative risk of 3.8 (95% confidence interval, 1.8 to 7.8) and 3.5 (95% confidence interval, 3.1 to 5.9) respectively. The influence of plaque morphology (thrombus, irregularity, absence of calcification), independently of its thickness, also seems to affect the prognosis. In this study, as in those reported by other groups, the influence of anti-thrombotic therapy was not specifically addressed. The definition of high risk plaques (thickness, irregularity, thrombus) could be useful in the evaluation of therapy which affects the atherosclerotic process (antiplatelet agents, anticoagulants, statins). We conclude that atherosclerosis of the ascending aorta and aortic arch is a potential source of systemic embolism and a powerful marker of overall vascular risk.
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PMID:[Evaluation of aortic atherosclerosis by transesophageal echocardiography. Prognostic implications]. 929 22

We evaluated risk factors involved in regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. Using ultrasonography, we examined the brachial, common carotid, and common femoral arteries in 65 hospitalized Japanese patients (15 controls, 18 patients with hypertension, 16 with diabetes mellitus, and 16 with both hypertension and diabetes mellitus). They ranged in age from 39 to 81 yr, mean 60.3 yr. The thickness of the intima-media complex of the far wall was measured, and the severity of atherosclerotic plaques was graded according to maximal lumen stenosis. The intima-media thickness in the carotid and femoral arteries was significantly greater in the hypertensive patients and the hypertensive patients with diabetes than in the controls. Severity of plaque was greater in the hypertensive patients with diabetes than in the controls. Plaque grades were higher in the carotid and femoral arteries than in the brachial artery. Multiple regression analysis revealed that age and mean blood pressure were strongly associated with the intima-media thickness in all three arteries. In the femoral artery, cigarette smoking and hyperglycemia also significantly correlated with the intima-media thickness. Plaque grades increased with age in the carotid and brachial arteries, while in the femoral artery the grade increased with cigarette smoking and serum cholesterol concentration. These findings suggest that the extent of atherosclerosis and its underlying risk factors differ among arterial sites. In addition, risk factors may partly differ according to the stage of atherosclerosis. To prevent or reverse atherosclerosis, the above differences should be taken into account.
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PMID:Ultrasonographic assessment of regional differences in atherosclerotic lesions in patients with hypertension, diabetes mellitus, or both. 932 98

Immunocompetent cells infiltrate atherosclerotic plaques of all stages. Plaque-infiltrating T-cells recognize oxidized LDL and heat shock proteins and this elicits antibody responses that have been proposed as markers of disease activity. Cytokines secreted by activated T-cells may control macrophage activation, scavenger receptor expression and metalloproteinase secretion. Furthermore, cytokines secreted by T-cells and macrophages modulate smooth muscle proliferation, nitric oxide production and apoptosis, and induce endothelial activation. However, both positive and negative signals, as well as feedback loops, may be induced because of the complexity of the immune system. The possibility that some of these signals may be protective against atherosclerosis is currently under investigation in several laboratories. Recent studies in experimental animals show that immunomodulation affects the development of plaques and that immunization with oxidized LDL can inhibit lesion formation. This review provides a brief overview of cellular immunology and an analysis of its potential role in atherogenesis.
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PMID:Cell-mediated immunity in atherosclerosis. 933 54

Multiple risk factors for cardiovascular disease, particularly hypercholesterolemia, are often present in the hypertensive patient. Recent guidelines, ranging from those prepared by the World Health Organization/International Society of Hypertension to those of the three European Societies of Cardiology, Atherosclerosis, and Hypertension, stress the importance of evaluating global risk, based on the presence of all cardiovascular risk factors in an individual or in a group of subjects. It has also been suggested that treatment should aim to correct all modifiable risk factors. This is a reasonable recommendation, but although observational epidemiologic studies have shown that the effects of concomitant risk factors are additive, if not multiplicative, it is surprising that no intervention trial has been undertaken to determine whether the benefits of treating more than one risk factor are also additive. The Plaque Hypertension Lipid-Lowering Italian Study (PHYLLIS) is the first such study. Its aim is to investigate the potential benefit of lowering blood pressure and plasma cholesterol on the progression of carotid plaque in hypertensive patients with elevated plasma cholesterol. Using a factorial design, the antiatherosclerotic effect of two different antihypertensive drugs, the angiotensin-converting enzyme (ACE) inhibitor fosinopril and the diuretic hydrochlorothiazide will be compared. The study aims to confirm animal experiments demonstrating the benefit of ACE inhibitors on experimental atherosclerosis. PHYLLIS will also compare the effects of two lipid-lowering regimens, diet plus placebo and diet plus pravastatin, in the study population. This 3-year, multicenter, double-blind, randomized Italian study, using B-mode ultrasound evaluation of the carotid walls with central reading of the ultrasound scans (Bowman Gray University, Winston-Salem, NC) is now underway and should provide useful evidence about the benefits of multiple risk factor treatment in the hypertensive patient.
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PMID:The hypertensive patient with multiple risk factors: is treatment really so difficult? 936 77

This prospective study was conducted to correlate the presence of angiographically significant coronary artery disease (CAD) and atherosclerotic disease in the aorta, carotid, and femoral arteries as measured by ultrasound. One hundred two consecutive patients admitted for coronary angiography for suspected CAD participated in the study. All patients underwent transesophageal echocardiography for the evaluation of thoracic aortic atherosclerosis and B-mode ultrasound for evaluation of carotid and femoral atherosclerosis. Intimal-medial thickness > 1 mm in the thoracic aorta or peripheral vessels was considered as evidence of atherosclerosis. Patients with CAD (n = 64) had a significantly higher incidence of atherosclerotic plaques in the thoracic aorta, carotid, and femoral arteries than subjects with normal coronary arteries: 91%, 72%, 77% vs 31%, 47% and 42%, respectively. Extracoronary plaque was a stronger predictor of CAD than conventional risk factors. Evidence of plaque in patients younger than median age (64 years) had a higher specificity than in patients above median age (77% vs 40%, respectively, p <0.0001). Plaque score of the extracardiac vessels was significantly higher in patients with multivessel CAD than in patients with 1-vessel CAD disease and in subjects with normal coronary arteries (p <0.001). Thus, atherosclerotic plaques in the aortic and femoral arteries and, to a lesser extent, in the carotid arteries are strong predictors of CAD.
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PMID:Relation of coronary artery disease to atherosclerotic disease in the aorta, carotid, and femoral arteries evaluated by ultrasound. 939 16

Atherosclerosis is one of the most prevalent fatal diseases in Western societies, and results from an intricate interplay between diverse factors such as lipid metabolism, blood coagulation elements, cytokines, hemodynamic stress, and behavioral risk factors. Atherosclerotic lesions are characterized by the infiltration of immune competent cells such as macrophages and T-lymphocytes, the proliferation of intimal cells of the arterial wall, the accumulation of lipids and the deposition of extracellular matrix components. For some years, endothelial cells, smooth muscle cells, and macrophages have been accorded crucial roles in the process of atherosclerosis. The mechanisms by which these cells contribute to atherosclerosis include augmented expression of adhesion molecules, as well as secretion of proinflammatory cytokines, matrix metalloproteinases, and tissue factor within human and experimental atheroma. Much evidence supports the role of tissue factor in inciting the thrombosis that causes most acute coronary syndromes. Macrophage content and expression of tissue factor correlate with rupture and instability of the atherosclerotic plaque. Matrix metalloproteinases can digest the plaque's extracellular matrix, and thus impair its stability. Plaque rupture exposes circulating blood components to the tissue factor-rich lipid-core, inciting thrombosis. Despite the increasing appreciation that atherogenesis involves participation of inflammatory pathways within cellular interactions, mediators of local communication between the major cell types within atherosclerotic plaques remain incompletely defined. By early appearance, activated T-cells may act as the orchestrator of atherogenesis. Both soluble and contact-dependent mediators from T-cells may be crucial in the development of this prevalent disease. Recent reports have helped explain some of these questions by pointing to a role of contact dependent interaction between CD40 and CD40 ligand (CD40L, renamed CD154) as a stimulus for atheroma-associated cells. We and others have recently showed that activated T-lymphocytes within the atherosclerotic vessel wall express the CD40 ligand surface molecule, known to play a major role in several immunological pathways. In addition to activated T-lymphocytes, functional CD40 and CD40L are coexpressed by human vascular endothelial cells, smooth muscle cells and human macrophages in vitro as well as in situ in human atherosclerotic lesions. Recent studies indicate that CD40L activates atheroma-associated cells by promoting the expression of molecules thought to be involved in atherosclerosis, such as adhesion molecules, cytokines, matrix metalloproteinases, and tissue factor. Thus, CD40 ligation on these vascular wall cells may promote mononuclear cell recruitment, participate in the weakening of the plaque and set the stage for thrombosis, mechanisms of crucial importance in the process of atherosclerosis. The involvement of the CD40 signaling pathway may play major roles during atherogenesis by regulating antigen-specific T-cell responses to yield activation instead of tolerance, and the presence of functional CD40L on non-leukocytic cells associated with atherosclerotic lesion indicates a novel T-cell-independent route of inflammatory activation, a now well recognized component of atherogenesis. These findings establish a possible crucial role for CD40-CD40L interactions in a prevalent human disease.
Atherosclerosis 1998 Apr
PMID:CD40 signaling in vascular cells: a key role in atherosclerosis? 969 47

Several factors may contribute to the development of unstable angina. These include underlying atherosclerosis, mural platelet thrombosis, dynamic stenosis, occlusive spasm and microvascular dysfunctions. Of these, thrombosis is the most visible event, but its actual causes remain elusive. Plaque fissure is widely assumed to be the cause of unstable angina. However, studies have shown no evidence of plaque fissure in about 40% of patients dying from acute coronary syndromes and, conversely, fissured plaques have been found in 10-25% of individuals dying of non-cardiac causes. An inflammatory process may activate the coronary intima and the haemostatic system to produce a platelet-rich thrombus. Activated inflammatory cells produce cytokines which can activate the endothelium making it prothrombotic and vasoconstrictive; they can also produce metalloproteases that can lyse the interstitial matrix. Thus, inflammatory lysis of thin atherosclerotic plaques may also cause plaque fissure at one or more sites. Waxing and waning inflammatory activity may explain the multi-layered thrombi and multiple simultaneous coronary fissure and thrombi that have been described in patients with acute coronary syndromes.
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PMID:The role of plaque fissures in unstable angina: fact or fiction? 979 Feb 81

Disruption of atherosclerotic plaques with associated thrombus is responsible for the majority of the acute coronary syndromes. Plaque instability is related closely to the degree of inflammation. Inflammatory cells within the plaque produce cytokines that inhibit collagen production by vascular smooth muscle cells and increase the production of metalloproteinases, which degrade the extracellular matrix in the fibrous cap. The recruitment of inflammatory cells into the vessel wall occurs in a coordinated sequence of events involving the expression of cellular adhesion molecules on the surface of activated endothelial cells and the production of chemoattractants, and occurs in part in response to oxidation of low-density lipoprotein within the vessel wall. The cellular adhesion molecules are shed into the circulating blood in several disease states, including clinically evident atherosclerosis. The acute-phase reactants C-reactive protein and interleukin-6, and markers of the fibrinolytic state (plasminogen activator inhibitor-1 and tissue plasminogen activator), are also elevated in the acute coronary syndromes and in healthy individuals at increased risk for developing coronary artery disease. These markers may reflect vascular inflammation and thereby the stability of atherosclerotic plaques. Their measurement may pinpoint the mechanisms of benefit of cholesterol-lowering therapy and other interventions designed to reduce coronary risk, and potentially could offer a new method for monitoring coronary risk factor reduction in patients.
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PMID:Inflammation, the endothelium, and the acute coronary syndromes. 988 50

An intravascular ultrasonic imaging device (40 MHz) was used to obtain in vitro ultrasonic images and matching histologic cross-sections, derived from human vascular specimens. The feasibility of assessing vessel wall morphology as well as the ability to accurately document plaque thickness was determined. Based on the echogenicity of the arterial media, intravascular ultrasound could distinguish muscular arteries from elastic arteries, veins, and bypass grafts. The hypoechoic media only present in the muscular type of artery proved to be an essential landmark to document superimposed atherosclerosis. Plaque thickness calculated in these arteries showed close relationship with the corresponding histologic cross-section. Using real-time in vivo intravascular imaging (30 MHz), the morphology of the vessels interrogated was studied. The dynamic change of the arterial wall, as well as the outcome after intervention, is discussed.
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PMID:Intravascular ultrasound and vascular intervention. 1015 Sep 20

Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. The risk for plaque disruption depends more on plaque vulnerability (plaque type) than on degree of stenosis (plaque size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a plaque's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap thinning, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a plaque's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.
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PMID:Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. 1038 96


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