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

Epidemiological surveys show the clear association of hypertension with an increased risk of developing ischaemic heart disease. One method of quantifying atherosclerosis is to measure, at necropsy, the percentage of the intimal surface of the coronary arteries or aorta which is occupied by raised plaques. When this is done in a large number of subjects the amount of intimal involvement in any particular geographical population correlates directly with the frequency of ischaemic heart disease. In all these populations, whether at a high risk or low risk of developing ischaemic heart disease, hypertensive subjects have a greater intimal involvement by plaques than normotensive subjects. Thus, the increased risk in hypertension is, in part, mediated by possession of more plaques. Plaque growth is due to the accumulation of lipid from the plasma, the ingress of monocytes with their conversion to lipid filled foam cells and the formation of collagen by smooth muscle cells. Hypertension may act by altering endothelial function to potentiate all these processes. Mechanical stress on endothelial cells will evoke the formation of growth factors for smooth muscle cells. Plaque growth in man is also episodic due to the formation of thrombi; a proportion of these episodes are symptomatic producing acute myocardial ischaemia but the majority are silent leading to sudden plaque expansion. Thrombi over plaques are either due to endothelial denudation injury or more commonly due to the tearing of the cap of a plaque leading to deep intimal injury. Necropsy surveys of control populations show that subjects with hypertension have a greater frequency of recent plaque tears compared with normotensive subjects.
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PMID:Hypertension and atherosclerotic (ischaemic) heart disease. 194 81

The in vivo acoustic and structural characteristics of atherosclerosis in the descending thoracic aorta have not been well delineated. We prospectively evaluated the descending thoracic aorta of 147 patients (35 women and 112 men; age, 61 +/- 14 years) who underwent clinically indicated transesophageal echocardiography. Patients with suspected disease of the aorta were excluded. Thirty-eight patients (26%) had protruding plaques (men, 25%; women, 29%). Six patients had mobile intimal densities with the mobile area ranging up to 1 cm2. As expected, aortic lumen area was decreased (plaque-free, 3.53 cm2; plaque, 3.19 cm2; p less than 0.05) and wall area was increased (plaque-free, 1.51 cm2; plaque, 1.92 cm2; p less than 0.05) in the regions of the plaque. However, total arterial area was not increased (plaque-free, 5.04 cm2; plaque, 5.09 cm2; difference not significant) in a compensatory manner as observed in other arterial beds. Plaque gray scale was less than the gray scale of plaque-free wall (plaque-free, 141.2; plaque, 122.7; p less than 0.05) when compared at the same level of the descending thoracic aorta or with a second aortic plaque-free level (plaque-free, 150.4; plaque, 122.7; p less than 0.05). Standard deviation of gray scale level was similar between plaque and normal regions. Unsuspected protruding plaques in the descending thoracic aorta occurred in one quarter of the patients referred for routine transesophageal examination. Plaques tended to have lower echogenicity and were differentiated from plaque-free walls within patients. Plaque formation did not result in increased total arterial area. These data suggest that the degree or character of compensatory atherosclerotic remodeling in the highly elastic descending thoracic aorta may differ from other arterial beds.
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PMID:Plaque and structural characteristics of the descending thoracic aorta using transesophageal echocardiography. 200 33

Atherosclerotic plaque rupture with superimposed thrombosis is recognized as the lesion causing greater than 90% of acute myocardial infarctions. To determine the severity of atherosclerosis at the site of plaque rupture, 184 coronary arteries from autopsies of 162 patients who died of acute myocardial infarction were studied. There were 102 men, 72 +/- 10 years old (mean +/- SD), and 60 women, 75 +/- 8 years old. All arteries were dissected from the heart, fixed, decalcified, cut at 2 to 3 mm intervals and processed routinely for histologic examination. A planimeter was used to measure artery, plaque, thrombus and luminal cross-sectional area at the site of plaque rupture with thrombosis in sections projected at x13.8 magnification. At the site of atherosclerotic plaque rupture with superimposed thrombosis, the degree of stenosis due to plaque was: 90 +/- 7% for the right (n = 67), 91 +/- 6% for the left anterior descending (n = 79) and 91 +/- 6% for the left circumflex (n = 38) coronary arteries. Plaque rupture in fatal acute myocardial infarction occurs at sites of severe narrowing (mean 91%, range 67% to 99%). Thus, plaque rupture with thrombosis is unlikely to cause the fatal acute myocardial infarction in patients with mild to moderate coronary stenosis.
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PMID:The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thrombosis. 200 14

In this unifying hypothesis directed to the etiology and pathogenesis of atherosclerosis, the importance of focal arterial lesion-prone sites has been emphasized. Key initial participants in these sites include the focal intimal influx and accumulation of low-density lipoprotein (LDL) and a preferential recruitment of blood monocytes. Both are further enhanced in the presence of hyperlipidemia, when the quantity of intimal LDL and the oxidative potential of the intima exceed the capacity of macrophages to remove, via the non-down-regulating scavenger receptor, cytotoxic anionic (Ox-LDL) macromolecules. Foam cells, pathognomonic of the fatty streak, form during the receptor-mediated uptake of Ox-LDL by the macrophages. Interstitial free radicals and the excess of Ox-LDL particles injure and kill cells, including the foam cells, with the formation of the necrotic extracellular lipid core, a key transitional step in lesion progression. Monocyte-macrophage recruitment to the intima is likely to be regulated not only by a multiplicity of endothelial adhesive cytokines, integrins, and selectins, but also by the monocyte-specific chemoattractant, MCP-1, constitutively synthesized and secreted by intimal smooth muscle and endothelial cells. Its synthesis and secretion is augmented by mildly oxidized LDL. Free radicals, pivotal in the oxidation of LDL, and derived from activated macrophages, and also endothelial and smooth muscle cells. Smooth muscle cells migrate from the media through the intimal endothelial layer (IEL) and proliferate under the regulation of a number of mitogens, including platelet-derived growth factor (PDGF). Collagen synthesis by smooth muscle cells is substantial. Lymphocytes, as a source of interferons, invade the plaque and are present in the adventitia in substantial numbers, likely representing an autoimmune response in the later stages of plaque development. Platelets and mural thrombosis directly contribute to subsequent plaque growth, particularly after plaque rupture or fissure and disruption of the thromboresistant endothelial cells (EC). Plaque regression in all likelihood involves the conversion of the inert pool of extracellular lipid to a metabolically active intracellular pool and subsequent clearance by the high-density lipoprotein mediated reverse cholesterol transport system. The atherogenic cascades so described conceptually represent arterial inflammatory and healing processes occurring in a hyperlipidemic environment. Many components of pathogenesis are the targets for modulation by genetic, hemodynamic and selected risk factors. The prevention and treatment of the disease should logically target reduction in plasma LDL levels, the inhibition of the oxidative modification of lipoproteins, including LDL, by free radical scavengers, and augmentation of the reverse cholesterol transport system.
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PMID:The pathogenesis of atherosclerosis: an overview. 204 53

This communication gives a brief account of the morphology and natural history of atherosclerosis. It defines atherosclerosis, in dynamic terms as the resultant of three interacting sets of processes: accumulation and modification of plasma-derived lipid within the arterial intima, connective tissue proliferation and connective tissue necrosis forming an atheromatous pool at the plaque base. The first of these leads to the accumulation of lipid-filled macrophages within the affected intima and this step is most probably mediated via oxidative modifications of the low density lipoprotein molecule. An alteration of the functional phenotype of the intimal smooth muscle cell as a result of interactions with growth factors (most notably PDGF) constitutes the basis for the connective tissue proliferation. Plaque necrosis, which is extremely important as a risk factor for acute thrombosis, is the least well understood area; the activated macrophage may well play a significant role in this connexion.
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PMID:Pathology of atherosclerosis. 210 Jun 93

Rupture of plaques followed by thrombosis and thrombo- or atheroembolism mark the clinical horizon of ischemic organ lesions in atherosclerosis. Initiation and development of lesions precede these often dramatic events by decades. Precursor lesions arise within the first, irreversible ones may develop from the second decade of life onwards. Two concurring or succeeding pathogenetic mechanisms dominate: 1. Discrete or functional endothelial injury (in conjunction with hemodynamic wall stresses and effects of endogenous or exogenous toxic factors such as hormones, immune- and other mediators, components of tobacco smoke, etc.) induces increased flow of low density lipoprotein (LDL) into arterial tissue. Immigrating monocytes capture LDL and accumulate its cholesterol as ester droplets becoming foam cells. Net flux and accumulation of cholesterol probably correlate with plasmatic LDL-cholesterol levels. 2. Endothelial denudation, also occurring under the influence of mechanical wall stresses and in particular over precursor lesions, incites platelet aggregation and clotting mechanisms. As a consequence, arterial smooth muscle proliferates in the sense of repair of injury, resulting in the formation of scar tissue. Lipid-rich lesions with scanty scars seem to be particularly prone to rupture and thus important complications. Plaque rupture is probably the most common complication leading to ischemic disease, whereby the extent of formation and organisation of thrombi might determine whether infarction or chronic ischemia is the outcome.
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PMID:[Current concepts of the pathogenesis of atherosclerosis]. 259 58

Unstable angina is a simple term used to describe a complex group of conditions with a heterogeneous pathogenesis and prognosis. In patients with cardiac disease, understanding pathogenetic mechanisms often influences decisions regarding prognosis and treatment. Potential causes for the development of acute myocardial ischemia include: 1. Extracardiac factors in the patient with severe coronary atherosclerosis. 2. Plaque disruption resulting in: a. Transient platelet aggregation in diseased vessels. b. Dynamic or intermittent coronary artery thrombosis. c. Hemorrhagic dissection into an atheromatous plaque. d. Abnormal constriction of a coronary artery. 3. Progression of atherosclerosis as a result of plaque "healing." It may not be possible to identify the appropriate mechanism responsible for unstable angina in every case but the clinician must attempt to do so since the selection of appropriate therapy for the individual patient depends on the mechanisms responsible for the symptoms.
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PMID:Unstable angina pectoris: pathogenesis and management. 268 40

The Simpson atherectomy device used for the recanalization of severely stenosed peripheral arteries is able to collect plaque material which can be further characterized. This study reports histological, immunohistochemical and transmission electron microscopic findings on advanced human primary atherosclerotic plaques of peripheral arteries percutaneously removed by a Simpson atherectomy catheter. Material from stenosing plaques consisted of dense connective tissue with abundant amounts of concentrically arranged elastic fibers and lamellae. This meshwork contained numerous cells, often arranged in clusters and oriented with their longer axis parallel to the direction of blood flow. The vast majority of these cells could be easily identified as vimentin-positive and desmin-negative smooth muscle cells containing lipid deposits in the perinuclear region and numerous glycogen particles. Monocytes/macrophages were observed only very infrequently. Plaque tissue contained a range of smooth muscle cell phenotypes. Most of the cells were of an intermediate phenotype, i.e. sparsely filled with myofilament bundles at the cell periphery and a high amount of organelles such as mitochondria, rough endoplasmic reticulum and Golgi cisterns. An intact lining of pieces of intimal tissue with endothelial cells was not observed. Two-dimensional gel electrophoresis of plaque tissue showed the presence of alpha-, beta- and gamma-actin isoforms with a clear predominance of the beta-isoform.
Atherosclerosis 1989 Dec
PMID:Cell constitution and characteristics of human atherosclerotic plaques selectively removed by percutaneous atherectomy. 269 72

Heart, aorta, and sciatic arteries were collected from 157 wild male turkeys (Meleagris gallopavo silvestris) by hunters in 9 states during the spring 1983 and 1984 hunting seasons. In descending order of extent and severity, intimal vascular changes were observed in the left sciatic artery, aorta at the celiac region, cranial abdominal portion of the aorta, sciatic bifurcation, caudal abdominal portion of the aorta, coronary arteries, and thoracic portion of the aorta. Only the aorta from the celiac region and right sciatic artery had significant differences (P less than 0.05) among turkeys from various locations. Turkeys from Indiana had significantly (P less than 0.05) larger plaque scores in the celiac region than did those from Alabama, Missouri, and South Carolina. Turkeys from Indiana also had significantly (P less than 0.05) greater plaque scores in the right sciatic artery than did turkeys from Arkansas. When all tissues were considered, tissues from turkeys from Michigan had the highest plaque scores and those from Iowa had the lowest. Plaque scores for turkeys from Michigan were significantly (P less than 0.05) higher overall (including all blood vessels) than were plaque scores for turkeys from Alabama, Arkansas, Iowa, and South Carolina. Few significant (P less than 0.05) correlations were detected among plaque scores in turkeys from within states of origin (geographic location). Also, only a few significant (P less than 0.05) correlations were determined between age or body weight and atherosclerosis for blood vessels from turkeys within various states.
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PMID:Atherosclerosis in coronary, aortic, and sciatic arteries from wild male turkeys (Meleagris gallopavo silvestris). 322 69

During 1979 to 1987, we collected 84 consecutive cases of juvenile sudden death which occurred in the Veneto Region, northeast Italy. Death was attributed to cardiovascular disease in 79 cases. Nineteen of these (24%), consisting of 17 males and two females, from 18 to 35 years of age, had 70% or greater atherosclerotic coronary stenosis, in the absence of other cardiac pathology and previous clinical evidence of angina pectoris or myocardial infarction. In 13 cases (68%), sudden death was the first manifestation of coronary artery disease; the remaining six patients had experienced atypical, non-diagnostic prodromal symptoms. At the moment of death, 16 patients were engaged in sedentary activity. Pathological examination disclosed that in 15 cases (79%), only one major vessel was stenosed, and in 12 cases it was the proximal descending coronary artery: the other four patients had three-vessel disease. Histologic study revealed uncomplicated, obstructive fibromatous plaques in 16 cases, and a preserved tunica media in all cases. Plaque fissuring with superimposed mural or occlusive thrombosis was present in only three cases. Overt myocardial infarction was not observed. Our findings indicate that coronary atherosclerosis is an important cause of sudden death in young persons. In this series, coronary disease was 'silent', and sudden death was its first clinical manifestation. The occurrence of death at rest, in the absence of an acute coronary lesion, with preservation of the coronary tunica media suggests that fatal outcome might be due to coronary vasomotor tone abnormalities culminating in ischaemia-induced cardiac arrest.
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PMID:Sudden death as the first manifestation of coronary artery disease in young people (less than or equal to 35 years). 324 45


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