Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The descending thoracic and abdominal aortas of normal and hypercholesterolemic Golden Syrian hamsters were examined with transmission electron microscopy and immunofluorescence microscopy. Serum cholesterol distribution in lipoproteins was determined by gradient ultracentrifugation. Luminal surfaces appeared free of lesions and no intimal thickening or foam cells were seen. The main rise of cholesterol during the hypercholesterolemic diet was in the VLDL + IDL fraction. These findings suggest differences in the localization of atherosclerotic lesions and lipoprotein cholesterol distribution between humans and hamsters, which hamper the use of this species as a model for human atherosclerosis.
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PMID:The hyperlipidemic hamster as an atherosclerosis model. 175 Aug 2

Atherosclerosis was induced in 13 Yorkshire pigs (4 weeks; 7-10 kg) by endothelial balloon denudation of the aorta and left anterior descending coronary artery and a diet containing 2% (wt/wt) of cholesterol, 8% (wt/wt) of lard fat and 0.5% (wt/wt) of bile acids. After 8 months 7 animals (group I) were sacrificed to determine the extent to which atherosclerosis had developed. The other 6 animals (group R) received a diet (no cholesterol, 5% (wt/wt) of lard fat and 5% (wt/wt) of fish oil) for 4 months. In I plasma cholesterol increased from 2.29 to 9.02 mmol l-1 after 8 months and in R it returned to 1.89 mmol l-1 after 12 months. Less marked changes occurred in plasma HDL cholesterol and triglycerides. ADP-induced platelet aggregation and the number of platelets remained constant in I whereas both parameters were reduced in R after 12 months. In the lesions of the abdominal aorta of I, cholesterol, cholesterol ester, phospholipid and triglyceride contents were 4.97, 2.08, 4.20 and 0.77 micrograms g-1 wet wt, respectively, whereas in R these values (3.02, 0.47, 2.70 and 0.44 micrograms g-1 wet wt, respectively), were close to the values measured in non-abraded vessel wall specimens. The Sudan IV-positive area of the aorta was 34 +/- 9% in I and 10 +/- 4% in R (P less than 0.05). Luminal encroachment of the denudated left anterior descending coronary artery was 11 +/- 3% in I and 13 +/- 3% in R (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of n-3 fatty acids on the regression of atherosclerosis in coronary arteries and the aorta of the pig. 262 Jun 86

Aortocoronary vein bypass surgery might not restore normal maximal coronary flow reserve to bypassed coronary vessels because residual diffuse coronary atherosclerosis might limit maximal hyperemia. To investigate the effect of diffuse atherosclerosis and a focal stenosis at the graft-coronary anastomosis, we measured coronary flow reserve with an extensively validated subselective Doppler catheter in 24 patients with 35 bypass grafts perfusing angiographically normal coronary vessels. The Doppler catheter was positioned in the midportion of the graft, and coronary flow reserve was measured as the peak/resting velocity ratio after selective graft injection of a maximally vasodilating dose of papaverine. Luminal dimensions of the bypass graft, graft-coronary insertion, and bypassed coronary vessel were measured by quantitative coronary angiography (Brown/Dodge method). Measurements of coronary flow reserve and coronary dimensions of vein bypass grafts were compared with similar measurements obtained from 13 patients with normal coronary vessels and normal myocardium. Seventeen of the 35 bypass grafts perfused unobstructed coronary-vein graft anastomoses (less than 50% area stenosis) and normal myocardium. The coronary flow reserve of these 17 bypass grafts was normal (5.0 +/- 0.4, mean +/- SEM) and not significantly different from that measured in normal arteries (5.1 +/- 0.6), even though the cross-sectional area of the native coronary artery just distal to the bypass insertion was 40% smaller than in matched normal vessels. Bypass grafts perfusing hypertrophied (n = 2) or infarcted (n = 6) myocardium had significantly reduced coronary flow reserve compared with normal vessels (2.7 +/- 0.3; p less than .01), even when the infarcted wall had only minimal hypokinesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does coronary artery bypass surgery restore normal maximal coronary flow reserve? The effect of diffuse atherosclerosis and focal obstructive lesions. 295 10

Luminal narrowing was assessed in 238 transverse segments obtained from coronary arteries removed at postmortem. In each segment, narrowing was assessed by gross visual estimation before and after fixation, and on histological sections by stereological point counting and computer-assisted planimetry. Computer-assisted planimetry was found to be accurate and reliable but the equipment needed is expensive, and requires specialized software and an experienced user. Morphometric measurement by stereologic point counting was accurate, rapid, simple, and inexpensive. In comparison with computer-assisted planimetry visual estimation was found to be neither accurate nor reliable. Our results indicate point counting as the method of choice for assessment of coronary artery luminal narrowing by atherosclerosis.
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PMID:Morphometric analysis of coronary artery stenosis: an accuracy and reliability study. 319 61

The performance of the self-expanding stainless steel (Gianturco) stent in atherosclerotic arteries was examined in a rabbit model. Atherosclerosis was induced by supplementing rabbit chow with 6% peanut oil and 2% cholesterol followed by endothelial disruption of the abdominal aorta with a balloon catheter and continuation on the atherogenic diet for the remainder of the study. Eighteen stents, 1 cm in length and 4 or 5 mm in diameter when fully expanded, were placed in atherosclerotic stenotic lesions in six rabbits. Luminal distention was consistently achieved. At 8 weeks follow-up, no luminal narrowing, stent migration, thrombus formation or branch vessel occlusion had occurred. Atherosclerotic neointimal proliferation occurred around the stent wires following placement, but did not cause significant luminal narrowing.
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PMID:Self-expanding metallic stents: preliminary evaluation in an atherosclerotic model. 357 26

Interleukin-1 beta (IL-1 beta) is known to have a number of effects on the different cell types present within coronary arteries. In this study we identified the location and phenotype of cells containing IL-1 beta in human coronary artery specimens from patients suffering from either coronary atherosclerosis or cardiomyopathy and correlated the presence of IL-1 beta with disease severity. Luminal endothelial cells, adventitial vessel wall cells, and macrophages were double labeled immunohistochemically for IL-1 beta protein and a cell type-specific monoclonal antibody for either endothelial cells or macrophages. In situ hybridization was performed to locate the presence of IL-1 beta mRNA within the coronary artery wall. In this study IL-1 beta protein was found to be increased in the adventitial vessel walls of atherosclerotic coronary arteries compared with coronary arteries from nonischemic cardiomyopathic hearts. This increase was directly proportional to the severity of coronary atherosclerosis. IL-1 beta protein was also detected in luminal endothelium and macrophages of atherosclerotic coronary arteries and coronary arteries from nonischemic cardiomyopathic hearts. IL-1 beta mRNA was found in luminal endothelial cells, adventitial vessel endothelial cells, and macrophages. We conclude that IL-1 beta is produced by endothelial cells and macrophages in coronary arteries from ischemic hearts and to a lesser extent from nonischemic cardiomyopathic hearts.
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PMID:Interleukin-1 beta in coronary arteries of patients with ischemic heart disease. 869 38

Endothelin (ET) is a very potent vasoconstrictor peptide, which was originally reported to be produced by endothelial cells and to act locally in a paracrine fashion to regulate vascular tone. Recent studies have demonstrated that endothelin-1 (ET-1) not only is produced by endothelial cells, but is also present in non-endothelial cells of atherosclerotic lesions. The present study was therefore designed to characterize the cell type and distribution of ET-expressing cells in different areas of human atherosclerotic coronary plaques, obtained by directional atherectomy of 30 patients. In addition, ET-1 messenger RNA (mRNA) distribution was studied in human atherosclerotic plaque tissue by in situ hybridization (ISH). The strongest ET-1-like immunoreactivity (ET-1-IR) was present in all cell-rich areas of 27 plaques. In fibrotic areas of 27 tissue samples, ET-1-IR was found in 44 per cent (12/27). ET expression was most prevalent in foamy macrophages (MPs, HAM 56-positive) and myofibroblasts (MFBs, alpha-actin-positive) in the vicinity of necrotic areas with signs of previous intraplaque haemorrhage. By contrast, ET-1-IR was weak and inconsistently found in MPs (11/27; 40 per cent) and MFBs (12/27; 44 per cent) in fibrous areas. Luminal endothelial cells (Ulex europeus agglutinin reaction-positive, UEA) exhibited strong ET-1-IR, whereas endothelial cells of intraplaque microvessels demonstrated inconsistent staining for ET-1. ISH revealed that ET mRNA is produced locally in intimal MPs showing strong ET-1-IR. These findings demonstrate that ET-1 is produced by human MPs, the principal inflammatory cell type in atherosclerosis, suggesting a role for ET-1 in the chronic inflammation associated with complicated atherosclerosis.
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PMID:Endothelin-1-like immunoreactivity in human atherosclerotic coronary tissue: a detailed analysis of the cellular distribution of endothelin-1. 877 87

Compensatory arterial enlargement in response to atherosclerosis has been demonstrated for the left main coronary artery. Only limited data is available on the interaction of patient characteristics and atherosclerosis with coronary artery dimensions. The purpose of the present study was to evaluate the influence of age, race, body habitus, heart weight and atherosclerosis on coronary artery dimensions of young males. Hearts from 137 young men (age 32 +/- 8 years; 78 black, 59 white) with unnatural deaths (homicide, suicide, accident, drug overdose) were perfusion-fixed, and histologic sections were obtained from the left main, proximal left anterior descending and left circumflex coronary arteries. Computerized planimetry was performed on Movat stained sections. Multiple regression analysis was used to evaluate the relative contribution of plaque size, age, race, heart weight and body surface area on coronary dimensions and compensatory enlargement in response to atherosclerosis. In the left anterior descending and left main coronary arteries, black race, body surface area and age were independent predictors of increased lumen area. In the left circumflex, age was a predictor of lumen area. Plaque area, black race and body surface area independently predicted increased area enclosed by the internal elastic lamina area. There was compensatory enlargement of internal elastic lamina with increasing plaque size in both races in the three arteries, but the percent luminal stenosis was greater in whites due to smaller artery size. Luminal narrowing did not develop until plaques occupied 30% of internal elastic lamina area. Among a population of young men with non-cardiac deaths, blacks have larger lumen and area enclosed by internal elastic lamina than whites. Age and body surface area are major determinants of lumen areas, and compensatory arterial enlargement was seen in all examined arteries in the present study.
Atherosclerosis 1996 Jun
PMID:Effect of age, race, body surface area, heart weight and atherosclerosis on coronary artery dimensions in young males. 878 55

Luminal stenosis can be based on large atherosclerotic plaques in compensatory enlarged segments or on relatively little plaques in shrunken segments. In the present study, the contribution of plaque formation and remodeling to luminal narrowing was compared among six types of arteries prone to symptomatic atherosclerosis. Cross-sections (n = 5195) were obtained at regular intervals from 329 arteries. For each artery, the cross-section that contained the least amount of plaque was considered to be the reference. For each cross-section, the percentage of lumen area decrease was expressed as a percentage of the lumen area at the reference site (luminal stenosis). Similarly, the area encompassed by the internal elastic lamina (IEL area) was expressed as a percentage of the IEL area at the reference site (relative IEL area). All cross-sections were categorized in three groups: relative IEL area > 105% (enlargement), 95% to 105% (no remodeling), and < 95% (shrinkage). The prevalence of enlargement (50% to 75%) was significantly higher compared with shrinkage (8% to 25%). Shrinkage was observed most frequently in the femoral arteries (25%) and infrequently in the renal arteries (8%). For all types of arteries, the relative IEL area correlated negatively with luminal stenosis (P < .001). Regression analysis of relative IEL area on luminal stenosis, however, showed significant differences in the first-order regression coefficients among artery types. On average, plaque increase was more compensated for by enlargement in the coronary, common carotid, and renal arteries compared with the arteries obtained from the lower extremities. Anatomic regional differences were observed in the impact of arterial wall remodeling on percent luminal stenosis in de novo atherosclerotic lesions.
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PMID:The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely within the arterial system. A postmortem study. 940 93

Several techniques have been used to demonstrate that human arteries respond to atherosclerosis by increasing their total arterial area to prevent a decrease in blood flow. Three-dimensional reconstructions of coronary arteries can document this compensatory response accurately and specifically. Seven human coronary arteries were reconstructed using intravascular ultrasound and biplane angiography, and vessel geometries were quantified. In all seven vessels, as plaque area increased, overall vessel area increased (R = 0.986, 0.933, 0.984, 0.678, 0.763, 0.963, and 0.830), but luminal cross-sectional area did not significantly decrease. Focal compensatory enlargement was identified in each vessel, and in some cases this response appeared to occur until the vessel was 65% occluded. Luminal enlargement near the proximal ends was attributed to the natural taper of the vessel. The semi-automated, three-dimensional segmentation technique used in this study allows reproducible quantification, as there is no subjective manual tracing involved. Following the intravascular ultrasound transducer in time and space with biplane angiography allows for accurate reconstruction with or without automated pullback devices. Information on the rate of change of vessel measurements is also presented, which, when combined with visualization of accurate 3D geometry, provides a unique assessment of coronary compensatory enlargement. This reconstruction technique can be applied in a clinical environment with no major modification.
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PMID:Assessment of coronary compensatory enlargement by three-dimensional intravascular ultrasound. 1092 43


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