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

In order to investigate the degree of similarity between renal transplant and non-renal hypercholesterolemia, serum and lipoprotein lipid compositions were compared in female transplant hypercholesterolemic patients (serum cholesterol greater than 240 mg/100 ml, serum triglyceride less than 150 mg/100 ml) and female non-renal hypercholesterolemic and normal subjects. A number of lipid abnormalities were demonstrated: (1) Serum and LDL cholesterol and phospholipid levels were significantly elevated in both transplant and non-renal hypercholesterolemic patients; (2) Serum triglyceride, VLDL choelsterol, triglyceride and phospholipid, and LDL and HDL triglyceride were significantly increased in transplant hypercholesterolemic patients. Changes of this nature are usually found in hypertriglyceridemia, and were not observed in non-renal hypercholesterolemic subjects. Finally, a number of changes in the ratio of esterified to free cholesterol and in the ratios of other lipoprotein-lipids, most of which did not correspond to any changes found in the common non-renal hyperlipidemias, were also demonstrated.
Atherosclerosis 1978 Aug
PMID:Hypercholesterolemia in renal allograft recipients. Comparison with non-renal hypercholesterolemia and normal subjects. 21 82

Studies on the pathogenic potential of the human cardiotropic enterovirus, coxsackievirus B5, show that this agent localizes and replicates in the aorta of mice. Nutritionally-induced hypercholesterolemia leads to an increased replication and persistence of virus in tissues, specifically the aorta. Coxsackievirus B cardiopathy is markedly augmented in the hypercholesterolemic host, resulting in a persistent cardiomyolysis which is not evident in virus-infected animals with normal cholesterol levels. Pathological changes in the aorta become evident only months after the acute infection, and only in hypercholesterolemic animals previously infected with coxsackievirus B5. Our findings of coxsackievirus B-induced angiopathy and cardiopathy in the hypercholesterolemic host extend the known pathogenic range of these human viruses, and further emphasizes their potential as etiological agents of cardiovascular disease.
Atherosclerosis 1978 Nov
PMID:Coxsackievirus B cardiopathy and angiopathy in the hypercholesterolemic host. 21 92

In 13 hypercholesterolemic children, re-screened for serum cholesterol after a 1-year interval, hypercholesterolemia was confirmed in only 61.5% of the cases. A tentative explanation seems to be the statistical principle of regression towards the mean. The lipid--lipoprotein analysis showed that serum and LDL cholesterol concentrations in the 13 hypercholesterolemic children and their parents were significantly higher compared to controls (children and parents). At re-screening, hyper-LDL cholesterolemia was present in only 8 of the 13 children (61.5%); 4 cases exhibited hyper-HDL cholesterolemia (30.7%). The high prevalence of the parents repeating the lipoprotein abnormality and the electrophoretic pattern found in the propositi (children) confirms the familial aggregation of the hypercholesterolemic states (hyper-LDL and hyper-HDL cholesterolemia). In conclusion the results of our study stress the importance of determining the lipid--lipoprotein composition, rather then merely evaluating total serum cholesterol in order to make a correct diagnosis of the hypercholesterolemic state. It should also be emphasized that the lipoprotein disturbances and their familial aggregation may be detected early in childhood, suggesting that the familial screening for risk factors of atherosclerosis should be done at pediatric age.
Atherosclerosis 1979 Feb
PMID:Lipid--lipoprotein composition in hypercholesterolemic children and their parents. 22 2

The turnover of apolipoprotein B (apo B) in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) was investigated in 2 homozygous and 3 heterozygous patients with familial hypercholesterolaemia. The effects of a marked reduction in plasma LDL concentration, brought about by plasma exchange, upon apo B turnover were studied in 4 patients. Specific activity-time curves for the the plasma apo B after intravenous radioactive VLDL before plasma exchange indicated that in the heterozygotes all IDL-apo B was derived from VLDL and all LDL-apo B was derived from IDL, but the curves from the homozygotes showed that a significant fraction of the LDL in the plasma was not derived from IDL. Plasma exchange did not increase the rates of synthesis of LDL-apo B or VLDL-apo B and had no significant effect on the precursor--product relationship between IDL-apo B and LDL-apo B in heterozygous or homozygous patients. These findings provide no support for the hypothesis that apo B synthesis is controlled by the plasma LDL.
Atherosclerosis 1979 Mar
PMID:Metabolism of apolipoprotein B-containing lipoproteins in familial hypercholesterolaemia: effects of plasma exchange. 22 91

Content of cholesterol and of collagen fractions (salt-, acid soluble and insoluble) in thoracal and peritoneal parts of aorta as well as concentration of products of collagen metabolism (protein-bound and free hydroxyproline) in blood plasma were studied in rabbits with various degree of atherosclerosis--separate lipid spots in aorta thoracal part (I group), total impairment of aorta (II group) and in control animals. Concentration of cholesterol and triglycerides was also studied in blood plasma and content of cholesterol, cholesterol and triglyceride esters, phospholipids and protein was measured in separate types of lipoproteins--lipoprotein of low (LPLD), of very low (LPVLD) and of high density (LPHD). Increase in content of cholesterol, salt-soluble and insoluble collagen from the both parts of aorta as well as in concentration of protein-bound and free hydroxyproline was found in rabbits of the II group as compared with the control animals. In animals of the I group content of collagen fractions in aorta was similar to that of control animals. Hypercholesterolemia, observed in both groups of rabbits, was most distinct in the II group, being related to the higher amount of cholesterol in LPLD fraction. The ratio of cholesterol esters, free cholesterol, triglycerides and phospholipids was similarly altered in LPVLD fraction of the groups of animals, mainly due to an increase in content of cholesterol esters. But rabbits of the I group were distinct from the II group of animals in the ratio of these components in LPLD: relative content of protein was lower and of cholesterol esters--higher in LPLD of the II group than of the I group. The data suggest that LPLD contained high amount of lipoproteins of intermediate density and cholesterol deposited into vessel wall from LPLD and lipoproteins of intermediate density at the increased rate. In LPHD from blood plasma of rabbits of the II group the ratios cholesterol/protein, cholesterol esters/protein as well as the molar ratio free cholesterol/phospholipids were increased; these data suggest that LPHD was saturated with cholesterol and LPHD appeared to lose the ability to eliminate cholesterol from the vessel wall. Differences in the degree of atherosclerotic impairments, existing between the I and II groups of animals, were apparently related to the variations in composition and content of lipoproteins, which regulate the level of cholesterol in vessel wall, as well as to content of collagen, i. e. they were due to features of metabolism of lipoproteins in blood plasma and of collagen in the vascular wall.
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PMID:[Plasma lipoproteins and aortic collagen fractions in rabbits with different degrees of atherosclerosis]. 22 99

In animal studies, hypercholesterolemia induced by cholesterol feeding results in the plasma cholesterol being transported by lipoproteins of lower densities. Little information is available for humans. To determine the specific lipoprotein responses to dietary cholesterol challenge in humans, four volunteer subjects ingested a liquid formula diet containing 5000 mg of egg yolk cholesterol per day for 30 days and the changes in their lipoprotein fractions were examined. The high dietary cholesterol (above the range of normal diet) was associated with marked increases in apolipoprotein B and low density lipoprotein (LDL) cholesterol levels. An elevated cholesterol : triglyceride ratio in the LDL fraction indicated that the diet altered both LDL level and composition. High density lipoprotein cholesterol and apolipoprotein AI increased slightly. Very low and intermediate density lipoprotein cholesterol and apolipoprotein E levels did not increase during the diet. Thus, high dietary cholesterol was associated with major changes in LDL level and composition, but only minor changes in the other lipoprotein fractions and suggested only minor accumulation of remnant particles.
Atherosclerosis 1979 Aug
PMID:Short-term egg yolk feeding in humans. Increase in apolipoprotein B and low density lipoprotein cholesterol. 22 79

Heterotopic cardiac allografts were placed in the necks of 48 rabbits. In rabbits that were not immunosuppressed, allografts beat as long as 12 days, while in immunosuppressed rabbits allografts beat as long as 101 days. Coronary arterial lesions in donor hearts of rabbits fed a lipid-poor diet were found in arteries of all sizes and were mainly proliferative without fatty change. In cholesterol-fed rabbits, arterial lesions were similarly distributed, but the majority of lesions in longer surviving transplants were fatty-proliferative and some bore close resemblance to chronic human coronary atheroselerosis. In contrast to findings in cardiac homotransplants, only occasional predominantly fatty lesions were induced in small intramyocardial arteries of cholesterol-fed recipients. By electron microscopy, early arterial lesions in allografts were characterized by platelet aggregates in widened junctions between endothelial cells, sloughing of endothelium without intimal thickening but with adherence of platelets to the denuded arterial wall, and platelets deep within essentially normal media. Platelets were also seen adhering to the lining cells overlying the thickened intima of more advanced arterial lesions. Results indicate that immunologic arterial injury due to allograft rejection acting in synergy with hypercholesterolemia resulting from a dietary supplement of cholesterol can lead to rapidly developing atherosclerosis. Observations of early and evolving lesions indicate that endothelial injury and platelet interaction with the arterial wall are early and continuing events and may be of primary importance in the pathogenesis of experimental graft-induced atheroarteriosclerosis. In man, similar mechanisms may be involved in the pathogenesis of graft-induced athererosclerosis and in other instances of atherosclerosis. (Am J Pathol 87:415-442, 1977).
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PMID:Studies on the pathogenesis of atheroarteriosclerosis induced in rabbit cardiac allografts by the synergy of graft rejection and hypercholesterolemia. 32 8

This paper reviews and discusses the evidence supporting the involvement of defective fibrinolysis in the pathogenesis of atherosclerosis, with emphasis on diabetes mellitus. According to the literature, defective fibrinolysis has been observed in association with virtually every major "risk factor" for coronary heart disease, including diabetes mellitus, hypercholesterolemia, hypertriglyceridemia, hypertension, obesity, cigarette smoking and lack of physical exercise. The interrelationships between disturbances in carbohydrate and fat metabolism and fibrinolysis are considered. Attention is drawn to the need for increased clinical attention to the potential role of defective fibrinolysis in atherogenesis, and periodic assessments of the fibrinolytic status are suggested as a promising approach toward early recognition of atherosclerotic tendency and risk. The judicious use of physiologic, dietary and pharmacologic means to correct defective fibrinolysis prophylactically and for the treatment of some forms of atherosclerosis is advocated.
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PMID:Fibrinolysis and risk factors of atherosclerotic disease, with special emphasis on diabetes mellitus. 35 70

Hypercholesterolemia was induced in rabbits by feeding Purina Chow supplemented with cholesterol (5 g/kg body weight/day). The serum cholesterol levels of these rabbits increased progressively and after 3 to 5 months were 4 to 9-fold greater than those of the control animals. Decrease in total hemolytic complement was not apparent during the feeding regimen. Morphologic examination of aortae of these hypercholesterolemic rabbits showed typical atherosclerotic intimal plaques. Immunofluorescent microscopy with fluorescein (F)-labeled anti-rabbit C3 showed deposition of C3 in the intimal and inner medial layers as early as 3 months on high cholesterol diet. C3 deposits were also observed in the renal glomeruli and in the walls of coronary arteries. However, fluorescent studies failed to demonstrate the presence of IgG, IgM, and C4 at these sites. Tissues from control animals fed normal diets were negative for immunoglobulins, C3, and C4. These results suggest that the complement system may be implicated in the pathogenesis of cholesterol-induced atherosclerosis in rabbits.
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PMID:C3 deposition in cholesterol-induced atherosclerosis in rabbits: a possible etiologic role for complement in atherogenesis. 38 17

A study was undertaken to determine the effects of long-term insulin therapy on the development and regression of lipid perturbations and experimental cholesterol atherosclerosis in rabbits: (1) Insulin administration for 15 days significantly reduced plasma lipid levels and free fatty acids in rabbits fed a high-cholesterol diet; it also inhibited the effects of a single dose of cholesterol. Paradoxically, continued insulin treatment led to the reinforcement of lipaemia through the stimulation of mobilization. Insulin administration during the development of atherosclerosis significantly aggravated the fatty infiltration of the aortic tissue and the lesions of the vessels, and also increased the frequency of coronary lesions. (2) In rabbits fed a cholesterol enriched diet during two months and then a normal diet, insulin treatment accelerated the rate of reduction of hypercholesterolaemia, but aggravated the lipid infiltration of the artery walls, and also prevented regression of coronary atherosclerosis.
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PMID:Effect of insulin in the induction and regression of experimental cholesterol atherosclerosis in the rabbit. 41 30


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