Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different segments of the aorta and its branches show differing susceptibilities to atherosclerosis. To identify metabolic features that may account for plaque formation and sparing, we studied aortic wall respiration and glycolysis proximal and distal to an aortic coarctation in 30 rabbits fed a standard or atherogenic diet. Three months after coarctation, blood pressure in the proximal aorta was elevated, and plaque occupied 98% +/- 28% of the intimal surface compared with 57% +/- 26% for control animals (p less than 0.05). Aortic pressure distal to the stenosis remained normal, but plaque formation was markedly decreased (5% +/- 4%) compared with controls (30% +/- 27%, p less than 0.05). Metabolic studies included measurement of oxygen consumption of proximal and distal aortic walls, lactic acid production, and 2-deoxyglucose uptake. Elevated pressure or hyperlipidemia increased respiration (22.6 +/- 4.0 or 16.3 +/- 6.0 pmol oxygen consumed/min/microgram deoxyribonucleic acid [DNA] vs 5.8 +/- 5.2 for controls; p values less than 0.05) without increasing glycolytic metabolism. The coexistence of hypertension and hyperlipidemia resulted in maximal plaque formation and a sevenfold increase in both oxidative metabolism (46.6 +/- 27.2 pmol oxygen consumed/min/microgram DNA vs 5.8 +/- 5.2 for controls, p less than 0.004) and glycolytic metabolism (44 +/- 10 ng lactic acid produced/90 min/microgram DNA vs 6 +/- 3 for controls, p less than 0.004). In the spared aortic segment distal to coarctation, glycolytic metabolism was increased (10 +/- 8 ng lactic acid produced/90 min/microgram DNA vs 2 +/- 1 for controls, p less than 0.05) but oxidative metabolism remained normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosis. 336 36

The authors examined the effects of splenectomy on serum lipids in patients with hematologic disease, in rabbits, and also in cholesterol-fed rabbits with experimental atherosclerosis. Serum cholesterol was determined in patients with hypersplenism before and after splenectomy. Meanwhile serum lipids were determined in two groups of rabbits: splenectomy group (Spx group, n = 19), and sham operation group (Sham group, n = 14) before and after the operation. Then the rabbits were divided into four subgroups: cholesterol-fed groups--Spx-C (n = 12) and Sham-C (n = (9), and normal-chow-fed groups--Spx-N (n = 7) and Sham-N (n = 5). The Spx-C and the Sham-C rabbits were fed 1% cholesterol diet and the Spx-N and Sham-N rabbits were fed normal chow for twelve weeks. In patients preoperative serum cholesterol levels were low, and significant increase in serum cholesterol was observed following splenectomy. In rabbits, the Spx-C group showed significantly higher levels of serum cholesterol, triglycerides, and phospholipids in contrast to lower levels of high density lipoprotein cholesterol, as compared with the Sham-C group. The percentage of aortic plaque area in the Spx-C group tended to be higher than that in the Sham-C group. On the other hand, the Spx-N and the Sham-N group showed no difference in serum lipids during twelve weeks. The worsening of atherosclerosis in the Spx-C group was considered to be mainly due to an enhanced hyperlipidemia. Their results suggest a possible role of the spleen in lipid metabolism, in particular the existence of a splenic factor that can cause hypocholesterolemia in hyperplenism and can suppress hyperlipidemia.
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PMID:Effects of splenectomy on serum lipids and experimental atherosclerosis. 337 69

Many human atherosclerotic lesions, showing no evidence of fissure or ulceration, contain a large amount of fibrin which may be in the form of mural thrombus on the intact surface of the plaque, in layers within the fibrous cap, in the lipid-rich centre, or diffusely distributed throughout the plaque. Small mural thrombi are invaded by SMCs and collagen is deposited in patterns closely resembling the early proliferative gelatinous lesions. In experimental animals, thrombi are converted into lesions with all the characteristics of fibrous plaques, and in saphenous-vein bypass grafts, fibrin deposition is the main cause of wall thickening and occlusion. There seems little doubt that fibrin deposition can both initiate atherogenesis and contribute to the growth of plaques. Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease. Fibrin may stimulate cell proliferation by providing a scaffold along which cells migrate, and by binding fibronectin, which stimulates cell migration and adhesion. Fibrin degradation products, which are present in the intima, may stimulate mitogenesis and collagen synthesis, attract leukocytes, and alter endothelial permeability and vascular tone. In the advanced plaque fibrin may be involved in the tight binding of LDL and accumulation of lipid. Thus there is extensive evidence that enhanced blood coagulation is a risk factor not only for thrombotic occlusion, but also for atherogenesis. Enhanced blood coagulation frequently coexists with hyperlipidaemia and, together, these may have a synergistic effect on atherogenesis.
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PMID:Fibrinogen, fibrin and fibrin degradation products in relation to atherosclerosis. 352 31

The effect of plasma lipid reduction on the progression of femoral atherosclerosis was studied in hyperlipidaemic patients with stable intermittent claudication. 24 patients were randomly assigned to treatment and usual-care groups, the former receiving dietary advice and cholestyramine, nicotinic acid, or clofibrate depending on their lipoprotein phenotype. Biplanar arteriography was performed when the study began and after a mean period of 19 months. Angiograms were assessed visually, with blinding, and by computerised image analysis. Therapy reduced mean plasma total cholesterol by 25%, mean low density lipoprotein (LDL) cholesterol by 28%, and mean plasma triglycerides by 45%. Significantly fewer arterial segments showed detectable progression of atherosclerosis in the treatment group. The mean increase in plaque area (mm2/segment/year) in the treatment group was only one third of that in the usual-care group. The mean increase in edge irregularity index (a measure of the severity of disease) in the treatment group was only 40% of that in the usual care group. Twice as many arterial segments showed improvement in the treatment group. In both groups changes in edge irregularity index were directly related to plasma LDL cholesterol concentration. This study, the first randomised controlled trial of its type, provides evidence that effective treatment of hyperlipidaemia favourably influences the natural history of symptomatic peripheral atherosclerosis.
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PMID:Treatment of hyperlipidaemia retards progression of symptomatic femoral atherosclerosis. A randomised controlled trial. 613 93

Atherosclerosis is a curious process of the intima of the vessel walls characterized by platelet aggregation, deposition of thrombotic material, lipid and fibrin which finally culminates in the intimal thickening, vascularization, and haemorrhage from the new vessels. The lipids demonstrated in the atherosclerotic plaque are mainly cholesterol, triglycerides, and phospholipids. Hyperlipidaemia initiates and maintains the atherosclerotic process and a diet rich in unsaturated essential fatty acids is known to be of benefit in arresting the process. Prostaglandins are formed from unsaturated essential fatty acids and are known to regulate platelet aggregation and thrombus formation. Thus atherosclerosis may be a disease of altered PG system and if so this would pave the way for new therapeutic strategies.
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PMID:Atherosclerosis and prostaglandins. 674 63

Clinical documentation of atherosclerotic plaque regression has been difficult to obtain. This is a report of a patient with severe and early atherosclerotic cardiovascular disease with regression of at least three major atherosclerotic lesions demonstrated by coronary arteriography 10 years after partial ileal bypass operation. The patient's total plasma cholesterol was reduced over these 10 years, ranging from 40% to 23%, from the preoperative level of 757 mg/dl. Sequential arteriograms were assessed independently by several arteriographers and blindly by the Arteriography Review Panel of the Program on Surgical Control of the Hyperlipidemias (POSCH). The readings were analyzed by 4 grading methods. Unanimously, marked regression was read in the proximal left circumflex artery (70% leads to 20%), middle segment of the right coronary artery (45% leads to 20%), and in the distal right coronary artery (80% leads to 50%). Thus, by any and all of the methods used, there was significant regression of arteriographically demonstrated atherosclerotic lesions.
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PMID:Clinical angiographic regression of atherosclerosis after partial ileal bypass. 683 88

Atherosclerosis occurred in a coronary artery saphenous vein bypass graft. Serial angiograms are presented documenting subtotal occlusion of this graft which occurred over a nine-month period. Pathologic examination of graft material obtained at surgery demonstrated ulcerating atherosclerotic plaque. The occurrence of early saphenous vein graft atherosclerosis is discussed with particular reference to the possible effects of hyperlipidemia, which was present in this patient.
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PMID:Rapidly progressive coronary artery bypass graft atherosclerosis. Report of a case documented by serial coronary arteriograms and pathologic examination. 696 50

Regression of the main components of atherosclerotic leseions is compared with regression of other related pathological masses in the body, notably the fatty liver, the large abscess, the large thrombus, the tuberculous granuloma, the lipid implantation granuloma, an the at first reversible but later irreversible proliferation of tissues in response to certain hydrocarbons. The unique obstacles to the regression of advanced artheromata -- as compared to regression of pathological masses elsewhere -- are identified as a lack of early capillarisation, a dependence on evacuation by a very slow unidirectional filtration across an extremely dense and contracted tissue, a lack of an unending imigration of leucocytes for the phagocytic or lysosomal removal of large extracellular lipid pools, and the massive deposits of collagen, an insulating material of extremely long half-life that seems, in addition, to promote wall fragility and supra-plaque thrombosis. The origin and the fate of the myocyte proliferation in hyperlipemia-induced plaques is scrutinized; arguments are presented in favor of its regenerative rather than platelet-induced origin and in favor of the possibility that protracted hyperlipemia may induce the development of some regression-resistsant myocytic mutants. The special difficulties and pitfalls of regression research are analysed. The current conclusions from the most critical experimental studies to date indicate that incipient or young lesions are capable of significant regression, but there is as yet no evidence that advanced or complicated plaques will regress in any species.
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PMID:Overview of studies on regression of atherosclerosis. 701 65

The carotid artery and abdominal aorta of hypertensive normocholesterolemic rats responded in similar manner to balloon denuding of the endothelium. One denuding resulted in an intimal fibrous plaque, while multiple such injuries increased the lipid content of the plaque and so yielded fatty-fibrous plaques, which perhaps represent an intermediate stage of atherosclerosis. In no instance did a single or multiple denuding lead to advanced atherosclerosis. Although the abdominal aorta of animals with one or with repeated denudings accumulated more lipid when placed on atherogenic died, the lesions remained essentially in the fatty-fibrous plaque category. Typical atherosclerosis was observed only occasionally and was limited to rats with multiple denudings. In rats with denuded carotid artery on an atherogenic diet classic atherosclerosis developed, especially when there were multiple episodes of injury. This was the first time the authors observed advanced atherosclerosis in the rat, and the lesions were quite comparable to human atherosclerosis. For the rat in this instance the principal factors in pathogenesis were hyperlipidemia and the repeated endothelial denudings, which promoted lipid deposit in the intimal plaques of the vessel.
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PMID:Atherosclerosis following balloon catheter injury to the carotid artery and the aorta of hypertensive rats with normolipidemia or hyperlipidemia. 722 58

On a diet with high levels of cholesterol and sucrose, a beta-lipoproteinemia developed in rhesus monkeys that is similar to type II human hyperlipidemia. Lesion regression appeared in response to drastic lowering of serum cholesterol (SC) levels. This experiment analyzed angiochemical responses on the addition of a bile-acid sequestrant to continued atherogenic feeding, which resulted in ranges of moderate cholesterolemia that mimick those that occur in man. After two years of atherogenic diet, fatty fibrous plaques were demonstrated in ten monkeys; then cholestyramine resin, 1.5 g/100 g of the atherosclerotic diet, was added to the food of eight monkeys, whereas two served as controls during a 12-month regression period. Six adult control monkeys that did not receive the atherosclerotic diet were also killed. Seven experimental animals overall showed plaque regression when SC level fell from 400 +/- 130 to 237 +/- 74 mg/dL; one animal showed angiographic combinations of progression and regression. Angiochemical evaluation demonstrated discordant data with instances of decreased plaque cholesterol content and increased levels of collagen. On the average, plaque regression and final composition were related to absolute levels of SC reduction induced by cholestyramine. Regression required that the threshold levels of cholesterol be below 200 mg/dL. Plaques regressed mainly by lipid absorption; in this experiment and, in particular, arterial segments, collagen content sometimes increased.
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PMID:Regression of atherosclerotic plaques in rhesus monkeys. Angiographic, morphologic, and angiochemical changes. 743 21


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