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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interrelationships between hypertension and atherosclerosis were investigated in a subhuman primate model (cynomolgus monkey) with hypertension produced by surgically coarcting the miathoracic aorta. The hypertensive coarcted monkey fed a low cholesterol diet for 6 months did not develop complicating atherosclerosis but did develop focal intimal lesions as well as marked thickening of the musculoelastic media of both the large and small arteries. Fibrocellular thickening of the intima and media occurred in the vessels proximal to the coarctation but not distal to the coarctation suggesting that a high level of blood pressure with resulting increase in arterial wall tension is responsible for these changes. The hypertensive coarcted monkey fed a hypercholesterolemic diet (2% cholesterol and 10% butter) for 6 months developed severe coronary atherosclerotic disease with fibrous plaque formation. The disease produced over 65% luminal narrowing of the major coronary arteries and their extramural and intramural branches. In contrast the noncoarcted normotensive animal fed the same diet developed mild atherosclerosis of only the major coronary arteries which caused an average luminal narrowing of 12%. Aggravation of atherosclerosis by hypertension also appeared to occur in the other arteries above the coarctation particularly the cerebral arteries. When the hypertensive coarcted monkey with preestablished coronary atherosclerosis was treated with a low cholesterol diet and a combination of antihypertensive drugs (hydrochlorothiazide, hydralazine, and reserpine), the progression of the disease was arrested. There also was evidence that treatment caused some regression of the coronary lesions which appeared to "heal" by fibrosis. The treatment of both hyperlipidemia and hypertension appeared to be more effective than the treatment of hyperlipidemia, alone.
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PMID:Aggravation of atherosclerosis by hypertension in a subhuman primate model with coarctation of the aorta. 81 49

The long term use of a glucose free dialysate in a group of 15 maintenance hemodialysis patients is associated with a significant decrease in serum cholesterol in 50% of the patients and a significant decrease in serum triglycerides in 25%. The lipid changes appear to be independent of changes in body weight. Hyperlipidemia is believed to be an associated risk factor in the genesis of atherosclerosis in the general population and perhaps in maintenance hemodialysis patients. The long term correction or palliation of the hyperlipidemia of some maintenance hemodialysis patients by the use of glucose free dialysate may be beneficial.
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PMID:Long-term effect of dialysate glucose on the lipid levels of maintenance hemodialysis patients. 82 Dec 4

These studies provide new insight into the complex mechanisms wherby hyperlipidemia causes progressive atherosclerosis. It has been shown that physical injury to the endothelial lining of arteries sets off a process which probably is an attempt at healing the injury but which can lead to atherosclerosis. It has also been found that chemical agents such as homocystine can produce a similar series of events leading to atherosclerosis. These events include focal loss of endothelium, exposure of subendothelial connective tissue, and adherence of platelets followed by release of factors that stimulate intimal smooth muscle proliferation. The present studies indicate that the effects of chronic hyperlipidemia are complex in that the condition results not only in the deposition of lipids in the atheromatous lesions but that it may produce the primary endothelial injury that initiates the process of atherosclerosis as well.
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PMID:Hyperlipidemia and atherosclerosis. 82 15

Atherosclerosis is the process responsible for our national epidemic of coronary heart disease. A primary and proven atherosclerotic risk factor is the plasma cholesterol concentration. Yet, proof that a reduction in plasma cholesterol level results in a reduction in the incidence or severity of atherosclerosis and atherosclerotic cardiovascular disease still requires conclusive documentation. The controversial methods of operation and inconclusive results of concluded first and second generation trials are reviewed. These data clearly demonstrate that a definitive test of the lipid hypothesis has not been reported. Evidence is presented to show that the partial ileal bypass operation most nearly fulfills the six features of an "ideal" lipid lowering trial modality: maximum effectiveness (50% cholesterol reduction); known mechanism of action; no response "escape" or "rebound"; obligatory effect without patient cooperation; minimal side effects; and relative safety. The basic design and protocol of the National Heart and Lung Institute Program on Surgical Control of the Hyperlipidemias, a secondary intervention trial using a combination of diet therapy and partial ileal bypass surgery, are outlined.
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PMID:Maximum lipid reduction by partial ileal bypass: a test of the lipid-atherosclerosis hypothesis. 83 23

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
Atherosclerosis 1977 Jan
PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

The prevalence and type of plasma lipoprotein abnormalities were determined in 114 French-Canadian patients with angiographically proven peripheral vascular disease (PVD). The severity of atherosclerosis was positively correlated with plasma triglyceride concentration, especially in the younger patients (r = 0.29, P less than 0.05), and (not significantly) with plasma cholesterol concentration. Of the risk factors believed to predispose individuals to atherosclerosis, cigarette smoking was the most frequently found in the PVD patients (72.8%), especially among the men. Combination of two or more risk factors was the rule. Findings were compared with those in 114 patients who had undergone coronary angiography for suspected coronary heart disease (CHD). The CHD patients were, on average, younger by 10 years. Hyperlipidemia was present in 58.8% of CHD patients, compared with 43.9% of PVD patients. A far higher proportion of CHD patients showed the type II plasma lipoprotein pattern (24.6% v. 7.9%), although the type IV pattern was more common in both groups (31.6% and 28.9%, respectively). A high proportion of all patients (56.1% with PVD and 41.2% with CHD) showed a normal lipoprotein pattern on paper electrophoresis.
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PMID:Plasma lipids and lipoprotein patterns in angiographically graded atherosclerosis of the legs and in coronary heart disease. 86 81

Plasma linoleic acid levels were found to be low in the atherosclerosis patients investigated. In contrast, platelet arachidonic acid levels were decreased only when atherosclerosis was combined with diabetes or mixed hyperlipidemia. In acute vascular thrombosis, a marked decrease in platelet arachidonic levels occurrrd, irrespective of whether the patient had atherosclerosis or not.
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PMID:[Platelets fatty acid variation in patients with atherosclerosis (author's transl)]. 89 Sep 91

We report the case of a 5-year-old girl who died two years after onset of the idiopathic nephrotic syndrome, which failed to respond to treatment with corticosteroid and cyclophosphamide. Severe atherosclerotic changes were noted in both coronary arteries. Prolonged hyperlipidemia in patients with long-standing nephrotic syndrome may represent a major risk factor predisposing to premature coronary atherosclerosis in children who are also destined to develop chronic renal failure.
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PMID:Premature coronary atherosclerosis in a 5-year-old with corticosteroid-refractory nephrotic syndrome. 90 86

This article presents a theory concerning the pathogenetic background for three diseases of civilization: essential hypertension, stable diabetes and atherosclerosis. Man and many other animals have mobilizing mechanisms for preparation for physical activity, expressed inter alia by an increase in blood pressure, hyperglycaemia and hyperlipidaemia. During physical activity, blood pressure falls almost to the resting level and hyperglycaemia and hyperlipidaemia are reduced parallel with the metabolism of glucose and fats in working muscles. In wealthy countries, this preparation for physical activity, which is dominated by the sympathetic-adrenergic system, comes into action just as frequently as in less wealthy countries -- or possibly even more frequently -- but this is rarely followed by muscular activity. How long is this sympathetic dominance maintained? How high are the blood pressure, hyperglycaemia and hyperlipidaemia? How slowly do these return to normal levels? It appears probable that this may be of fundamental pathogenetic significance in the three abovementioned diseases, the causes of which we have difficulty in finding or agreeing upon. Various prophylactic possibilities are mentioned briefly.
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PMID:[An hypothesis concerning the pathogenetic background of 3 diseases of civilization]. 90 6

Rats were fed for 24 days a liquid diet with ethanol as 36% of calories to produce hyperlipemia and hepatic steatosis. The catabolism of chylomicrons doubly-labeled in the triacylglycerol and cholesteryl ester moieties was studied in conscious rats after ingestion of their usual liquid diets with or without ethanol. A constant intravenous infusion of chylomicrons revealed a defect in chylomicron catabolism after chronic treatment with ethanol. The plasma clearance of chylomicron cholesteryl ester was impaired to a greater extent than clearance of chylomicron triacylglycerol. These findings are consistent with defective catabolism of chylomicron remnants, and suggest that the accumulation of chylomicron remnants in the plasma contributes to the development of increased post-prandial hyperlipemia and chronic hyperlipemia in association with excessive ethanol consumption.
Atherosclerosis 1977 Sep
PMID:Effects of chronic ethanol consumption on the catabolism of chylomicron triacylglycerol and cholesteryl ester in the rat. 91 70


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