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

Restenosis within 24 months of carotid endarterectomy was discovered in 3.6% of 361 operations. The patients in this group of restenosis tended to be younger than the overall group. Hypertension and hyperlipidemia were also more frequent. Restenosis recurred within an average of 12.5 months of the first operation, with a range from five to 24 months. No surgical technical causes could be found. Restenosis is attributed to rapid, exuberant myointimal proliferation. This process is histologically distinct from the atherosclerotic plaque which is the cause of late restenosis. Reoperation on this group of patients with the fibrous myointimal proliferative type of lesion was difficult and was infrequently associated with improvement in the patients' signs and symptoms.
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PMID:Early restenosis after carotid endarterectomy. 63 92

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

Experimental studies have shown the regression of atherosclerosis in animals given a cholesterol-rich diet and then given a normal diet or hypolipidemic therapy. Despite favourable results of clinical trials of primary prevention modifying the lipid profile, the concept of atherosclerosis regression in man remains very controversial. The methodological approach is difficult: this is based on angiographic data and requires strict standardisation of angiographic views and reliable quantitative techniques of analysis which are available with image processing. Several methodologically acceptable clinical coronary studies have shown not only stabilisation but also regression of atherosclerotic lesions with reductions of about 25% in total cholesterol levels and of about 40% in LDL cholesterol levels. These reductions were obtained either by drugs as in CLAS (Cholesterol Lowering Atherosclerosis Study), FATS (Familial Atherosclerosis Treatment Study) and SCOR (Specialized Center of Research Intervention Trial), by profound modifications in dietary habits as in the Lifestyle Heart Trial, or by surgery (ileo-caecal bypass) as in POSCH (Program On the Surgical Control of the Hyperlipidemias). On the other hand, trials with non-lipid lowering drugs such as the calcium antagonists (INTACT, MHIS) have not shown significant regression of existing atherosclerotic lesions but only a decrease on the number of new lesions. The clinical benefits of these regression studies are difficult to demonstrate given the limited period of observation, relatively small population numbers and the fact that in some cases the subjects were asymptomatic. The decrease in the number of cardiovascular events therefore seems relatively modest and concerns essentially subjects who were symptomatic initially. The clinical repercussion of studies of prevention involving a single lipid factor is probably partially due to the reduction in progression and anatomical regression of the atherosclerotic plaque.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is regression of atherosclerosis possible?]. 129 45

The progression of atheroarteriosclerosis was shown to be age dependent. This designation covers two separate entities: arteriosclerosis, the progressive and diffuse hardening of the walls of arteries with loss of elasticity, and atheromatous plaque formation, which can start early in life according to nutrition and genetic factors (LDL-receptor expression). Lipoprotein-receptor interactions play a crucial role in lipidic plaque formation. There is, however, no indication that the diffuse hardening of the vascular wall would also be influenced by these mechanisms. We described recently a high-affinity receptor for elastin peptides, present on smooth muscle cells, fibroblasts, and also on monocytes and PMNs. When activated, this receptor will increase intracellular calcium. Circulating elastin peptides were determined by a sensitive Elisa method and found to be between 0.1 and 20 micrograms/ml, in the range of activation of the elastin receptor. They increase in obliterative arteriopathies and type IIb hyperlipidemia. Elastolysis accompanies aging and vascular pathology; the sensitivity of this receptor changes with age, intracellular Ca++ increases, but the receptor appears to be uncoupled from its normal transmission mechanism. These results may well explain the increasing diffuse calcification of the vessel wall. The previously demonstrated potentiation of cholesterol deposition in elastic fibers by calcium is in agreement with simultaneous deposition of calcium and lipids. The recent demonstration of the efficient competition of fibronectin for LDL in proteoglycan-LDL complexes suggests that this reaction may be involved in foam cell formation by the opsonization of LDL for phagocytosis. Fibronectin was shown to accumulate in atherosclerotic plaques. Altogether these recent results confirm the importance of cell-matrix interactions in atherogenesis and lead to a better understanding of the age dependence of these disease processes.
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PMID:Cell-matrix interactions in the genesis of arteriosclerosis and atheroma. Effect of aging. 133 48

To study the mechanisms by which monocytes/macrophages and smooth muscle cells contribute to atherosclerotic lesions, we studied atherosclerotic plaque formation in cholesterol-fed rabbits treated with etoposide, a drug that has been shown to have several effects that could interfere with the proposed interactions between these two cell types (M.W. Aarnoudes et al, Virchows Arch B 1984;47:211-216 and M. Rozencweig et al, Cancer 1977;40:334-342). Our results show that long-term etoposide treatment of New Zealand White rabbits maintained on a high-cholesterol diet decreases the extent of fatty streak formation in the aortic intima. Moreover, the plaques formed in the presence of etoposide are thinner and at least focally have less fibrous tissue and fewer smooth muscle cell-derived foam cells than do plaques in control rabbits. These effects are independent of the extent of the diet-induced hyperlipemia or an effect of etoposide on blood cell count and may be related to the inhibition of intimal cell proliferation by etoposide.
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PMID:Etoposide treatment suppresses atherosclerotic plaque development in cholesterol-fed rabbits. 142 96

Under certain circumstances the effect of insulin to promote glucose uptake in peripheral tissues is reduced because of a resistance to insulin action. This insulin resistance and the resulting hyperinsulinaemia are now recognised as common background factors that may be responsible for hypertension, hyperlipidaemia, decreased thrombolysis and also impaired glucose tolerance and diabetes. Hyperinsulinaemia has also been identified as an independent risk factor for coronary heart disease and promotes smooth muscle cell growth and plaque formation. A series of studies have now demonstrated that treatment with selective beta-blockers as well as thiazide diuretics impair insulin sensitivity by 15-30% and causes a compensatory increase in insulin concentrations. Furthermore, lipoprotein concentrations are affected in an unfavourable way. This is in contrast to the drugs belonging to ACE-inhibitors, calcium-channel blockers and alpha 1-blocker classes that are either neutral or may have the opposite effects in these respects.
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PMID:Insulin resistance and cardiovascular drugs. 154 Oct 35

In the development of atherosclerosis (AS), circulating monocytes emigrate into and accumulate in the intima as foamy cells. Interaction of the lipid laden macrophage (M phi) with cells of the arterial wall may contribute to the formation of atheromatous plaque. Using subcutaneous and peritoneal foamy cells (FC) collected from diet-induced hyperlipemia rabbits, the authors observed the influence of lipid laden on macrophage's functions relevant to AS lesion formation. In comparison with normal M phi, peritoneal FC were 4.8 and 5.4 fold more adhesive to the endothelial surface of intima preparation and the smooth muscle cells (SMC), while the adhesion rate produced by subcutaneous FC were increased 0.79 and 0.16 fold. SMC migration stimulated by both FC-conditioned medium slowed 5.78 and 5.90 fold increased respectively as in comparing with the control's, whereas normal M phi-conditioned medium only gave a 2.3 fold increase of SMC migration stimulation. In addition, both FC-conditioned medium stimulated SMC growth making 1.96 and 2.59 fold increase, and normal M phi-conditioned medium produced a 1.3 fold increase as compared with the control's. The results suggest that lipid-laden macrophages, may accelerate AS development due to changes of their biological properties. Since more than 95% of peritoneal macrophages as well as macrophages in the pleura, pericardial and synovial cavities from experimental hyperlipidemia rabbits are fully filled with lipid assuming the morphologic characteristics of atheromatous intimal foamy cells, it is considered that these cells will be valuable as the model.
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PMID:[Interaction of foamy cells from experimental hyperlipemia rabbits with smooth muscle cells and the endothelial surface of intima preparation]. 161 48

Stimulation by macrophage secretory products of the migration of arterial smooth muscle cells was studied in vitro with a modified system. Round cell colonies were formed by plating subcultured smooth muscle cells into the middle wells of agarose gels. Following irradiation (1500 rads) and refeeding with test medium, cell migration was observed by measuring the increase in surface area of cell colonies at specific time intervals. The cell colonies expanded under the agarose gels with an increment of approximately 10.6 mm2 per day when exposed to macrophage conditioned medium, and the average increase in surface area of the colonies was approximately 5.7 and 8.6 mm2 per day when exposed to platelet-deficient serum and whole blood serum, respectively. The results indicate that macrophages may contribute to atheromatous plaque formation by stimulating smooth muscle cell migration into the intima in the case of arterial damage due to hyperlipemia or other causes.
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PMID:[Secretory products of macrophages stimulate arterial smooth muscle cell migration in vitro]. 183 18

In the last years, a plasmatic fibrinogen increase, a fibrinolytic system activity reduction and platelet activation, seemed to play a significant role on the genesis and progression of atheromatous plaques, especially when combined to a plasmatic lipoprotein increase. The results obtained in normolipidaemic patients (2000 asymptomatic subjects, 364 non-insulin diabetic patients randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 69 nifedipine-30 mg/daily-treated subjects, and 38 patients submitted to nifedipine-30 mg/daily-combined to indobufen-400 mg/daily-therapy), are reported. The results obtained in hyperlipidaemics (blood cholesterol level > 240 mg/dl; 356 patients, randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 56 patients with simvastatin 40 mg/daily and 85 with low saturated fat and low cholesterol diet), are also reported. Follow-up of all the patients was 4 years, but the simvastatin group followed-up only 1 year. An ultrasound examination of carotid and femoral arteries was performed in all the patients by means of a Duplex Scanner ATL Ultramark 5, with a high resolution probe (10 MHz). Subjects were graded into I-VI classes, according to the vessel progressive atherosclerotic impairment. In normolipidaemics, wall atheromatous changes were seen with increasing frequency with age, and a significant relationship among plaque progression rate and developed cerebrovascular symptoms, developed symptomatic peripheral symptoms, increased cardiovascular events and mortality rate, was evidenced. Non-insulin dependent diabetes, combined to normal levels of blood lipoproteins, appears an independent risk factor, superimposable to hyperlipidaemia. In this group of patients, bezafibrate therapy significantly reduced plaque progression, acting on blood coagulation factors and similar results were obtained in nifedipine and nifedipine plus indobufen groups. Also in hyperlipidaemics treated with diet, simvastatin and bezafibrate, the plaque progression was significantly reduced with respect to control group, especially when blood lipoproteins and coagulation were normalized. In conclusion, hyperlipidaemia, Ca++ and blood coagulation disorders, appear to be the main factors affecting the plaque progression, and the prevalence of each factor in the atheroma development must be well evaluated in the single patients to establish an adequate therapeutic strategies.
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PMID:[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]. 184 88

The pathogenesis of atherosclerosis has been extensively studied and the cellular aspects increasingly characterized. This review will focus on the basic pathology, presumed cellular events, cellular interactions, cell-lipid relationships, and potential therapies of atherosclerosis. Fatty streaks, fibrous plaques, and complicated plaques are the pathologic hallmarks of atherosclerosis. These lesions insidiously progress, and symptoms appear to develop when the plaque luminal surface destabilizes. The major cellular contributors to plaque development are monocytes/macrophages, endothelial cells, smooth muscle cells, and, to a lesser degree, lymphocytes and platelets. They interact in a complicated fashion. Growth factors and cytokines produced by these cells are also of great importance for cell-cell interaction. Hemodynamic factors contribute to atherogenesis at preferential sites within the arterial vasculature, presumably by effects on the cellular mechanisms. Hyperlipidemia, especially elevations of total and LDL-cholesterol, has been well characterized as an atherosclerotic risk factor. Cellular modification of LDL-cholesterol, primarily by oxidation, leads to more rapid uptake by macrophage-derived foam cells, enhancing plaque growth by this and other mechanisms. These observations may unify the cellular and lipid contributors to atherogenesis. Therapies directed at the cellular contributors to atherosclerosis are being assessed. Dietary n-3 fatty acid supplementation reduces the extent of experimental atherosclerosis, and human studies are in progress. Many potential cellular effects of n-3 fatty acids have been demonstrated. Other potential therapies for atherosclerosis that probably work at the cellular level include calcium channel blockers, antioxidants, and heparinoids. An exciting new era of atherosclerosis research and, hopefully, therapy has dawned, as knowledge about its cellular basis accrues.
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PMID:Atherosclerosis: cellular aspects and potential interventions. 185 95


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