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

The predictors of premature coronary atherosclerosis were examined in 203 patients (99 men aged less than or equal to 50 years, and 104 women aged less than or equal to 60 years) undergoing elective diagnostic coronary arteriography. Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. In men, age (p less than 0.05), smoking (p less than 0.05), and plasma triglyceride (p less than 0.02) and apoA-1 (p less than 0.05) levels were independently associated with CAD. In women, smoking (p less than 0.001) and plasma apoB levels (p less than 0.04) were the strongest variables independently associated with CAD. It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors.
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PMID:Comparison of the plasma levels of apolipoproteins B and A-1, and other risk factors in men and women with premature coronary artery disease. 156 71

Fourteen women and five men participated in a 20-week controlled, cross-over trial of the interaction of simvastatin, an HMGCoA reductase inhibitor, with high and low fat diets. Simvastatin was found to be just as effective at lowering LDL cholesterol whether the subjects were on a 22% fat diet or a 38% fat diet (25% and 29% falls, respectively). Nevertheless, the lowest cholesterol levels were achieved by combining simvastatin with a low fat diet, the latter adding a further 5% reduction in plasma cholesterol. Simvastatin plus a low or high fat diet increased HDL cholesterol by 10.0% and 2.9% respectively (P = 0.003 overall) and reduced triglyceride concentration by 15.9% and 19% respectively (P less than 0.001). Significant diet-drug interactions were seen in LDL and HDL3 cholesterol. Simvastatin blunted the effect of dietary fat change so that the difference in LDL cholesterol, which was 0.71 mmol/l between high and low fat in the absence of simvastatin, was only 0.22 mmol/l with simvastatin. On a high fat diet, simvastatin produced almost no rise in HDL3 cholesterol whereas on a low fat diet HDL3 cholesterol was increased by 8.8% with simvastatin. The cholesterol content of VLDL and LDL were significantly reduced by simvastatin. The effects of diet and drug on apoproteins A-I and B resembles those on HDL and LDL cholesterol. The findings show interactions between simvastatin and dietary fat which have a bearing on the treatment of hypercholesterolemia.
Atherosclerosis 1992 Mar
PMID:Is fat restriction needed with HMGCoA reductase inhibitor treatment? 159 4

It has been suggested that the antioxidant drug probucol can prevent arterial cholesterol accumulation in part by promoting HDL-mediated cholesterol removal from cells. In this study, the effect of probucol in vitro on the interaction of HDL3 with cultured skin fibroblasts, bovine aortic endothelial cells and human monocyte-derived macrophages was tested. Treatment of cholesterol-loaded cells with up to 20 microM probucol had no effect on [3H]cholesterol efflux from plasma membranes. No effect of probucol on HDL3-mediated efflux of labeled sterol was seen after intracellular sterol was labeled either with the biosynthetic precursor [3H]mevalonolactone or after incubation with lipoprotein-associated [3H]cholesterol linoleate. Further, no effect of probucol on cell cholesterol mass efflux was observed. Thus these results demonstrate that probucol does not affect movement of sterol from different cellular radiolabeled sterol pools. Within the limitations of cell culture studies, it is suggested that the proposed antiatherogenic effect of probucol in vivo is not likely to be the result of modulation of major cellular pathways for removal of cholesterol.
Atherosclerosis 1992 May
PMID:The effect of probucol on HDL-mediated sterol translocation and efflux from cells. 163 59

The excess risk of atherosclerosis that is associated with diabetes mellitus cannot be completely accounted for by other known risk factors. Recent studies have suggested that increased glycation of high density lipoproteins (HDL) at high glucose concentrations causes functional abnormalities that might contribute to accelerated atherosclerosis. Other investigators also have shown that elevated glucose concentrations can stimulate the activity of protein kinase C in cultured cells. Because protein kinase C appears to be involved in HDL receptor-mediated efflux, the hypothesis that a high glucose concentration in vitro might modulate HDL-mediated efflux of cholesterol from human fibroblasts was tested. These studies indicate that a high glucose level alone does not affect the interaction of normal HDL3 with cultured human skin fibroblasts.
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PMID:High glucose levels do not directly impair cellular binding of HDL3 or HDL-mediated efflux of cholesterol from human skin fibroblasts. 166 7

Literature data suggest that identification of the conditions preventing lecithin:cholesterol acyltransferase (LCAT) to produce normal cholesterol esterification might be of utmost importance in the follow-up of atherosclerosis. Interrelationship between LCAT activity, and total cholesterol (TC), unesterified cholesterol (UC), esterified cholesterol (EC), low and high density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides (TG), phospholipids (PL), free fatty acids (FFA), l-lactate (LAC), and electrolytes, i.e. zinc (Zn), calcium (Ca) and magnesium (Mg), was investigated in 60 patients with acute myocardial infarction (AMI), 30 patients with coronary heart disease (CHD) and 30 healthy control subjects. Results of the study revealed LCAT activity to be significantly decreased in atherosclerotic patients, with a significantly increased ratio of unesterified-esterified cholesterol (UC/EC), as compared to the control group of normal subjects. A decreased LCAT activity was accompanied by elevated values of phospholipids and LDL-C, a moderate increase in triglycerides, and a decreased quotient of HDL3/HDL2 cholesterol. Accordingly, a decreased activity of LCAT could with great certainty be considered a high-risk biochemical factor for atherosclerosis.
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PMID:Lecithin:cholesterol acyltransferase activity in patients with acute myocardial infarction and coronary heart disease. 175 Aug 5

The abnormalities of lipid metabolism in nephrotic syndrome consist in an increase in total and low-density lipoprotein (LDL) cholesterol, apolipoproteins B (ApoB), C-II and C-III, associated in patients with heavier or marked hypoalbuminemia with an increase in triglycerides and very low-density lipoprotein (VLDL) cholesterol, while the high-density lipoproteins (HDL) are distributed abnormally (increased HDL3 fraction and decreased HDL2 fraction) and the Apo A-I to Apo B ratio is reduced. Both increased hepatic lipoprotein synthesis and reduced removal capacity contribute to this hyperlipidemia. Proteinuria may lead to the lipoprotein abnormalities through stimulation of VLDL synthesis by the liver induced by hypoalbuminemia, although it has been more recently suggested that urinary protein loss is associated with the urinary loss of some important cofactor for the regulation of lipid synthesis or catabolism. Treatment of lipid abnormalities in patients with long-lasting heavy proteinuria is mandatory, because they may cause or contribute to accelerated atherosclerosis, but also because they appear to accelerate progression of renal disease by favouring mesangial sclerosis. Four groups of lipid-lowering drugs have been tested: 1) bile acid-binding resins; 2) fibric acid; 3) probucol; 4) inhibitors of HMG CoA reductase. The drugs of the last group appear to be effective and safe in short-term experiments, but long-term studies are necessary to confirm their validity. A dietary approach, consisting in a strictly vegetarian soy diet, very rich in poly- and monounsaturates fatty acids, has been recently tested by the author, with very promising results.
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PMID:Lipid changes in the nephrotic syndrome: new insights into pathomechanisms and treatment. 175 84

A Caucasian family of mediterranean origin comprising a patient whose parents were first cousins, his wife and their three children, and his two sisters have been studied. The patient and his two daughters were afflicted with the same corneal opacities and hypoalphalipoproteinaemia. The disease was shown to be transmitted as a non-sex-linked recessive trait. The corneal opacities develop at the end of the second decade of life and consist of numerous minute greyish dots in the entire corneal stroma that give the cornea a misty appearance. Vision slowly deteriorated from 40 years of age. At about 50 years of age, except in one of the two daughters who showed Marfanoid syndrome, the three patients had good general health and no symptoms of atherosclerosis. Biochemical investigations showed hypoalphalipoproteinaemia (with a faint fast-moving HDL band on polyacrylamide gel gradient electrophoresis and small arcs of HDL2 and HDL3 of low mobility determined by agarose gel immunoelectrophoresis), low total cholesterol (3.5-4.9 mmol l-1), slightly decreased cholesteryl ester/total cholesterol ratio (0.52-0.63), extremely low HDL cholesterol (0.20-0.21 mmol l-1), mild hypertriglyceridaemia (1.94-3.80 mmol l-1), and striking deficiency in apo A-I and apo A-II (0.45-0.72, 0.08-0.16 g l-1, respectively). The esterification of HDL cholesterol was low while that of LDL and VLDL was nearly normal. Other laboratory values were normal. The HDL subspecies and major apolipoprotein isoforms have been studied to differentiate FED from Tangier disease, LCAT deficiency, as Apo A-I, A-II, C-II, C-III deficiencies and variants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A 'Fish-eye disease' familial condition with massive corneal opacities and hypoalphalipoproteinaemia: clinical, biochemical and genetic features. 177 23

The Spatholobus suberectus (SS) of hexue type, the Euonymus alatus (EA) of huoxue type and the Eupolyphaga sinensis (ES) of poxue type were selected and their influence on plasma lipid in the experimental hyperlipidemia quails was observed. The ES could raise plasma HDL-C/TC ratio and increase LCAT activity. The SS could raise plasma HDL2-C/HDL3-C ratio. The effect of EA on plasma HDL-C/TC, HDL2-C/HDL3-C and LCAT levels was between SS and ES. All the three huoxue huayu Chinese drugs could lower plasma HDL3-C level and slow down the progress of atherosclerosis to a certain degree. The above-mentioned results show that certain orders exist between the action range of huoxue huayu drugs and their effect on regulating plasma lipid.
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PMID:[Comparison of Spatholobus suberectus Dum, Euonymus alatus (Thunb.) Sieb. and Eupolyphaga sinensis Walker on regulation of plasma lipid]. 178

In a contribution to a prolonged multicenter study 15 patients with primary hypercholesterolemia were treated with simvastatin, a competitive inhibitor of HMG-CoA reductase. The first part of the study was done in a double-blind fashion comparing the effect of this new drug with that of gemfibrozil during 12 weeks, and after this period on open-label treatment was started with the administration to all the patients of simvastatin in doses ranging from 2.5 to 40 mg q.p.m. Persistent and significant reductions (P less than 0.001) were achieved for total serum cholesterol (TC), LDL-cholesterol (LDL-C), apo B and triglycerides: by 38, 49, 44 and 33%, respectively, after 40 weeks of the open-label extension. From week 12, LDL-C levels were maintained at a cut point less than or equal to 140 mg/dl in every patient throughout the study. At week 40, cholesterol values of HDL subfractions showed a significant increase in HDL2-C (28%, P less than 0.01) and a concomitant reduction in HDL3-C (12%, P less than 0.01) in spite of a nonsignificant elevation of total HDL-C (by 6%). The HDL2-C/HDL3-C ratio rose by 47% (P less than 0.001) and the TC/HDL-C ratio was significantly reduced by 43%: from 6.1 +/- 1.2 to 3.5 +/- 0.7 (mean +/- SD, P less than 0.001). No adverse effects were detected. Our results suggest a conversion of HDL3 into HDL2, which could imply a beneficial effect of simvastatin upon the so-called reverse cholesterol transport, in addition to the striking reduction in atherogenic lipoproteins.
Atherosclerosis 1991 Dec
PMID:Significant increase of high-density lipoprotein2-cholesterol under prolonged simvastatin treatment. 178 12

The effects of 12 weeks eicosapentaenoic acid (EPA) administration (2.7 g/day) on plasma lipoprotein subfraction levels and on activities of lecithin: cholesterol acyltransferase (LCAT) and lipid transfer protein (LTP) were investigated. Plasma VLDL-C, VLDL-TG, VLDL-PL, VLDL-apo B, VLDL-apo C-II and VLDL-apo C-III levels were decreased by 32.8% (P less than 0.05), 31.2% (P less than 0.01), 31.5% (P less than 0.05), 32.5% (P less than 0.05), 34.7% (P less than 0.05) and 34.1% (P less than 0.05), respectively. EPA did not change plasma IDL-TC, IDL-TG, IDL-PL and IDL-apo B levels. Plasma large, light LDL (LDL1)-TC, LDL1-PL and LDL1-apo B levels were decreased by EPA by 18.7% (P less than 0.02), 19.1% (P less than 0.01) and 23.3% (P less than 0.01) while LDL1-TG level was not changed. Plasma small, heavy LDL (LDL2)-TC level was increased by 25.7% (P less than 0.02) while LDL2-TG, LDL2-PL and LDL2-apo B levels were not altered. Plasma HDL2-TC, HDL2-TG, HDL2-PL and HDL2-apo A-I levels stayed unchanged by EPA treatment. EPA did not affect plasma HDL3-TC, HDL3-PL and HDL3-apo A-I levels but decreased HDL3-TG level significantly (P less than 0.02). LCAT activity was not altered by EPA. LTP activity was increased by 24.8% at 4 weeks (P less than 0.02) and by 32.1% (P less than 0.001) at 12 weeks EPA treatment. We conclude that EPA reduces plasma large, light LDL levels as well as plasma VLDL amounts and stimulates LTP activities.
Atherosclerosis 1991 Nov
PMID:Effects of eicosapentaenoic acid on plasma lipoprotein subfractions and activities of lecithin:cholesterol acyltransferase and lipid transfer protein. 181 49


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