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Biomedical subjects

R I Levy

Publications and source records attributed to R I Levy.

At least 19 recordsLinked to original sources
PubMed1987

Intermediate-density lipoproteins and progression of coronary artery disease in hypercholesterolaemic men.

Lipoprotein mass concentrations were measured by analytical ultracentrifugation in a subset of 57 hypercholesterolaemic male participants in the National Heart, Lung, and Blood Institute Type II Coronary Intervention Study. 2-year changes in levels of intermediate-density lipoproteins (IDL) of flotation rate 12-20 were strongly predictive of progression of coronary artery disease at 5 years. Changes in serum mass concentrations of low-density lipoproteins (LDL; flotation rate 0-12), very-low-density lipoproteins (VLDL; flotation rate 20-400), high-density lipoproteins (HDL), and the HDL2 and HDL3 subfractions did not differ significantly between men with and without definite progression of coronary artery disease. The relation of IDL mass to disease progression remained significant (p less than 0.05) after adjustment for group assignment to cholestyramine treatment or placebo and was only slightly reduced (p less than or equal to 0.06) by adjustment for changes in LDL mass concentrations. Changes in IDL mass and ratios of HDL-cholesterol to total-cholesterol or LDL-cholesterol were inversely correlated and had a similar ability to predict progression. The findings are consistent with earlier evidence that IDL are directly involved in the development of coronary artery disease and suggest that ratios of HDL-cholesterol to total-cholesterol or LDL-cholesterol may be indicators of coronary disease risk partly owing to relations with IDL metabolism.

Adult↗
PubMed1987

Report on the Lipid Research Clinic trials.

The Lipid Research Clinic Coronary Primary Prevention Trial was a randomized, double-blind, placebo-controlled intervention trial performed in 3806 hypercholesterolaemic (greater than 265 mg dl-1) but asymptomatic men aged 35-59 at entry. The bile acid sequestrant cholestyramine was used to achieve the cholesterol differential in the treatment group. Both groups received a modest low cholesterol-low fat diet. All subjects were followed for at least seven years (mean duration 7.4 years) during which time a mean fall of 8% and 12% in plasma total cholesterol and LDL cholesterol levels respectively relative to levels in placebo controls were achieved and maintained. The cholestyramine group experienced a 19% reduction in risk (P greater than 0.05) of the primary end point-definite coronary heart disease death and/or definite non-fatal myocardial infarction. In addition, the incidence rates for new positive exercise tests, angina, and coronary bypass surgery were all significantly reduced by 25%, 20% and 21%, respectively, in the cholestyramine group. In the treated group, risk reduction was related directly to reduction in total and LDL cholesterol. In a similar but considerably smaller double blind, placebo-controlled, secondary prevention trial where coronary artery lesion change as determined by serial coronary angiography was the end point (The NHLBI Type II Intervention Trial), cholestyramine treatment significantly delayed the progression of atherosclerotic lesions. Plaque progression related directly to both a fall in low density lipoprotein and a rise in high density lipoprotein.

Adult↗
PubMed1986

Changing perspectives in the prevention of coronary artery disease.

Today the question is no longer whether cholesterol reduction is beneficial for those at risk for coronary artery disease; the questions now are when, whom and how to treat. Areas of great interest include extrapolation of current trial results to low density lipoprotein reduction by diet and drugs, and assessment of the value of increasing high density lipoprotein levels by pharmacologic means. We will need to decide what measurements (total cholesterol, lipoprotein cholesterol or lipoprotein apoprotein levels) are of most value to the diagnosis, treatment and follow-up of the at-risk patient. Recommendations, including those of the recently published National Institutes of Health Consensus Panel on Cholesterol Lowering, suggest that our index for diagnosis and treatment should be set considerably lower than it is today. To be successful with a more aggressive approach to cholesterol lowering, we will need to better support, educate and motivate the at-risk patient. Physicians need to become more knowledgeable about what plasma cholesterol is and how to change it. Methods that enhance patient adherence to diet and drug therapy must be developed. We will need to alter lifetime habits and will need the help of both the food industry and better informed consumers, knowledgeable on how to read food labels, if we are to succeed. Ultimately, we will need a 2-pronged approach, focusing on both the physician and the public at large.

Animals↗
PubMed1979

The composition and metabolism of high density lipoprotein subfractions.

The composition and metabolism of high density lipoprotein (HDL) subfractions were investigated in seven normal individuals. Mean HDL2 (d, 1.063-1.125 g/ml) composition (by weight) was 43% protein, 28% phospholipid, 23% cholesterol, and 6% triglyceride, and mean HDL3 (d, 1.125-1.21 g/ml) composition was 58% protein, 22% phospholipid, 14% cholesterol, and 5% triglyceride. The mean apoA-I; apoA-II weight ratio was 4.75 for HDL2 and 3.65 for HDL3. HDL2 protein was proportionally slightly richer in C apolipoproteins and higher molecular weight constituents (including apoE) than HDL3. Kinetic studies utilized radiolabeled HDLA (d, 1.09-1.21 g/ml), HDL2, and HDL3 demonstrated rapid exchange of apoA-I and apoA-II radioactivity among HDL subfractions, similar fractional rates of catabolism of apoA-I and apo A-II within HDL, and similar radioactivity decay within HDL subfractions. Mean plasma residence time was 5.74 days for radiolabeled HDL2 and 5.70 days for radiolabedled HDL3. Differences in HDL protein mass among individuals were largely due to alterations in catabolism, and in general both HDL2 and HDL3 were catabolized via a plasma and a nonplasma pathway. Data from simultaneous radiolabeled very low density lipoprotein and HDL studies in 2 individuals are consistent with the concept that apoC-II and apoC-III are catabolized at a different rate than are apo A-I and apo A-II within the HDL density range.

Adult↗
PubMed1979

Progress toward prevention of cardiovascular disease. A 30-year retrospective.

Since its creation as the National Heart Institute in 1948, the National Heart, Lung, and Blood Institute (NHLBI) has led a national biomedical research program in heart, lung, blood, and blood vessel diseases, and has become increasingly involved in complex clinical trials to validate its research findings. In addition, NHLBI sponsors demonstrations and educational activities to apply proved research findings in the health care community. NHLBI's approach to these responsibilities involves acquiring new and basic information, testing and evaluating the information, and applying it to improve prevention, detection, and treatment of disease. New equipment such as the heart-lung machine and the pacemaker, better diagnostic procedures, new operative and treatment devices, new drugs, and increased use of preventive medicine have dramatically reduced mortality from heart attack, hypertension and stroke.

Academies and Institutes↗
PubMed1978

Metabolism of high-density lipoprotein apolipoproteins in Tangier disease.

To define the metabolic defect in Tangier disease, we studied the kinetics of [125I]-high-density lipoprotein apolipoproteins (apolipoproteins A-I and A-II) in 11 normal subjects, two obligate heterozygotes, and two homozygotes. Mean synthesis of apolipoproteins A-1 and A-11 was 8.24 mg per kilogram per day in the normal group, 7.94 in heterozygotes and 3.66 in homozygotes. The mean plasma-residence time for both apolipoproteins was 5.21 days in the normal subjects, 3.41 days in heterozygotes, and 0.52 days in homozygotes. In normal subjects and heterozygotes the apolipoproteins were catabolized at similar rates, whereas in homozygotes apolipoprotein A-I was catabolized at a much greater fractional rate than apolipoprotein A-II. These findings indicate that the deficiency of these apolipoproteins in Tangier disease is largely due to rapid and altered catabolism.

Adult↗
PubMed1978

Plasma-triglycerides in regulation of H.D.L.-cholesterol levels.

Plasma-high-density-lipoprotein (H.D.L.) cholesterol concentrations are lower in patients with coronary-artery disease than in control subjects. In an investigation of the relationship of H.D.L. cholesterol to other lipid and lipoprotein parameters in normal and hyperlipoproteinaemic subjects inverse correlations were found between H.D.L. cholesterol and very-low-density-lipoprotein (V.L.D.L.) cholesterol, and between H.D.L. cholesterol and plasma-triglyceride levels. Mean H.D.L.-cholesterol concentrations in normal subjects were 50 mg/dl, and in hyperlipoproteinaemic patients they were: type I, 17 mg/dl; type II, 44 mg/dl; type III, 38 mg/dl; type IV, 37 mg/dl; and type V, 27 mg/dl. H.D.L.-cholesterol levels were lowest in patients with fasting chylomicronaemia and were diminished in hypertriglyceridaemic subjects, suggesting a relationship between the metabolism of triglyceride-rich lipoproteins and H.D.L.

Cholesterol↗