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

In addition to high concentrations of LDL cholesterol, high levels of triglycerides and low concentrations of HDL cholesterol are now known to be independent risk factors in the development of atherosclerosis. The use of Gemfibrozil, with its LDL cholesterol-reducing, HDL cholesterol-raising, and triglyceride-lowering effects, would thus appear to make good sense for the treatment of lipid metabolism anomalies with no selective elevation of LDL cholesterol; it would thus also appear to be superior to HMG-CoA-reductase inhibitors.
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PMID:[Gemfibrozil in the differential therapy of disorders of fat metabolism]. 139 12

We studied the effect of gemfibrozil on the compositions of VLDL, LDL and distribution of LDL subspecies in type II hyperlipidemic patients. Gemfibrozil significantly lowered serum triglyceride levels in this group of patients who had normal to moderately elevated triglyceride prior to therapy. Gemfibrozil also changed the composition of VLDL by lowering its free cholesterol, cholesterol ester and raising the protein content. In contrast, no measurable changes in LDL chemical composition were found following gemfibrozil therapy. Changes in LDL, however, can be detected using ultracentrifugal and electrophoretic methods. Peak densities of LDL were lowered and LDL subspecies shifted to larger, slower-moving bands on gradient gel electrophoresis in patients receiving gemfibrozil treatment. These results suggest that gemfibrozil treatment resulted in qualitative changes in both VLDL and LDL even in patients with moderately elevated baseline serum triglyceride levels.
Atherosclerosis 1992 Jul
PMID:Effect of gemfibrozil on composition of lipoproteins and distribution of LDL subspecies. 164 90

Normalization of serum lipid levels should be initiated as soon as possible in patients with myocardial, cerebrovascular, or peripheral vascular disease. Clinical trials indicate that coronary artery disease and overall mortality rates can be reduced and atherosclerosis stabilized or reversed by lipid-lowering therapy. Treatment should lower low-density lipoprotein cholesterol levels to 130 mg/dL or less and total triglyceride levels to 150 mg/dL or less and increase high-density lipoprotein cholesterol levels to at least 52 mg/dL in men and 66 mg/dL in women. Nonlipid coronary risk factors should be eliminated when possible. Lipid-lowering therapy may consist of dietary modification and drug treatment with colestipol hydrochloride (Colestid), cholestyramine (Cholybar, Questran), lovastatin (Mevacor), gemfibrozil (Lopid), and nicotinic acid (Nicolar).
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PMID:Treating serum lipid abnormalities in high-priority patients. 198 20

Gemfibrozil lowers triglycerides, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol. It also promotes a significant increase of high density lipoprotein (HDL) cholesterol. It has been established that normalization of apolipoproteins is an important protective factor against atherosclerosis. The present report examines the effectiveness of 12 months of gemfibrozil treatment on plasma lipids and apolipoproteins in types IIa (VLDL 18 +/- 2 mg cholesterol/dL) and IIb (VLDL 58 +/- 7 mg cholesterol/dL) hypercholesterolemic patients. Gemfibrozil lowered plasma triglycerides, VLDL cholesterol and apolipoprotein B (apoB), increased HDL cholesterol and apoAI levels in both groups, and induced a very substantial reduction in LDL cholesterol in type IIa patients only. Even though HDL particles were enriched in cholesterol, indicating improvement in the reverse cholesterol transport and lower risk of atherosclerosis in both groups, it is important to note that production of cholesterol-poor LDL particles and reduction in LDL cholesterol and the LDL/HDL cholesterol ratio were observed only in the normotriglyceride group (type IIa). Due to the initially elevated concentration of plasma triglycerides and VLDL in type IIb patients and the increased catabolism of VLDL to LDL during gemfibrozil therapy, this drug has a more efficient regulating effect on LDL particles in type IIa compared with type IIb hyperlipidemia.
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PMID:Gemfibrozil therapy in primary type II hyperlipoproteinemia: effects on lipids, lipoproteins and apolipoproteins. 202 87

Simvastatin, 10-40 mg/d (n = 11), bezafibrate, 600 mg/d (n = 6), and gemfibrozil, 1200 mg/d (n = 5) were administered for 12 weeks after a 4-week placebo period to subjects with initial plasma levels (mg/100 ml. mean +/- SD) of cholesterol (346 +/- 77), and of triglycerides (180 +/- 54). Total LDL-C plasma concentration was lowered 32% by simvastatin and 35% by bezafibrate, but only bezafibrate diminished the triglyceride (41%) and increased HDL-C plasma levels (35%). Plasma lipoprotein fractions obtained by discontinuous gradient ultracentrifugation, namely, VLDL, lighter LDL (LDL-1), heavier LDL (LDL-2) and bulk HDL were chemically analyzed. Simvastatin and bezafibrate significantly diminished the quantity of VLDL and LDL-1 particles, although barely modifying their composition. Neither drug influenced the LDL-2 plasma concentration. Bezafibrate increased the total plasma HDL level little interfering with its chemical composition. Gemfibrozil was the least effective of all drugs but decreased the lipid and protein contents and their ratios in VLDL and LDL-2.
Atherosclerosis 1990 Dec
PMID:Effects of simvastatin, bezafibrate and gemfibrozil on the quantity and composition of plasma lipoproteins. 210 85

Pharmacologic intervention for altering plasma lipoproteins is aimed principally at reducing atherogenesis and thereby preventing coronary artery disease. These drugs should be prescribed only after nonpharmacologic interventions (reduction of saturated fat and cholesterol consumption, weight reduction, aerobic exercise, cessation of cigarette smoking) have failed to achieve an adequate effect. The plasma concentration of the atherogenic low-density lipoprotein (LDL) may be reduced in hypercholesterolemic patients by increasing hepatic LDL receptor synthesis (bile acid sequestering resins, 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors) or by reducing hepatic very low density lipoprotein synthesis (gemfibrozil, nicotinic acid). LDL concentration may also be reduced by treatment with one of the fibrates (e.g., fenofibrate). Several classes of lipid-lowering drugs also increase the plasma high-density lipoprotein (HDL) cholesterol concentration. In the case of the fibrates, this appears to be principally mediated through an increase in lipoprotein lipase activity. Gemfibrozil additionally stimulates apolipoprotein AI synthesis. The increase in HDL cholesterol produced by nicotinic acid is due primarily to decreased clearance of HDL particles from the circulation. The increase in HDL concentration produced by gemfibrozil was shown in the Helsinki Heart Study to make a major contribution to a reduced incidence of coronary artery disease, independently of that made by the decrease in LDL. The Cholesterol-Lowering Atherosclerosis Study demonstrated that combined therapy with a resin (colestipol) and nicotinic acid can reduce the progression of coronary atherosclerosis and the development of graft lesions in patients who have undergone coronary artery bypass graft surgery.
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PMID:Pharmacotherapy of disorders of plasma lipoprotein metabolism. 220 45

Recent pharmacological studies confirmed the role of hypercholesterolemia in the pathogenesis of coronary atherosclerosis. A 10% reduction in cholesterol levels can reduce the risk of coronary heart disease by 15%. However many hypercholesterolemic patients often suffer from arterial hypertension and drugs such as thiazide diuretics cause an imbalance in lipid metabolism. The efficacy and the tolerability of simvastatin (a inhibitor of HGM-CoA reductase) with that of gemfibrozil (a fibric acid derivative, which can reduce the VLDL level) were compared in a placebo-controlled study in 2 groups of patients with primary hypercholesterolemia and mild-to-moderate essential hypertension treated with hydrochlorothiazide. After 10 weeks standard hypolipidemic diet and hydrochlorothiazide (25 mg od) therapy, 30 patients whose cholesterol levels were still greater than or equal to 250 mg/100 ml and whose diastolic blood pressure was less than 95 mmHg were randomized to one of the following treatments: simvastatin, 20 mg od, gemfibrozil, 600 mg bid or placebo, while continuing dietetic and diuretic treatment. After 24 weeks treatment, simvastatin induced a 37% reduction in cholesterol plasma levels, a 9% increase of HDL and a 16% reduction of LDL. APO-A1 showed a 4% increase, while APO-B showed a 3% reduction. Gemfibrozil induced a 20% reduction in plasma triglycerides and a 13% decrease in plasma cholesterol, with a significant 19% increase in HDL and a 11% reduction in LDL. No significant variations in any of the lipid parameters monitored were observed in the placebo group. Treatment with simvastatin or gemfibrozil in hypertensive patients in hydrochlorothiazide monotherapy can reduce total cholesterol and LDL-cholesterol plasma levels, while significantly increasing HDL plasma levels compared to placebo. Simvastatin, however, resulted more efficient than gemfibrozil on total cholesterol or cholesterol fractions.
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PMID:[Simvastatin versus gemfibrozil in the treatment of primary hypercholesterolemia in hypertensive patients treated with hydrochlorothiazide]. 224 35

In 25 patients with primary dyslipoproteinemias and severe premature atherosclerosis, during an average combined Lopid-Mevacor treatment span of 12.5 months per patient, our specific aim was to assess safety and efficacy of open-label therapy with diet, gemfibrozil (Lopid), and lovastatin (Mevacor). Because targeted lipid values were not reached on diet alone (low-density lipoprotein cholesterol [LDLC] less than 120 mg/dl, high-density lipoprotein cholesterol [HDLC] greater than 35 mg/dl or total cholesterol [TC]/HDLC less than 4.5), the patients received Lopid, 1.2 gm/day as their initial lipid-lowering drug. Because targeted lipid levels were not reached with Lopid treatment alone after 3 or more months, Mevacor was added, with 17 subjects receiving 20 mg/day, five receiving 40 mg, two receiving 60 mg, and one receiving 80 mg. Outpatient visits were repeated during combined therapy every 6 to 8 weeks, with an average of 6.4 visits per subject, 162 measurements of fasting lipids and liver function tests, and 127 measurements of creatine phosphokinase (CPK). By selection, all patients had normal liver function (gamma-glutamyltransferase, serum glutamic-oxaloacetic transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) levels) and normal CPK levels at baseline. No gamma-glutamyltransferase levels were high during combined therapy. Of the 162 liver function test measurements, five (3.1%) SGOT levels and three (1.9%) SGPT levels were high. Of 127 CPK measurements, three (2.4%) were high; one subject had a high CPK measurement, and one subject had two high measurements for CPK. No symptomatic myositis or myalgias developed in the subjects; none had palpable skeletal muscle tenderness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of combined gemfibrozil-lovastatin therapy for primary dyslipoproteinemias. 234 62

We investigated the modulating effect of serum total triglycerides on the lipid composition of various lipoproteins, and on the response to gemfibrozil treatment. This placebo controlled study was conducted blind in 60 participants of the Helsinki Heart Study. An inverse relationship was observed between cholesterol content in all lipoprotein fractions and serum total triglyceride level. Gemfibrozil, in addition to changing the absolute amounts of lipoprotein lipids, also normalized the qualitative abnormalities associated with hypertriglyceridemia. Gemfibrozil increased the level of HDL-cholesterol with the main effect on HDL3-subfraction. The observed reduction in LDL-cholesterol was dependent on the initial triglyceride level.
Atherosclerosis 1990 Feb
PMID:Effect of gemfibrozil on the concentration and composition of serum lipoproteins. A controlled study with special reference to initial triglyceride levels. 240 50

Serum high density lipoproteins (HDL) are a protective factor against atherosclerosis. Many epidemiological studies show a strong inverse relationship between serum HDL-cholesterol (HDL-C) and the likelihood of developing coronary artery disease (CAD). HDL-C levels appear to be a stronger predictive factor for CAD than serum total or low density lipoprotein cholesterol (LDL-C) levels. In the presence of high HDL-C levels, the development of CAD is unlikely even in persons with increased total or LDL-C. Conversely, subjects with low serum levels of HDL-C are at increased risk even if their total and LDL-C is within the "desirable" range. A number of studies have also shown that increasing HDL-C levels is associated with both primary and secondary prevention of atherosclerosis. HDL-C levels should be estimated in individuals with family and/or personal history of premature atherosclerosis, even if they have normal total cholesterol. Only the current problems with the accuracy and precision of the serum HDL-C assay prevent it from being the single most important test for assessment of the lipid risk factors for CAD. The most frequent causes of low HDL-C are smoking, obesity, and hypertriglyceridemia. Treatment of low HDL-C includes removal of these factors, and if this is ineffective, use of drugs. Gemfibrozil and niacin are most effective in raising serum HDL-C, although a number of other medications can markedly improve the total:HDL-C ratio.
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PMID:The clinical significance of serum high density lipoproteins. 269 72


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