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

New Zealand White rabbits fed a low-level cholesterol-enriched diet (0.1%) were used to study and characterize a possible model of experimental atherogenesis. For the determination of the degree of atherosclerosis, more consistent and reproducible morphometric methods were used. Simultaneously the influence of plasma cholesterol levels on vascular noradrenaline content was studied. The effect of a new lipid-regulating drug (0.1% L 44-0, the N-oxide of a nicotinic acid derivative) on analyzed parameters was studied as well. This study suggests that the low-level cholesterol-enriched diet is atherogenic, with macroscopically detectable lesions of atherosclerosis becoming apparent by week 12 of the study. The same diet increases the vascular noradrenaline content in the renal artery and in the femoral artery and vein; however, it does not influence that content in the carotid and mesenteric arteries. L 44-0 counteracts most of the observed effects.
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PMID:Experimental atherogenesis and vascular noradrenaline content in NZW rabbits and activity of a new nicotinic acid derivative (L 44-0). 179 52

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

There is overwhelming evidence that atherosclerosis is caused by elevated cholesterol levels and that the process can be prevented, arrested, and even reversed by altering the cholesterol fractions. The National Cholesterol Education program established guidelines for the management of hypercholesterolemia. Classification of cholesterol values are: Desirable 200 mg./dl, Borderline high 200-239 mg./dl high risk 240 mg./dl and above. Total cholesterol is used for case finding and screening, but LDL cholesterol is the key index for decisions requiring treatment. Classification of LDL levels is as follows: High risk 160 mg/.dl and over, Borderline 130 to 159 mg./dl, Acceptable 130 mg./dl and below. Secondary and familiar disorders should be identified. Dietary therapy is the cornerstone of cholesterol reducing interventions. Steps one and two diets are described, with limitations of saturated fats to 10% of total calories and cholesterol to 300 mg./daily in step one; step two diet limits saturated fats to 7% of total calories-and cholesterol to 200 mg./daily. Pharmacotherapy is based on 5 groups of hypolipidemics agents: A--Resins (cholestyramine and colestipol) B--Nicotinic acid C--Probucol D--Fibric acids (gemfibrozil) E--Reductase inhibitors (lovastatin). Some areas of criticism and controversies regarding the guidelines are discussed and identified.
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PMID:The National Cholesterol Education program: guidelines and commentaries. 207 38

Niacin reduces the incidence of non-fatal myocardial way infarction, confers a significant long-term survival benefit after recovery from myocardial infarction, and has had many years of study and usage by the medical community. Recent evidence suggests that via mechanisms which elevate HDL cholesterol and also release endogenous prostacyclin, niacin should be a potent agent in the long-term treatment of atherosclerosis.
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PMID:Atherosclerosis: the importance of HDL cholesterol and prostacyclin: a role for niacin therapy. 211 21

The bile acid sequestrants, cholestyramine and colestipol, are the drugs of choice for the treatment of patients with hypercholesterolemia caused by increases in LDL-cholesterol levels without concurrent hypertriglyceridemia (type IIA and type IIB hyperlipoproteinemia). Longitudinal clinical studies with these drugs have shown their ability to slow the progression of atherosclerosis and to limit the consequences of the disease. Bile acid sequestrants can be used with other lipid-lowering drugs such as nicotinic acid or HMG CoA reductase inhibitors, to maximize the cholesterol-lowering effects. The side effect profile of the bile acid sequestrants is tolerable, with most complaints related to effects on the gastrointestinal tract and the bulkiness of the resins.
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PMID:Bile acid sequestrants. 217 78

Coronary heart disease is the leading cause of death among patients with non-insulin-dependent diabetes mellitus (NIDDM). NIDDM patients have a high frequency of dyslipidemia, which along with obesity, hypertension, and hyperglycemia may contribute significantly to accelerated coronary atherosclerosis. Because risk factors for coronary heart disease are additive and perhaps multiplicative, even mild degrees of dyslipidemia may enhance coronary heart disease risk. Therefore, therapeutic strategies for management of NIDDM should give equal emphasis to controlling hyperglycemia and dyslipidemia. The National Cholesterol Education Program recently issued guidelines for treatment of hyperlipidemia in adults including diabetic patients. Because of the unique features of diabetic dyslipidemia, however, we suggest that certain modifications in these guidelines be made to meet specific needs of diabetic patients. For example, therapeutic goals for serum cholesterol reduction should be lower in diabetic patients than in nondiabetic subjects. Particular emphasis should be given to weight reduction in NIDDM patients. In some diabetic patients, monounsaturated fatty acids may be a better replacement for saturated fatty acids than carbohydrates. The target for cholesterol lowering should include both very-low-density lipoprotein and low-density lipoprotein (LDL) (non-high-density lipoprotein) rather than LDL alone. To obtain a substantial reduction of cholesterol levels, drug therapy may be required in many patients. However, first-line drugs for nondiabetic patients (nicotinic acid and bile acid sequestrants) may be less desirable in NIDDM patients than hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors and even fibric acids. In fact, HMG CoA reductase inhibitors may be the drugs of choice for NIDDM patients with elevated LDL cholesterol and borderline hypertriglyceridemia, whereas gemfibrozil appears preferable for NIDDM patients with severe hypertriglyceridemia.
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PMID:Management of dyslipidemia in NIDDM. 219 Jul 70

As hypercholesterolemia is an essential risk factor of atherosclerosis, a strategy for diagnosis and treatment of hyperlipidemia is indispensable. Differences in mortality from coronary heart disease in different cultures seem to be due to environmental, not to genetic factors. Trials in Finland and the United States have shown that cholesterol levels and smoking can be reduced by information and education with an ensuing drop in cardiovascular mortality. This experience warrants national programmes for cholesterol-lowering in high risk countries. Programmes should be directed to doctors and health officials as well as legislators and the public. Within any given population individual differences of lipid levels are due to both nutritional habits and genetic variations concerning e.g. LDL-receptors and lipase activity. At present the only means of identifying subjects at risk is to measure their lipid levels and to scrutinize their family history. Measurements should be repeated to exclude biologic and laboratory variability. Drugs currently available include HMG CoA reductase inhibitors, bile acid binding resins, clofibrate derivatives and nicotinic acid. Formerly defined age groups with regard to therapeutic measures have meanwhile been abandoned.
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PMID:Strategy for diagnosis and treatment of hyperlipidemia. 219 53

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

The goals of treatment for patients with hyperlipoproteinemia are to reduce plasma concentrations of known atherogenic lipoproteins, thereby exerting a favorable effect upon lipid deposition in the arterial wall and, less commonly, to prevent the adverse sequelae of hyperchylomicronemia in patients with severe hypertriglyceridemia. Diet is the cornerstone of the therapy after the exclusion of secondary factors; the decision to begin drug therapy should be made only after an adequate trial of diet has failed to achieve satisfactory concentrations of plasma lipids and lipoproteins. For patients without evidence of atherosclerosis the goals is to reduce the plasma concentrations of low density lipoproteins to below 160 mg/dl (4.2 mM/L); for those individuals with atherosclerosis or the concurrent presence of two risk factors, a lower level of LDL is desirable (less than 130 mg/dl; 3.4 mM/L). For regression to occur the LDL level may need to be below 100 mg/dl (2.6 mM/L). The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate, and inhibitors of HMG CoA reductase (e.g., lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolemia and these agents reduce plasma concentrations of total and LDL cholesterol by 15-45%. For those patients with concurrent hypertriglyceridemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use. Fibric acid derivatives (e.g., clofibrate, gemfibrozil, bezafibrate, or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinemia, as is nicotinic acid or lovastatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of hyperlipidemia: goals for the prevention of atherosclerosis. 220 37

Twenty-three consecutive hyperlipidaemic patients were treated with 4 g nicotinic acid daily for 6 weeks. The treatment resulted in the expected reduction of serum very low density (VLDL) and low density lipoproteins (LDL) and in the increase of high density lipoproteins (HDL). The cholesterol concentration of the latter fraction rose by 45%. The HDL fraction was isolated by ultracentrifugation and then subjected to gradient gel electrophoresis (gge), in order to determine the HDL particle size distribution, before and after treatment. The increase of HDL was almost exclusively confined to the largest HDL (gge) subclass HDL-2b, the protein content of which rose by 183%. In contrast, there was about a 25% decrease in the concentration of the smallest HDL(gge) subclasses, HDL-3b and HDL-3c. The levels of HDL-2b and VLDL triglycerides showed a significant inverse correlation before, as well as after, treatment. Multiple partial correlation analysis demonstrated, however, that the nicotinic acid induced increase in HDL-2b concentration showed a highly significant inverse correlation to the decrease in LDL cholesterol, but not to the decrease in VLDL triglyceride levels. Recent studies, in particular those regarding the negative correlation between both the degree and progression of coronary atherosclerosis and the HDL-2b concentration in young male myocardial infarct patients, suggest that the profound increase of HDL-2b levels by nicotinic acid treatment in hyperlipidaemic patients might be of considerable importance in the protection of coronary atherosclerosis.
Atherosclerosis 1990 Aug
PMID:The effects of nicotinic acid treatment on high density lipoprotein particle size subclass levels in hyperlipidaemic subjects. 224 98


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