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

Obesity is known to be associated with an elevated risk for cardiovascular disease. Rheological disturbances could be factors contributing to these vascular complications. Therefore we have evaluated blood viscosity parameters in 128 obese (BMI greater than 28 kg/m2) adults and in 90 non-obese healthy subjects. Whole blood, plasma and erythrocyte viscosity values were determined with a Contraves LS30 viscosimeter. Plasma and whole blood viscosity were significantly (all P less than 0.001) increased in the obese subjects. The increased low shear erythrocyte viscosity suggested a diminished erythrocyte deformability in obesity. The rheological abnormalities were present even in the absence of impaired glucose tolerance, diabetes, hypertension or hyperlipidaemia. In the obese group the rheological parameters showed significant correlations (at least P less than 0.05) with BMI, insulin or C-peptide area during an oral glucose tolerance test and plasma lipids. Our findings demonstrate that obesity per se may be associated with abnormal blood viscosity properties.
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PMID:Blood viscosity in human obesity: relation to glucose tolerance and insulin status. 269 80

We evaluated the changes in frequency of pharmacologic treatment of hyperlipidemia in 345 hyperlipidemic patients with symptomatic cardiovascular disease requiring cardiac catheterization between 1982 and 1987. The frequency of pharmacologic treatment increased from 13% (1982) to 59% (1987), with the major increase occurring in 1984. Increases in the frequency of treatment were paralleled by increases in prescriptions for lipid-lowering drugs nationwide. During this period the percentage of hyperlipidemic patients we evaluated who were treated with various agents changed, and at the end of the study the use of gemfibrozil, bile acid-binding resins, and nicotinic acid had increased, whereas clofibrate and probucol use decreased. Although the data showed an increase in prevalence of treatment, almost half the patients remained untreated, and of those treated over half remained hypercholesterolemic despite treatment. The results suggest increasing but incomplete physician awareness of hyperlipidemia as a cardiovascular disease risk factor and the need for further physician education in the pharmacologic management of hyperlipidemia.
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PMID:Changes in pharmacologic treatment of hyperlipidemia. 273 Jul 96

Cardiovascular disease is the leading cause of morbidity, disability, and death among patients with type II (non-insulin-dependent) diabetes mellitus. Moreover, hyperlipidemia is also common among these patients. Despite this, there are virtually no data regarding the level of awareness and treatment of hyperlipidemia among diabetic subjects at the community level. We therefore examined 374 Mexican-Americans and 86 non-Hispanic whites with type II diabetes identified in an epidemiologic survey that involved 3279 Mexican-Americans and 1847 non-Hispanic whites who resided in San Antonio, Tex. More than 40% of the diabetic subjects were hyperlipidemic according to the criteria of the National Cholesterol Education Program, and an additional 23% had hypertriglyceridemia and/or low levels of high-density lipoprotein cholesterol. By contrast, less than one fourth of the nondiabetic subjects were hyperlipidemic. Only approximately 25% of non-Hispanic whites with diabetes were aware of their hyperlipidemia, and less than 10% were receiving treatment. Awareness and treatment were even less frequent among Mexican-Americans with diabetes. Community physicians should be encouraged to give early attention to the management of lipid disorders in their diabetic patients.
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PMID:Lack of awareness and treatment of hyperlipidemia in type II diabetes in a community survey. 249 11

Recent epidemiologic studies have shown that rates of cardiovascular disease are lower in populations such as the Greenland Eskimos than in those that do not eat seafood, even though the levels of dietary fat intake are often similar. Dietary fish oils are rich in eicosapentaenoic acid (EPA), a polyunsaturated fatty acid of the omega-3 series. EPA has been shown to prolong bleeding time and to decrease platelet aggregation and blood viscosity. EPA inhibits the production of prostaglandins from endogenous arachidonic acid, which is associated with the formation of thromboxane A2 and may also dampen cyclo-oxygenase and lipoxygenase metabolites involved in mediating endothelial cell proliferation. Dietary fish oils are now available in the form of EPA-enriched capsules. Short-term trials in humans have shown that EPA significantly reduces the levels of plasma triglycerides and may increase the levels of high-density lipoproteins; however, no consistent effect on serum cholesterol levels has been shown. The results of evaluations of EPA's use in patients with renal disorders, mild hypertension, inflammatory disorders or hyperlipidemia have been promising. On the basis of the epidemiologic and biologic evidence dietary fish oils warrant further study in extensive clinical trials.
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PMID:Dietary fish oils containing eicosapentaenoic acid and the prevention of atherosclerosis and thrombosis. 284 22

It is generally acknowledged that hypertension is associated with an increased risk of cardiovascular morbidity and mortality, and that lowering elevated blood pressure is effective in reducing that risk. However, hypertension is more likely to cause cardiovascular disease in those with additional risk factors, such as cigarette smoking, hyperlipidemia, diabetes mellitus, hypokalemia, loft ventricular hypertrophy, or electrocardiographic abnormalities. The evidence to date indicates that not all patients with mild hypertension need to be treated with drugs; not all of those receiving drug therapy should be treated with the same drugs; and the benefit of the same degree of reduction in blood pressure may not be equivalent for different drugs. The use of traditional step 1 diuretic therapy is not uniformly appropriate. As an alternative, the vasodilator prazosin can be effective as monotherapy in the treatment of mild hypertension, and its addition to diuretic or beta blocker therapy appears to blunt or prevent the adverse effects of those agents on lipid levels. Since prazosin therapy is least likely to worsen existing risk factors or precipitate their occurrence, it should enhance the benefit of blood pressure reduction in delaying or preventing cardiovascular disease.
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PMID:Antihypertensive therapy and lipids. Paradoxical influences on cardiovascular disease risk. 286 58

Some of the genetic factors and environmental factors such as diet and drug therapies that are known to increase the risk of hyperlipidemia and possibly the predisposition to cardiovascular disease are reviewed. The cholesterol associated with the low-density lipoproteins (LDL), accounting for 60-75% of the plasma levels, is responsible for the powerful and direct relationship which exists between plasma cholesterol and coronary heart disease. Also, the cholesterol that accumulates in atheromatous lesions is derived primarily from plasma LDL. Hyperlipidemia is defined by elevated levels of the plasma levels; the risk for atherosclerosis is associated with the classification types IIa, IIb, III, and possibly IV, a classification system based on phenotypic manifestations of increased lipoprotein fractions. The Lipid Research Clinics Program reports data on plasma lipid and lipoprotein cholesterol distributions of a large-scale screening of white men and women (both with and without sex hormone usage) aged 20-59 years in the US. They found age-related trends for rising triglycerides and cholesterol with differences between the sexes clearly demonstrated. It has been established that normolipemic individuals are not immune to the development of atherosclerosis. The recent focus on the apolipoprotein moieties has revealed a number of normolipemic dyslipoproteinemias associated with tissue lipid infiltration. Multifactorial population studies provide a strong case for the powerful role of the environment, i.e., predominantly dietary intake of total fat, saturated fat, saturated fats, and calories, in hyperlipidemia. According to the Seven Countries Study, populations with higher levels of cholesterol and LDL cholesterol (and increased atherosclerosis) have saturated fat intakes of 10% or more of calories. Migration studies of Japanese populations in Japan and in the US also show the influence of diet. As was shown early on, oral contraceptive (OC) use predisposes to the development of hyperlipidemia. OCs also predispose to other cardiovascular risk factors that, when combined with smoking, bring about a greatly magnified risk for myocardial infarction. Also reviewed in terms of their effect on the lipoprotein profile are antihypertensive therapies, retinoids, and hypolipidemic agents. Regarding genetic predisposition, single-gene mutations in apoproteins, lipoproteins, and some of the enzymes involved in lipoprotein may underlie disorders of hyperlipoproteinemia or hypolipoproteinemia.
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PMID:Risks for hyperlipidemia. 287 33

Whether or not obesity per se is an independent risk factor remains controversial. However, a variety of studies have shown that obesity precipitates certain well-known risk factors, such as glucose intolerance, hyperlipidemia, hyperestrogenemia, hypertension, and left ventricular hypertrophy. Distribution of adipose tissue also seems to influence cardiovascular risk; patients with predominantly male-pattern obesity exhibit more profound risk for cardiovascular disease.
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PMID:Risks for obesity. 293 52

A randomized double blind, placebo-controlled crossover design was used to determine the efficacy of gemfibrozil and clofibrate in the treatment of familial combined hyperlipidemia and to determine which one of these agents would be more effective. Sixteen patients, 12 men and 4 women, mean age 49.5 years (40-68 yrs), had the entry criteria of increased cholesterol and/or triglyceride with an increase in triglyceride and/or cholesterol in one or more first degree relatives and/or family history of premature cardiovascular disease. Patients received 6 weeks of placebo followed by clofibrate 1000 mg bid or gemfibrozil 600 mg bid for 12 weeks, placebo for 6 weeks and the other drug for 12 weeks. Plasma total cholesterol, triglycerides, HDL-C, LDL-C, apo B and apo A-I were measured every 6 weeks during the study. Gemfibrozil was associated with a significant (P less than 0.05) decrease in plasma triglyceride concentration compared to placebo but it was not significantly different compared to clofibrate. For ease of comparison, the mean value for serum triglycerides during gemfibrozil treatment (average of the 6 and 12 week measurements) was calculated and was 232 +/- 198 mg/dl (mean +/- 1 SD) compared to the average of the placebo treatment values of 381 +/- 410 mg/dl and the average value during the clofibrate treatment period of 217 +/- 178 mg/dl. HDL-C was significantly (P less than 0.05) increased with both drugs and to the same extent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of gemfibrozil and clofibrate on serum lipids in familial combined hyperlipidemia. A randomized placebo-controlled, double-blind, crossover clinical trial. 305 31

There is good epidemiologic evidence that hypertension is associated with a high risk of cardiovascular disease. However, primary intervention trials have failed to demonstrate that a reduction in blood pressure in hypertensive patients reduces morbidity and mortality from cardiac events. Since various antihypertensive drugs adversely affect lipoprotein metabolism, these drugs may increase associated coronary risk and offset the beneficial effects of lowering blood pressure. This article reviews the effects of various antihypertensive drugs on plasma lipids, lipoproteins, and apolipoproteins. They can be summarized as follows: thiazide-type diuretics cause a marked elevation of plasma triglycerides and very low-density lipoprotein (VLDL) and minor increases in total cholesterol and low-density lipoprotein (LDL), but have little effects on high-density lipoprotein (HDL). The nonselective beta-blockers do not significantly affect total cholesterol and LDL, but increase total triglycerides and VLDL and decrease HDL. The changes in plasma lipids and lipoproteins caused by cardioselective beta-blockers and beta-blockers with intrinsic sympathomimetic activity are qualitatively similar but less pronounced. Calcium antagonists and angiotensin-converting enzyme inhibitors appear to have no significant effects on plasma lipids. alpha 1-Inhibitors reduce total triglycerides, total cholesterol, VLDL, and LDL and increase HDL. The possible mechanisms by which antihypertensive drugs affect cellular lipid metabolism (e.g., LDL receptor, lipid synthesis, lipoprotein lipase, lecithin cholesteryl acyltransferase, acylcholesteryl acyltransferase, and cholesteryl ester hydrolase) are described. The clinical significance of changes in blood lipids and cellular lipid metabolism caused by antihypertensive drugs is not yet totally clear. Nevertheless, before antihypertensive drug treatment is initiated, blood lipid levels should be measured to identify preexisting hyperlipidemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of antihypertensives on plasma lipids and lipoprotein metabolism. 305 88

The present study was undertaken to determine the relationship between plasma lecithin: cholesterol acyl transfer (LCAT) rate and cholesterol and bile acid turnover in hyperlipidaemia. Nineteen healthy controls, 19 patients with hyperlipoproteinaemia (HLP) type IIa and 12 patients with HLP type IV were studied under standardized dietary conditions. Bile acid kinetics was determined with the aid of [14C]labelled cholic acid and chenodeoxycholic acid. In the hyperlipidaemic patients, cholesterol balance was calculated as the sum of bile acid synthesis plus daily faecal excretion of neutral C27 steroids minus dietary intake of cholesterol. The plasma LCAT rate was determined simultaneously. The mean values of bile acid formation, cholesterol balance, and LCAT rate in HLP type IV patients exceeded those in HLP type IIa patients or in the controls. An increased plasma LCAT rate was found among HLP type IV patients with and without evidence of cardiovascular disease. Plasma LCAT rate correlated positively with bile acid formation (Rs = +0.78, p less than 0.01) and cholesterol balance (Rs = +0.88, p less than 0.002) in HLP type IV. No such relationships were obtained in the controls or in HLP type IIa. It is suggested that an increased production and/or flux of VLDL in HLP type IV is linked to an enhanced plasma LCAT rate and to an increased formation and metabolism of cholesterol in the liver.
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PMID:Plasma cholesterol esterification rate in hyperlipoproteinaemia: relation to cholesterol elimination. 320 95


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