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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of exercise on the progression of atherosclerotic diseases is reviewed. Prospective studies have reported that a low daily physical activity is associated with a lower incidence of coronary artery disease. Mild aerobic exercise improves survival in patients with coronary artery disease, lowers blood pressure in patients with mild hypertension, improves insulin resistance in diabetes mellitus, lowers weight in obesity and increases HDL-cholesterol and decrease triglyceride in patients with dyslipidemia. Mild exercise therapy may be beneficial in the management of atherosclerotic diseases.
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PMID:[Exercise therapy of atherosclerosis]. 841 77

An ever-increasing body of evidence supports active intervention in patients with dyslipidemia. Newly formulated recommendations call for evaluation of and treatment decisions based on not only total cholesterol and low-density lipoprotein (LDL) cholesterol levels but also high-density lipoprotein (HDL) cholesterol and triglyceride levels. HDL cholesterol determinations are now encouraged as part of routine coronary risk assessment in healthy adults. In addition, both HDL cholesterol and triglyceride measurements are recommended in patients with coronary artery disease, cardiovascular risk factors, or potentially atherogenic disorders such as hypertension or diabetes. If hygienic measures fail to normalize lipid values, a variety of drugs may be used. Future management strategies may include novel agents that inhibit different steps in lipid metabolism or in cholesterol biosynthesis, drugs that modify the lipoproteins themselves rather than change their concentrations, and drugs that protect the vessel wall from atherogenesis. A problem still to be resolved is that only about 10% of candidates for antihyperlipidemic drug therapy are receiving such treatment.
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PMID:Overview of current issues in management of dyslipidemia. 843 59

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

The insulin resistance syndrome has been noted as an interesting and important new risk factor for coronary artery disease. The syndrome consists of hypertension, glucose intolerance, and dyslipidemia, all of which are likely to be derived from insulin insensitivity. In subjects with nonobese and nondiabetic essential hypertension, steady-state plasma glucose (SSPG) was higher than in normotensive subjects during an insulin sensitivity test, indicating reduced insulin sensitivity to glucose metabolism in the hypertensive group. SSPG correlated with the percentage decrease of branched chain amino acids, free fatty acids, and serum potassium during the insulin sensitivity test. With a 2-h insulin infusion, serum norepinephrine, epinephrine, plasminogen activator inhibitor 1, and intraplatelet Ca2+ decreased significantly, but 6-keto-prostaglandin (PG) F1 alpha and PGE2 did not change. Insulin resistance decreased by using antihypertensive treatments with bunazosin, cilazapril, amlodipine, and benidipine in hypertensive subjects. Diagnostic criteria for the insulin resistance syndrome, including clinical values for each risk factor, were developed. Lowered insulin sensitivity and hyperinsulinemia were demonstrated in subjects with both vasospastic and coronary artery stenotic angina. The insulin resistance syndrome together with hyperinsulinemia is likely to induce atherosclerotic changes, possibly through reduced rather than excessive action of insulin.
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PMID:Mechanism and clinical implication of insulin resistance syndrome. 867 91

Disorders in lipoprotein metabolism (dyslipidemia) can result in premature atherosclerosis or pancreatitis. Dyslipidemias can be classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low density lipoprotein cholesterol and decreased levels of HDL cholesterol predispose to premature atherosclerosis. Triglyceride levels greater than 1,000 mg/dL increase the risk for pancreatitis. In the appraisal of the dyslipidemias, measurement of serum cholesterol, triglycerides, HDL-cholesterol and obtaining the LDL cholesterol by Friedewald equation is usually sufficient in the majority of patients. However, in some cases, such as the diagnosis of the Type III dyslipidemia and when triglycerides are > or = 400 mg/dL, ultracentrifugation is required to determine the VLDL or LDL cholesterol. Lipoprotein electrophoresis can be useful in the diagnosis of Type III dyslipidemia (broad beta band) and also to detect chylomicrons. In young subjects with coronary artery disease with a normal LDL cholesterol an apolipoprotein B-100 level may be a useful test. In children and young adults with severe hypertriglyceridemia, measurement of lipoprotein lipase activity or assaying apolipoprotein C-II levels can be useful in elucidating the cause. Also, laboratory tests are useful in excluding a secondary cause of dyslipidemia (urinalysis, plasma creatinine, TSH, glucose, protein electrophoresis, alkaline phosphatase and transaminases). Thus, laboratory investigations play an important role in the management of dyslipidemia.
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PMID:A practical approach to the laboratory diagnosis of dyslipidemia. 870 23

Dyslipidemia in end-stage renal disease is a common problem and may contribute to the high rates of morbidity and mortality in this population. Recent studies indicate that defective lipolysis is a major factor in the development of this disorder which is characterized by increased levels of very-low-density-lipoprotein remnant particles, hypertriglyceridemia and occasionally hypercholesterolemia. There are no prospective long-term studies on the effect of lipid-lowering treatment on morbidity and mortality related to dyslipidemia. Therefore, at present pharmacologic treatment of hyperlipidemia should be undertaken in patients with severe hypertriglyceridemia (> 500 mg/dl) or hypercholesterolemia (LDL > 130 mg/dl) who are at high risk for coronary artery disease. This review discusses the pathogenesis of dyslipidemia, common clinical patterns of hyperlipidemia and various nonpharmacologic and pharmacologic treatment options.
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PMID:Treatment of dyslipidemia in chronic renal failure. 871 69

The prevention of coronary artery disease (CHD) and particularly of myocardial infarction (MI) is based on some well designed strategies aimed at treating both asymptomatic high-risk patients (primary prevention) and patients with established CHD (secondary prevention). A positive impact from primary prevention can be basically achieved trough a reduction in high blood pressure and by correcting dyslipidemia. The benefit can be substantially increased by smoking cessation, increasing physical exercise, reduction of body weight, use of post-menopausal oestrogen, moderate alcohol consumption and use of high doses of vitamin E in those patients who are compliant with the specific strategies. Secondary prevention of MI can be again obtained by controlling blood pressure and reducing serum cholesterol in patients surviving acute MI who can also benefit from the administration of beta-blockers, aspirin and probably ace-inhibitors particularly in presence of left ventricular dysfunction. We suggest that in both arms of prevention, significant results can be achieved mainly by a multifactorial approach capable of correcting all the modifiable risk factors that contribute to the rather complex pathogenesis of CHD.
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PMID:Primary and secondary prevention of myocardial infarction. 874 42

Hyperlipidemia occurs frequently after heart transplantation, and accelerated coronary artery disease remains the major cause of morbidity and mortality in patients who survive more than 1 year after heart transplantation. However, the risks and benefits of lipid-lowering therapy after heart transplantation remain poorly defined, and national guidelines for lipid-lowering drug therapy do not specifically address treatment of dyslipidemia in transplant recipients. Since the initial reports in the 1980s of rhabdomyolysis in heart transplant patients receiving high-dosage lovastatin, results of 11 post-transplantation series that used lovastatin, simvastatin, or pravastatin at lower dosages as drug monotherapy have been published. These studies have shown an overall 1% incidence of rhabdomyolysis, defined as creatine kinase > 10 times the upper limit of normal plus muscle symptoms. One randomized, controlled prospective trial has investigated the effects of lipid-lowering pharmacotherapy on patient outcome in cardiac transplant recipients. At 1-year follow-up in this nonblinded, single-center trial, patients treated with pravastatin (20 or 40 mg/day) initiated within 2 weeks of transplantation had a significant reduction in mortality rate and a significantly lower incidence of transplant arteriopathy. A number of important issues remain unanswered regarding treatment guidelines in patients with hyperlipidemia after heart transplantation. In January 1995 we began the Heart Transplant Lipid Registry, with 12 participant centers, to gather data prospectively on the efficacy and safety of lipid-lowering drugs in the treatment of dyslipidemia after heart transplantation.
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PMID:Treatment of hyperlipidemia after heart transplantation and rationale for the Heart Transplant Lipid Registry. 880 37

The long-term clinical benefits of lowering serum lipid levels have been demonstrated in multiple clinical trials in recent years. These include coronary artery disease regression and decreases in the incidence of adverse clinical events, such as myocardial infarction or refractory ischemia. Reductions in overall mortality have also been demonstrated. The health risk of dyslipidemia led the National Cholesterol Education Program expert panel to recommend intervention to bring low-density lipoprotein cholesterol values to within certain goal levels through a variety of interventions. This article reviews the available pharmacologic agents and compares their efficacy, safety, and cost-effectiveness.
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PMID:Clinical pharmacologic concepts for the rational selection and use of drugs for the management of dyslipidemia. 882 16

It has been reported that insulin resistance is associated with essential hypertension and that an aggregation of risk factors-hypertension, dyslipidemia, and glucose intolerance-together with insulin resistance leads to the more frequent appearance of coronary artery disease. We examined the relation between early asymptomatic atherosclerosis and these risk factors in 72 nondiabetic subjects with essential hypertension (41 men, 31 women) aged 50 to 59 years. Intima-media thickness and plaque formation of the carotid artery were assessed by B-mode ultrasonography, and insulin sensitivity was measured by the steady-state plasma glucose method. Lipoprotein profile was analyzed by ultracentrifugation. The intima-media thickness of the common carotid artery significantly correlated with systolic pressure; mean blood pressure; steady-state plasma glucose, indicating insulin resistance; fasting insulin; area under the curve of plasma insulin and glucose; body mass index; apolipoprotein B; apolipoprotein B in low-density lipoprotein; lower ratio of cholesterol to apolipoprotein B of low-density lipoprotein; and decreased high-density lipoprotein cholesterol. By multiple regression analysis, steady-state plasma glucose was the strongest risk, followed by lower high-density lipoprotein and systolic pressure. These three factors accounted for 54.9% of all the risk for increased intima-media thickness of the common carotid artery. In conclusion, insulin resistance was the strongest risk factor for carotid intima-media thickness, followed by lower high-density lipoprotein cholesterol and hypertension. An effort to maintain normal insulin sensitivity is essential for the prevention of early atheromatous lesions in essential hypertension.
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PMID:Insulin resistance as an independent risk factor for carotid wall thickening. 884 83


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