Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension directly predisposes to all of the major atherosclerotic cardiovascular disease outcomes, including coronary artery disease, stroke, cardiac failure, and peripheral artery disease. Coronary artery disease deserves a high priority in treatment of hypertension because it is the most common and lethal sequela. However, reduction of blood pressure as the sole therapeutic goal of antihypertensive therapy is no longer appropriate. Hypertension tends to cluster with other atherogenic risk factors, including dyslipidemia, glucose intolerance, insulin resistance, obesity, and elevated uric acid. Hypertension is only one of the many risk factors for atherosclerotic cardiovascular disease and is variably hazardous, depending on the number and severity of these coexistent metabolically linked risk factors. The presence of coexistent, already overt cardiovascular disease and left ventricular hypertrophy also greatly influence the hazard and choice of therapy. The urgency for, and choice of, therapy should be based on the multivariate cardiovascular risk profile rather than relying solely on the character and severity of the blood pressure elevation. In this way at-risk hypertensive persons can be more appropriately targeted for treatment designed to improve their multivariate risk profile and to provide maximum benefit and cost effectiveness.
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PMID:Cardioprotection and antihypertensive therapy: the key importance of addressing the associated coronary risk factors (the Framingham experience). 884 93

Coronary angiographic trials have demonstrated that the lowering of cholesterol slows the progression of atherosclerosis, enhances atherosclerotic regression, limits the formation of new lesions, and reduces the incidence of coronary events. Atherosclerotic progression has been shown to be associated with an increased risk of cardiac death, cardiac death plus nonfatal myocardial infarction (MI), and all coronary events. Most of the atherosclerotic regression trials were too small and of too short duration to demonstrate a significant difference in hard coronary events between patients receiving cholesterol-lowering intervention and controls. However, when data from these studies were pooled, total mortality was found to be reduced by 26% and the rate of nonfatal MI by 39% in actively treated patients. The first events trial to demonstrate clearly a reduction in overall mortality was the Scandinavian Simvastatin Survival Study (4S), in which lowering of serum cholesterol in patients with coronary artery disease (CAD) and hypercholesterolemia also reduced coronary mortality, fatal and nonfatal MI, sudden cardiac death, and the need for revascularization. Reductions in major coronary events were seen consistently in all subgroups of patients studied and regardless of concomitant therapy with aspirin, beta blockers, or calcium antagonists. Further evidence of the benefit of cholesterol-lowering therapy was provided by the West of Scotland Coronary Prevention Study (WOSCOPS), which evaluated men with hypercholesterolemia but no history of CAD. Those receiving active treatment had less overall mortality, lower risk of definite nonfatal MI or death from definite or suspected CAD, and less need for revascularization. The Cholesterol and Recurrent Events (CARE) Study recently showed that lipid-lowering therapy is also beneficial in CAD patients with less severe dyslipidemia.
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PMID:Review of cholesterol-lowering therapy: coronary angiographic and events trials. 890 Mar 35

It is well known that hyperlipidemia is often present in patient with impaired glucose tolerance, obesity and/or hypertension. All of these are risk factors for coronary artery disease (CAD). The coexistence of these risk factors markedly increase the likelihood of CAD. Recently, it has been reported that the impaired glucose tolerance and insulin resistence are associated with the increased proinsulin, which is linked to the risk of CAD. We review that the impaired glucose tolerance is an important factor causing dyslipidemia. The characteristic of dyslipidemia associated with the impaired glucose tolerance include hypertriglyceridemia, high level of VLDL and low level of HDL cholesterol. They also associate with accumulation of remnant lipoproteins and appearance of small dense LDL. In addition, we pointed out that the increased number of risk factors is associated with elevated insulin and proinsulin level.
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PMID:[The impaired glucose tolerance in the pathogenesis of dyslipidemia]. 891 26

Secondary prevention of arteriosclerosis tries to inhibit progression of the atherosclerotic process. Therapeutic measures focus on modification of cardiovascular risk factors and antithrombotic treatment. Hypercholesterolemia is the main risk factor for coronary artery disease. The risk of a coronary event is correlated to the plasma cholesterol level. Lowering plasma cholesterol results in reduction of vascular morbidity and mortality. Cigarette smoking is the predominant risk factor for peripheral arterial occlusive disease (PAOD). Smoking cessation reduces progression of PAOD and lowers cardiovascular morbidity and mortality. The preventive effect of antihypertensive therapy in hypertensive patients is most pronounced for cerebrovascular events. Antihypertensive measures improve prognosis after stroke and myocardial infarction. The increased cardiovascular risk in diabetics is in part explained by hyperglycemia and hyperinsulinemia, but also depends on coexisting dyslipidemia and hypertension. Intensive treatment of elevated blood glucose levels, dyslipidemia and hypertension are important preventive measures. Aspirin is highly effective in secondary prevention of vascular events. For the coronary arteries, low-dose aspirin is well established. Whether low-dose aspirin is equally effective for reducing progression of arteriosclerosis in the cerebrovascular and in the peripheral vessels is questionable. Ticlopidine serves as an alternative to aspirin; however, neutropenia may occur, which requires supervision of the patient.
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PMID:[Secondary prevention of arteriosclerosis]. 892 4

A group of metabolic disorders including insulin resistance and hyperinsulinemia, impaired glucose tolerance, visceral obesity, hypertension, dyslipidemia, hyperuricemia, hypercoagulability and microalbuminuria determine the risk for the development of atherosclerosis, coronary artery disease and cerebral vascular disorders. Although available studies on the pathogenesis of the metabolic syndrome are equivocal, it is most frequently hypothesized that hereditary of insulin resistance leads to the remaining metabolic disorders including diabetes mellitus, atherosclerosis and coronary artery disease. Despite pathogenetic controversies, there are convincing arguments for the diagnosis of the metabolic syndrome and search for therapy improving insulin sensitivity and reducing hyperinsulinemia thus preventing the development of diabetes mellitus and coronary artery disease.
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PMID:[Insulin resistance and hyperinsulinemia--clinical aspects]. 899 30

We previously reported a compound heterozygote [T(-39)C/T(-93)G] in the human lipoprotein lipase (LPL) gene promoter in one out of 19 patients with familial combined hyperlipidemia (FCHL) and reduced post-heparin plasma LPL levels. The T(-39)C substitution resulted in 85% decrease in LPL promoter activity. Further screening of Caucasian patients with FCHL, coronary artery disease (CAD), and of unselected Caucasian subjects revealed four additional LPL promoter variants. Among the same 19 FCHL patients with reduced LPL levels, we found one heterozygote for a G(-53)C substitution. Among 115 CAD patients, we found five heterozygotes and one homozygote for the T(-93)G substitution and one heterozygote for a CC insertion between +13 and +19 of the 5' untranslated region. In a group of 183 unselected subjects, three heterozygotes with the T(-93)G substitution were found. The G(-53)C substitution led to approximately 70-75% decrease in promoter activity as assayed by transient transfections of THP-1 (macrophage-like) and C2C12 (myotube-like) cells. The T(-93)G substitution resulted in reduction of promoter activity by approximately 40-50%. The CC insertion between +13 and +19 caused a decrease in promoter activity by 20% in THP-1 and 50% in C2C12. Substitutions at -79 and -95, which had no effect on promoter function, were also discovered in the population samples studied. The finding of two promoter mutations (-39 and -53) among 19 FCHL patients with diminished LPL, but not among the other groups of subjects, suggests a potential role of regulatory mutations of the LPL gene in the development of dyslipidemia in FCHL.
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PMID:Regulatory mutations in the human lipoprotein lipase gene in patients with familial combined hyperlipidemia and coronary artery disease. 901 14

In addition to the goal of controlling elevated blood pressure in patients with hypertension improving Dyslipidemia associated with insulin resistance may be an important element in preventing coronary artery disease. Antihypertensive treatment may differ based on the pathophysiology present. It appears that the evidence that supports the development of lipid abnormalities in patients who have insulin resistance is growing. In such patients the morbidity and mortality associated with coronary artery disease may be significantly decreased by selecting agents with favourable metabolic consequences.
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PMID:Insulin resistance: a common factor in the triad of dyslipidemia, hypertension, and coronary artery disease? 903 Jun 76

Arterial occlusive disease (AOD) which is rarely described in patients with inflammatory bowel disease, is mainly associated with Crohn's disease (CD), and its etiology and natural course are unknown. We studied six patients (five women, one man) with CD and major lower extremity AOD who were treated at the Cleveland Clinic between 1985 and 1994. These were relatively young patients (age range 24-48 years) with steroid-dependent Crohn' colitis. On their presentation, five had acute onset of severe ischemic symptoms ("blue toe" syndrome in three) and one had rapid progression of claudication. All the patients had active CD and/or prior extensive bowel resections, and had no evidence of extraintestinal manifestation. Cardiovascular risk factors were smoking (n = 5), dyslipidemia (n = 3), family history of coronary artery disease (n = 3), premature menopause (n = 2), diabetes mellitus (n = 1). Arteriograms showed iliac artery involvement in all six patients and bilateral AOD in three. None of the patients had arteriographic or clinical signs of vasculitis. Five patients required arterial revascularizations, i.e., endovascular (n = 2), surgical (n = 2), and combined in one. Three patients had microscopic evidence of atherosclerosis. Lower extremity AOD in patients less than 50 yr of age and with CD may be partially related to premature atherosclerosis. Prospective screening for cardiovascular risk factors, subclinical disease, and hypercoagulability might be indicated in patients with active CD to prevent major arterial complications.
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PMID:Lower extremity arterial occlusions in young patients with Crohn's colitis and premature atherosclerosis: report of six cases. 906 77

Coronary artery disease (CAD) is the most common cause of death in women in the United States. Dyslipidemia is a risk factor for CAD in both men and women. Low levels of high-density lipoprotein (HDL) cholesterol and hypertriglyceridemia, especially in association with a dense low-density lipoprotein (LDL) phenotype, may be of greater importance in women than in men. The relationship between CAD and dyslipidemia and the therapeutic approach to disorders of lipid metabolism in women have unique features because of the effects of exogenous and endogenous hormones on lipid pathways. Estrogen decreases LDL cholesterol and Lp(a) lipoprotein and increases triglyceride and HDL cholesterol levels. Progestogens decrease triglycerides, HDL cholesterol, and Lp(a), and they increase LDL cholesterol. Thus, oral contraceptives increase plasma triglycerides, whereas the effect of these agents on LDL cholesterol and HDL cholesterol levels is related to the androgenicity and dose of progestogen. Postmenopausal hormone replacement therapy increases triglycerides and decreases LDL cholesterol. The effect of hormone replacement therapy on HDL cholesterol is influenced by the addition of progestogen. Although no primary prevention studies have analyzed lipid lowering and CAD in women, secondary prevention studies have suggested that the response to drug treatment and the benefit of lipid lowering are similar in women and in men. Hormone replacement therapy should be considered in the treatment of hypercholesterolemia in postmenopausal women; however, individualization of treatment is important to avoid adverse effects.
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PMID:Lipids and lipoproteins in women. 907 Jan 99

The metabolic syndrome consists of a cluster of metabolic diseases which often coexist: abdominal obesity, glucoseintolerance, diabetes mellitus type II, dyslipidemia, hypertension and impaired fibrinolysis. The common pathophysiologic link of these diseases in insulin resistance. All clinical disorders of the metabolic syndrome are risk factors for the vascular system. Since several diseases are present at the same time the risk for atherosclerotic complications such as coronary artery disease and apoplexy is potentiated. As a consequence the costs for direct and indirect health care are high. Besides a genetic predisposition the metabolic syndrome is mainly caused by the typical life style in industrialized countries with high energy and fat intake, physical inactivity, alcohol consumption, smoking, and stress. Therefore, prophylaxis and therapy imply the removal of these factors. In order to be successful experienced physicians and motivated patients are prerequisites. Even more affective than therapy is prophylaxis which is, however, not established in Germany. The metabolic syndrome is up to now not identified as a major health problem neither by the medical profession nor by health insurances and politicians. An effective therapy and prophylaxis would induce far-reaching changes in our health system and diminish health costs.
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PMID:[Metabolic syndrome]. 908 43


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