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)

The burden of ischemic heart disease is high in dialysis patients. Ischemia may result from atherosclerotic and nonatherosclerotic disease and may cause myocardial infarction and angina. The impact of diminished perfusion is intricately associated with the underlying cardiomyopathy, both of which predispose to heart failure. The etiology of ischemia is complex and associated with the underlying cardiomyopathy, whether it be concentric left ventricular hypertrophy, left ventricular dilatation, or systolic dysfunction. Hypertension, diabetes, dyslipidemia, abnormalities of divalent ion metabolism, hypoalbuminemia, and left ventricular hypertrophy are probably adverse risk factors for ischemia, but the relative importance of each is unknown.
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PMID:Ischemic heart disease in chronic uremia. 887 58

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

An epidemiological study was conducted to investigate the distribution of serum insulin and the relation of environmental factors to serum insulin concentrations in an urban population. In 1992 and 1993, 75 g oral glucose tolerance tests (OGTT) were performed and serum insulin concentrations determined for 2,147 subjects aged 30 to 79, randomly selected from residents of S-city in Osaka Prefecture. The subjects had received a health examination for cardiovascular disease at the National Cardiovascular Center. Median values of area under the insulin curve (AUIC), which is an index of insulin resistance, were similar for men and women, but were higher for older than younger women. Sex and age specific estimated upper limits of AUIC were set at the 95 percentile level of AUIC for the subjects without a history of stroke or myocardial infarction, and who did not have diabetes mellitus, obesity, hypertension, or dyslipidemia. Prevalence of hyperinsulinemia in the subjects was about 10 to 16%. The sex and age specific proportion of obesity, hypertriglyceridemia, hypo-HDL-cholesterolemia, and hypertension was higher for hyperinsulinemic than normoinsulinemic subjects. Relation of AUIC to obesity, dietary intake, physical activity, alcohol consumption, cigarette smoking, and antihypertensive drug use was examined in 2,039 subjects who were diagnosed as non-diabetic by OGTT. Of the environmental factors analysed, body mass index alone correlated independently with AUIC for all sex and age specific classes. For men aged 30 to 59 the waist/hip ratio correlated independently and positively with AUIC. This indicates that control of obesity, especially of upper-body obesity or visceral type obesity, should be considered important for improvement of insulin resistance.
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PMID:[Serum insulin distribution and the relationship between environmental factors and serum insulin levels in a Japanese urban population]. 891 97

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

It has not been definitely established whether elevated circulating triglyceride-rich lipoproteins constitute an independent risk factor for hypertension, atherosclerosis, myocardial infarction, and coronary heart disease. To investigate some aspects of the physiopathology of this lipid metabolism abnormality, a model of experimental hypertriglyceridemia and hypertension in rats was studied. The animals received commercially refined sugar (30%) in their drinking water during a period of 12 to 17 weeks. Monthly measurements of blood pressure and serum triglycerides were taken during and at the end of the treatment period; the levels of glucose and insulin were also determined. The blood, the aorta, and mesenteric artery were removed. Age- and weight-matched controls were used. The reactivity of the isolated vessels to norepinephrine and acetylcholine and the effect of control and hypertriglyceridemic serum on the same preparations were investigated. In hypertriglyceridemic rats, the response to acetylcholine in the tissues was reduced compared to the control arteries; the hypertriglyceridemic serum elicited contractions that were greater than those induced by control serum. The impaired response of hypertriglyceridemic tissue to the vasodilator and the effect of the hypertriglyceridemic serum on artery contraction suggest that the overall dyslipidemia could contribute to a chronic increase in vascular tone and, consequently, to hypertension.
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PMID:Vascular reactivity and effect of serum in a rat model of hypertriglyceridemia and hypertension. 912 3

The epidemiologic approach to investigation of atherosclerotic cardiovascular disease has provided many insights into the preclinical and clinical spectrum of the disease. The hazard of developing atherosclerotic cardiovascular disease is substantial with coronary heart disease (CHD), the most common and most lethal feature. The outlook in those who manage to survive the initial episode is also serious, with a 10-year mortality rate of 37% for persons with angina and a 55% rate for those sustaining a myocardial infarction. Fifteen percent of persons developing CHD present with a fatal event, and 38% of infarctions go unrecognized. The presence of atherosclerosis in one vascular territory imposes an increased risk of its appearing in another area at two to six times the general population rate. The major cardiovascular risk factors adversely affect all arterial vascular territories so that correction of risk factors targeted at one particular atherosclerotic outcome may also favorably influence the other risk factors. Coronary disease is the most prevalent lethal hazard of hypertension, dyslipidemia, glucose intolerance, and cigarette smoking. These risk factors cluster and optimal therapy must improve the whole risk profile. Women share the same risk factors for CHD as men. Although women have a lower absolute risk for most risk factors, a high total/HDL cholesterol ratio, left ventricular hypertrophy, and diabetes each tend to eliminate the female advantage. Menopause also promptly escalates risk threefold. Although women tend to have a lower incidence than men, the initial attack is just as highly lethal in women, and their subsequent outlook as survivors is at least as serious as for men. Sudden death is a pre-eminent feature of coronary disease and cardiac failure. Coronary disease increases sudden death risk 3.3-fold and cardiac failure 4.8-fold. Sudden death incidence varies in relation to the same cardiovascular risk factors as coronary heart disease, with no unique risk factors identified. However, multivariate combinations of these in a profile can identify high-risk candidates for sudden death as well as coronary attacks in general. The key to prevention of sudden death is to prevent coronary attacks and cardiac failure. Despite aggressive cardiac revascularization and treatment of hypertension, congestive heart failure (CHF) has not decreased in prevalence, and innovations in the treatments of overt failure have not substantially improved survival. Median survival is only 1.7 years for men and 3.2 years for women. The conditional probability of developing CHF can be estimated using a logistic function comprised of age, systolic pressure, vital capacity, heart rate, ECG-left ventricular hypertrophy (LVH), glucose intolerance, x-ray enlargement, and presence of CHD and heart murmurs. Eighty percent of CHF events occur in persons in the upper quintile of multivariate risk. Continued clinical, metabolic, and epidemiologic research have expanded and refined atherosclerosis risk factors. The lipid connection is now concerned with the apoprotein makeup of the lipids, subfractions of lipids, and Lp(a). The diabetic influence is now focused on insulin resistance. Ambulatory monitoring is being used to evaluate blood pressure and silent ischemia. Fibrinogen and leukocyte counts have emerged as possible indicators of unstable lesions. Prospects for primary and secondary prevention are good if public health measures, health education, and preventive medicine are implemented based on existing knowledge of correctable or avoidable risk factors. The potential for more effective prevention continues to expand, and great advances have already been made in countries where aggressive preventive measures have been implemented to correct the major established risk factors.
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PMID:Hazards, risks, and threats of heart disease from the early stages to symptomatic coronary heart disease and cardiac failure. 921 Oct 12

Several recent studies have shown that 60-70% of coronary occlusions that cause acute coronary syndromes (such as unstable angina, myocardial infarction, or sudden ischemic death) evolve from atherosclerotic plaques that are only mildly to moderately obstructive. Numerous studies have demonstrated that coronary thrombosis, the immediate cause of acute coronary syndromes, is a consequence of plaque disruption. Most thrombotic events are related to deep plaque fissure, while superficial plaque erosion is the cause in a significant minority of cases. Thus, the mechanisms by which stable coronary artery disease (CAD) evolves into an unstable and potentially lethal acute coronary syndrome are related to plaque disruption and thrombosis. The vulnerability of a plaque to disruption appears to be determined by the presence of a large lipid-rich core, a thin fibrous cap, and an inflammatory cellular infiltrate, rather than by the size of the plaque or the severity of stenosis caused by a plaque before disruption. In addition to plaque disruption and thrombosis, enhanced vasoconstriction--a characteristic feature of CAD and dyslipidemia-may contribute to the clinical manifestations of CAD. Angiographic studies have demonstrated that risk factor modification produces a disproportionately greater reduction in ischemic clinical events than in anatomic regression of plaque, suggesting "plaque stabilization" may be the major mechanism of such clinical benefit. The relatively rapid attenuation of endothelial-mediated vasomotor dysfunction with the treatment of dyslipidemia lends credence to this concept.
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PMID:New insights into the pathogenesis and prevention of acute coronary syndromes. 922 53

Patients with NIDDM are at increased risk for coronary heart disease (CHD). However, information on the predictive value of cardiovascular risk factors and the degree of hyperglycemia with respect to the risk for CHD in diabetic patients is still limited. Therefore, we carried out a prospective study on risk factors for CHD, including a large number of NIDDM patients. At baseline, risk factor levels of CHD were determined in 1,059 NIDDM patients (581 men and 478 women), aged from 45 to 64 years. These patients were followed up to 7 years with respect to CHD events. Altogether, 158 NIDDM patients (97 men [16.7%] and 61 women [12.8%]) died of CHD and 256 NIDDM patients (156 men [26.8%] and 100 women [20.9%]) had a serious CHD event (death from CHD or nonfatal myocardial infarction). A previous history of myocardial infarction, low HDL cholesterol level (<1.0 mmol/l), high non-HDL cholesterol (> or =5.2 mmol/l), high total triglyceride level (>2.3 mmol/l), and high fasting plasma glucose (>13.4 mmol/l) were associated with a twofold increase in the risk of CHD mortality or morbidity, independently of other cardiovascular risk factors. High calculated LDL cholesterol level (> or =4.1 mmol/l) was significantly associated with all CHD events. The simultaneous presence of high fasting glucose (>13.4 mmol/l) with low HDL cholesterol, low HDL-to-total cholesterol ratio, or high total triglycerides further increased the risk for CHD events up to threefold. Our 7-year follow-up study provides evidence that dyslipidemia and poor glycemic control predict CHD mortality and morbidity in patients with NIDDM.
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PMID:Dyslipidemia and hyperglycemia predict coronary heart disease events in middle-aged patients with NIDDM. 923 62

The polymorphisms (Pvu II and Hind III) on the lipoprotein lipase (LPL) gene locus was investigated in a sample of 100 patients surviving previous myocardial infarction and 100 age matched healthy individuals selected from Han Chinese of Beijing area. In patient group a strong association was found between H+ allele of Hind III polymorphism and raised TG levels (P < 0.01). In control group P-P- genotype was observed to be associated with higher TG levels compared with P+P genotype of Pvu II polymorphism (P < 0.05). Combination of H+H+ genotype with P-P- genotype showed the highest TG levels among all nine kinds of genotypic combinations in patient group (P < 0.01). However, comparison of distribution of alleles and genotypes of these polymorphisms between patient group and control group demonstrated no significant difference. Our data suggest that the polymorphisms at the LPL gene, as the linkage markers with an aetiologic mutation at or around LPL gene, may constitute one of the genetic determinants for the population variation in plasma TG levels, as well as for the common dyslipidemia in Chinese populations.
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PMID:Polymorphisms of the human lipoprotein lipase gene: possible association with lipid levels in patients with coronary heart disease in Beijing area. 938

Millions of Americans are at risk for cardiovascular morbidity and mortality related to disorders of glucose intolerance--particularly type 2 diabetes and prediabetic conditions, including the insulin resistance, or "cardiovascular dysmetabolic," syndrome. The latter is apparently more intricately associated with macrovascular disease--myocardial infarction, stroke, and peripheral vascular disease. In some situations the risk of cardiovascular disease might be reduced by the prevention of diabetes and also by prevention or treatment of the cardiovascular dysmetabolic syndrome. Studies have shown that intensive glycemic control can delay the development of microvascular complications in type 1, and possibly type 2, diabetes. Several longitudinal observational studies have demonstrated a relationship between glycemic control and the development of cardiovascular disease. Prospective clinical intervention trials to address this issue are underway. Insulin may have a role in atherogenesis, both directly and by promoting development of such risk factors as hypertension and dyslipidemia. Genetic factors and mechanisms promoting or discouraging development of glucose intolerance are also under investigation. Lifestyle changes--dietary and exercise modification, weight loss, and smoking cessation--have been shown to have a positive effect on cardiovascular disease risk. Clinical trials suggest that oral antidiabetic agents--particularly the new noninsulin secretagogues (including troglitazone and metformin, which act on the liver and on skeletal muscle)--may be useful in delaying or preventing development of type 2 diabetes and the cardiovascular dysmetabolic syndrome, as well as in their treatment, when present. Both agents, acting primarily by different mechanisms of action, have also demonstrated potential beneficial effects on serum lipid profiles and other cardiovascular risk factors and may be useful in patients with cardiovascular dysmetabolic syndrome who do not yet meet the criteria for diabetes.
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PMID:Type 2 diabetes care: the role of insulin-sensitizing agents and practical implications for cardiovascular disease prevention. 970 64


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