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)

Lipid abnormalities are major risk factors for premature coronary artery disease (CAD). However, the type and prevalence of dyslipidemia in these patients have not been well characterised, especially in some ethnic groups. The purpose of the present work was to determine the lipid disorders in patients of Northwestern Greece with premature CAD. The study population comprised of 132 men and 38 women who underwent elective diagnostic arteriography in our University Hospital. Subjects with > or = 1 lesion that narrowed the lumen of any of the 15 coronary artery segments by > or = 70% were considered to be CAD cases (n=108), whereas those with narrowing < 70% were excluded (n=54). Asymptomatic subjects (n=104) matched for age and sex were taken as controls. Compared with the controls, patients with premature CAD had increased serum levels of total cholesterol, LDL cholesterol, triglycerides, Apo B, and Lp(a), and decreased serum levels of HDL cholesterol and Apo A1. A lipoprotein or apolipoprotein abnormality was identified in 89 CAD patients (82.4%). The increased serum Apo B level (> 130 mg/dl) was the most common lipid abnormality observed in 72 patients. However, the most prevalent dyslipidemic phenotypes in our patients were type IIA followed by hypoalpha and hyperApoB. Compared to the control population, CAD patients had increased incidence of IIA and hypoalpha phenotypes. On the contrary, a normal lipoprotein phenotype was more common in the control population compared to CAD patients (56.7% vs. 17.6%, P<0.001). We conclude that the majority of Greek patients with premature CAD exhibit lipid and lipoprotein abnormalities, which to a large extent can be defined by determining the traditional lipid parameters (total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides). However, in some cases the value of the quantification of other lipid parameters such as apolipoproteins and Lp(a) should be taken into account.
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PMID:Lipid abnormalities in Greek patients with coronary artery disease. 915 72

In this review we examine the complex interactions between lipoprotein metabolism, immunosuppressive drug therapy, and inflammation and the potential benefits of lipid-lowering drug therapy after heart transplantation. The newer formulations of cyclosporine, Neoral (Novartis Pharmaceuticals; Basle, Switzerland), and other newer agents such as tacrolimus may have advantages in regard to lipid metabolism as compared with traditional triple-drug immunosuppression. Lipoprotein levels may influence both the toxicity and efficacy of cyclosporine. Dyslipidemia may adversely influence inflammation and rejection in the allograft. Two recent clinical trials have shown that lipid-lowering therapy with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor alone or in combination with low-density lipoprotein apheresis may confer significant benefits toward preventing transplant coronary artery disease.
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PMID:Pathophysiology and treatment of lipid perturbation after cardiac transplantation. 919 84

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

Hypertension is often accompanied by a host of metabolic defects. Investigations have shown an association between insulin resistance, hyperinsulinemia, central/visceral obesity, and hypertension. Recent interest has focused on the fact that untreated hypertensive individuals have compensatory hyperinsulinemia, are resistant to insulin-mediated glucose uptake, and frequently have coexisting lipid abnormalities. Data from prospective studies appear to indicate that fasting hyperinsulinemia is an independent predictor of coronary artery disease. Additionally, there is evidence that hyperinsulinemia and diabetes eliminate the normal sex differences in the prevalence of coronary artery disease. The salutary effects of ovarian hormones on the prevalence of hypertension and cardiovascular disease in postmenopausal women are well established. Hyperandrogenism, in particular elevated serum levels of dehydroepiandrosterone sulfate, is believed to be a risk factor promoting sex-specific impairments of glucose and lipid metabolism, obesity, and hypertension in women. Clinical and epidemiologic evidence have linked elevated blood pressure to disturbances in lipoprotein metabolism, fibrinolytic activity, plasminogen activation inhibitor levels, and dyslipidemia. This review briefly presents the current understanding of various metabolic disturbances associated with hypertension, the pathophysiologic mechanisms involved, and the significance of the interplay between them relative to the complications of this disease.
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PMID:Metabolic abnormalities in hypertension. 926 63

The effect of changes in physical activity levels during chronic exercise on plasma lipids and lipoproteins has not been reported. We examine the relationships between changes in VO2max, leisure time physical activity (LTPA), and percent body fat on changes in plasma lipids and lipoproteins in 137 men without coronary artery disease (CAD) and/or dyslipidemia, hypertension, or diabetes mellitus who participated in an employee exercise program. Measurements obtained at entry and 1- and 4-yr follow-up include VO2max, LTPA in kcal.wk-1, percent body fat, and plasma lipids and lipoproteins. The relationship between changes in the measurements between 1 and 4 yr of follow-up (N = 34) revealed the following significant (P < 0.05) correlations: i) changes in VO2max with changes in percent body fat (r = -0.289) and changes in plasma triglycerides (r = -0.354), ii) changes in LTPA with changes in percent body fat (-0.361), and iii) changes in percent body fat with changes in the total/high density lipoprotein (HDL)-cholesterol ratio (0.358), HDL-cholesterol (-0.212), and triglycerides (0.289). Multiple regression analysis revealed that changes in percent body fat affected changes in plasma triglycerides (P < 0.05). The effects of chronic physical activity on plasma triglycerides appear to result from exercise-related effects on body adiposity. These findings support the role of regular physical activity as mandated by Healthy People 2000 for CAD risk reduction.
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PMID:Changes in VO2max, physical activity, and body fat with chronic exercise: effects on plasma lipids. 930 25

At least one-third of Americans are obese, as defined by body mass indexes corresponding to body weight > or = 120% of ideal body weight, and this figure is rising steadily. Women and nonwhites have particularly high rates of obesity. Obesity greatly increases risks for many serious and morbid conditions, including diabetes mellitus, hypertension, dyslipidemia, coronary artery disease, and some cancers. Obesity is clearly associated with increased risk for mortality, but there has been controversy regarding optimal weight with respect to mortality risk. We review the literature concerning obesity and mortality, with reference to body fat distribution and weight gain, and consider potential effects of sex, age, and race on this relation. We conclude that when appropriate adjustments are made for effects of smoking and underlying disease, optimal weights are below average in both men and women; this appears to be true throughout the adult life span. Central obesity, most commonly approximated by the waist-to-hip ratio, may be particularly detrimental, although this requires further study. Weight gain in adulthood is also associated with increased mortality. These observations support public health measures to reduce obesity and weight gain, including recent recommendations to limit weight gain in the adult years to 4.5 kg (10 lb).
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PMID:Obesity and mortality: a review of the epidemiologic data. 932 85

Coronary artery disease (CAD) remains the leading cause of morbidity and mortality in the United States. Although risk factors contributing to the development of this disease are well known and effective interventions exist, the majority of patients eligible for pharmacotherapy are inadequately treated or not treated at all. Multiple factors contribute to this treatment gap. With respect to dyslipidemia, 2 of the major challenges facing healthcare organizations are: (1) how to ensure continued monitoring and medication adherence for patients with known atherosclerosis (secondary prevention); and (2) how to select the high-risk patients who will most benefit from treatment from the larger population of individuals who have not had a known coronary event (primary prevention). In Southern California Kaiser Permanente, 2 approaches being used to address these issues are dyslipidemia treatment guidelines and a computerized monitoring system. The guidelines stratify patients based on CAD risk and expected benefit from drug therapy. The computerized monitoring incorporates an "expert system" algorithm that facilitates patient selection in primary prevention and tracking to encourage patient compliance. This article describes these 2 approaches that attempt to maximize the effectiveness and efficiency of dyslipidemia management.
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PMID:Dyslipidemia treatment guidelines and management systems in Kaiser Permanente. 937 6

Studies on monozygotic twins support a role for genetic determinants of plasma lipid, lipoprotein, and apolipoprotein levels. Gene variants of the enzyme lipoprotein lipase have been shown to associate with dyslipidemia and coronary artery disease. We assessed the gene-environment interaction by investigating the relationship between the lipoprotein lipase gene and plasma lipid, lipoprotein, and apolipoprotein variability and levels among 54 male monozygotic twin pairs (aged 18-28 years). The Ser447-Ter mutation (C-->G transversion) was associated with significantly smaller within-pair differences in plasma high density lipoprotein-cholesterol (CG [n = 10] vs. CC [n = 44], 3.7+/-5.3 mg/dl vs. 6.4+/-5.2 mg/dl, P < 0.03) and total cholesterol (CG [n = 10] vs. CC [n = 44], 7.9+/-9.4 mg/dl vs. 15.8+/-12.7 mg/dl, P < 0.05), indicating attenuated variability in response to environmental stimuli. This observation of a restrictive variability gene effect further supports a role for the lipoprotein lipase gene in the genetic regulation of lipids and lipoproteins and suggests that the Ser447-Ter mutation exerts multiple effects. This study also raises the possibility of a genetically determined responsiveness to dyslipidemia therapies.
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PMID:The Ser447-Ter mutation of the lipoprotein lipase gene relates to variability of serum lipid and lipoprotein levels in monozygotic twins. 950 3

Patients with diabetes mellitus have an increased risk for coronary artery disease due to hyperglycemia, hypertension, dyslipidemia, and other risk factors. The diabetic dyslipidemia in these patients is characterized by moderately high levels of (1) serum cholesterol and triglycerides; (2) small, dense low-density lipoprotein (LDL) particles; and (3) low high-density lipoprotein (HDL) cho-lesterol concentrations. Recent clinical trials have demonstrated the benefits of cholesterol-lowering therapy in both diabetic and nondiabetic patients, thus supporting aggressive treatment of diabetic dyslipidemia for coronary artery disease prevention. A 3-step approach is recommended for the treatment of diabetic dyslipidemia. First, modification of diet and lifestyle, including decreased intakes of cholesterol, cholesterol-raising fats, and total energy, and increased physical activity should be advised. Second, good glycemic control should be achieved with diet and hypoglycemic drugs, if needed. Third, lipid-lowering drugs should be used, if necessary. Non-HDL cholesterol levels, which include both very-low-density lipoprotein (VLDL) and LDL cholesterol, should be the target of cholesterol-lowering therapy. The use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (the "statins") has become the first-line drug therapy for diabetic dyslipidemia. Bile acid sequestrants are effective cholesterol-lowering agents in normotriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients with severe hypertriglyceridemia may require fibric acids or n-3 polyunsaturated fatty acids. Nicotinic acid worsens hyperglycemia; therefore, it should be avoided in most cases. The efficacy and safety of estrogen-replacement therapy in postmenopausal women with diabetes needs to be determined. The combination of two lipid-lowering agents may be appropriate for some NIDDM patients but should be used judiciously.
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PMID:Treatment of diabetic dyslipidemia. 952 14

We studied the allelic frequency of the variable number of tandem repeats region 3' of the apolipoprotein B gene (apoB 3' VNTR) and its impact on coronary artery disease (CAD) in 150 patients with CAD and 153 normal controls in a Taiwan population. apoB 3' VNTR alleles were classified according to the number of repeats of a 15-bp hypervariable elements (HVE), the sequence of which was determined using the polymerase chain reaction and direct sequencing. Thirteen alleles comprising from 26 to 54 HVEs were identified. The CAD patients had greater heterozygosity (0.58 vs 0.42) and a higher frequency of long (> 36-HVE) apoB 3' VNTR alleles than the controls (18.7% vs 10.8%, p < 0.01). CAD patients with two HVE-36 alleles and no HVE-32 alleles (the two most common forms) had significantly higher concentrations of LDL-cholesterol, apolipoprotein B, and triglycerides, and significantly lower values of HDL-cholesterol and apolipoprotein AI than the control group (p < 0.01 for all comparisons). The length of the apoB 3' VNTR was not correlated with the plasma concentrations of any of the lipids. We conclude that long apoB 3' VNTR alleles occur more frequently in CAD patients, but that apoB 3'VNTR genotypic variation has little impact on the risk of dyslipidemia in Taiwanese.
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PMID:Polymorphisms of the apolipoprotein B 3' variable number of tandem repeats region associated with coronary artery disease in Taiwanese. 958 73


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