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

Cardiovascular disease, and in particular ischemic heart disease, is the principal cause of morbidity, functional disability, and mortality in patients with non-insulin-dependent (type II) diabetes. The main risk factors for the macrovascular complications of diabetes are dyslipidemia, hypertension, and cigarette smoking. Although degree of hyperglycemia is a risk factor for microvascular complications, it is not a prominent risk factor for macrovascular complications. Nevertheless, there are theoretical reasons for believing that glycemic control could lower cardiovascular risk. For example, glycemic control may both improve clearance and suppress hepatic overproduction of very-low-density lipoprotein. Moreover, there is direct empirical evidence that improved glycemic control can favorably alter lipid profiles in type II diabetic patients. Despite this, the only clinical trial that has assessed cardiovascular mortality as an end point in diabetic subjects (i.e., the University Group Diabetes Program) failed to demonstrate a benefit of glycemic control. In this study, the insulin-variable group, which achieved sustained glycemic control relative to the placebo group, had essentially the same cardiovascular mortality as the latter group. All of the conventional lipid-lowering agents have been shown to produce favorable changes in lipid profiles in diabetic subjects. However, the optimum regimen remains to be defined. Metabolic differences between diabetic and nondiabetic subjects mean that the optimum lipid-lowering regimens for the two categories of patients may differ. For example, nicotinic acid, which is a powerful lipid-altering drug, may worsen glucose intolerance. The characteristic lipid abnormalities in type II diabetic subjects are hypertriglyceridemia and low high-density lipoprotein cholesterol, not hypercholesterolemia. Although the role of hypertriglyceridemia as a cardiovascular risk factor in the general population has been questioned, there is evidence that this lipid abnormality may play a stronger role in diabetic subjects. For all of the above reasons, there is an urgent need for large-scale clinical trials assessing cardiovascular end points and testing various strategies of improving lipid profiles in diabetic subjects, particularly given the fact that all of the current generation of lipid-lowering trials have systematically excluded diabetic patients.
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PMID:Dyslipidemia in type II diabetes. Implications for therapeutic intervention. 177 1

Several epidemiologic and clinical studies over the past years have shown that insulin resistance and hyperinsulinemia are related to dyslipidemia, hypertension, android obesity and non-insulin-dependent diabetes mellitus (NIDDM). The insulin-resistance syndrome is thus closely associated with a cluster of potent cardiovascular risk factors, thereby explaining the 3-4 times higher incidence of cardiovascular disease in NIDDM. Recent observations point to the fact that insulin resistance is genetically determined and can be diagnosed a long time before the clinical manifestation of diabetes mellitus in the prediabetic stage (stage of hyperinsulinemia, hypertension and hyperlipidemia). Hence, it is not surprising that many NIDDM subjects suffer from cardiovascular complications already at the time diabetes is diagnosed. The pathogenetic mechanism of insulin resistance/hyperinsulinemia as cardiovascular risk factor is considered to be a direct atherogenic action of insulin on vessel wall cells and an indirect effect on upper body obesity, blood pressure, lipids and hemostasis.
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PMID:[Insulin resistance and cardiovascular complications]. 784 94

The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria frequent examinations are warranted for early detection of retinopathy, blood-pressure rise, and for optimizing the glycemic control. In patients with non-insulin-dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk factors (hypertension, dyslipidemia, tobacco, and obesity). In the nondiabetic population, there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to clarify further the role of microalbuminuria as an independent risk factor in the background population.
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PMID:Microalbuminuria: an important diagnostic tool. 808 48

Four-year-old schoolchildren with a positive family history for atherogenic dyslipidemia and/or clinical atheroma before 55 years of age were screened for hypercholesterolemia. Investigations included determination of serum levels of total cholesterol, triglycerides, HDL cholesterol, apolipoprotein A1, apolipoprotein B, and Lp(a); an agarose lipidogram; acrylamide gradient electrophoresis; and determination of LDL composition by ultracentrifugation. Normal values were defined as values under the 90th centile, i.e., 1.97 g/l for total cholesterol, 0.89 g/l for triglycerides, 1.36 g/l for LDL-cholesterol, and 1.26 g/l for apolipoprotein B. Among 3,565 children routinely evaluated at 4 years of age, 525 (16.2%) had a positive family history; of these, 72 underwent lipid investigations. Eight children (11%) had hypercholesterolemia type IIA, eight had a variety of lipid disorders, and 14 (20.6%) had increased Lp(a) levels as an isolated anomaly or concomitantly with an atherogenic dyslipidemia. Because Lp(a) is a cardiovascular risk factor independent from total cholesterol levels, we believe this parameter should be determined in high risk children.
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PMID:[Screening in the school milieu, at 4 years old, for hypercholesterolemia]. 823 96

The concept of microalbuminuria is reviewed. Measuring the urinary albumin excretion rate and testing for microalbuminuria is well established in the control and treatment of patients with insulin-dependent diabetes mellitus. Microalbuminuria predicts nephropathy and early cardiovascular death. In the presence of microalbuminuria, frequent examinations are warranted for early detection of retinopathy, hypertension and for optimizing the glycaemic control. In patients with non-insulin dependent diabetes, the independent value of microalbuminuria as a cardiovascular risk factor is not yet clarified. The urinary albumin excretion rate should be measured at diagnosis, because the indications are that presence of microalbuminuria reinforces the urge to intervene against other well-documented cardiovascular risk-factors (hypertension, dyslipidemia, tobacco and obesity). In the non-diabetic population there is accumulating evidence that an elevated urinary albumin excretion rate is associated with early cardiovascular morbidity and mortality. Large scale cross-sectional and prospective studies are needed in order to further clarify the role of microalbuminuria as an independent risk factor in the background population.
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PMID:[Microalbuminuria--a valuable diagnostic parameter]. 827 36

There are several types of obesity, and the metabolic conditions associated with these phenotypes are also heterogeneous. Obesity of the male (android) type shows a dominant visceral and upper thoracic distribution of adipose tissue, whereas in the feminine (gynecoid) type adipose tissue is found predominantly in the lower part of the body (hips and thighs). Android obesity is clearly a cardiovascular risk factor, more so than gynecoid obesity. Hereditary factors contribute significantly to the occurrence of this pathology in families, although environmental factors play a role in its development. Android obesity is associated with metabolic anomalies which also characterize the syndrome X: resistance to insulin, arterial hypertension and dyslipidemia. The predisposition of individuals with android obesity to become diabetic rests in part on genetic and in part on environmental factors. Hyperinsulinemia and a high flux of free fatty acids act at the level of liver and endocrine pancreas to increase resistance to insulin and to decrease insulin secretion, two determining factors for type II diabetes. Other functional anomalies have been involved to explain android obesity such as dysregulation of adrenocortical and sexual steroids or a global derangement of stress mechanisms. No significant proof, however, seems to support either one of these hypotheses.
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PMID:[Android-type obesity and gynecoid-type obesity]. 899 75

Hypertension is a very important cardiovascular risk factor and directly leads to major atherosclerotic cardiovascular diseases, including coronary artery disease, stroke cardiac failure and peripheral artery disease. Hypertension tends to cluster with other atherogenic risk factors like dyslipidemia, insulin resistance, obesity and others. The association between hypertension and dyslipidemia is very frequent and the risk is more than additive and its possible pathogenesis may be of a common mechanism. Insulin resistance is the main cause of both risk factors. Endothelium dysfunction is present in arterial hypertension and dyslipidemia and the pathogenesis of atherosclerosis. The treatment of hypertensive patients must be individualized to accommodate both the concomitant dyslipidemia and other atherogenic factors.
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PMID:[Hypertension and dyslipidemia]. 988 66

End-stage renal failure (ESRF) is associated with dyslipidemia and accelerated atherosclerosis. Triglyceride-rich lipoproteins accumulate and qualitative changes take place in low-density lipoprotein (LDL), with a predominance of the small dense LDL phenotype. Increased small dense LDL (LDLIII) is a known risk factor for cardiovascular disease. To assess the extent of LDLIII formation in ESRF and identify factors contributing to LDLIII production, we analyzed LDL subfractions by density-gradient ultracentrifugation, very low-density lipoprotein subfractions, and lipase activity in 75 patients with ESRF (25 hemodialysis [HD], 25 peritoneal dialysis [PD], and 25 predialysis patients) and 40 age- and sex-matched controls. The percentage of LDLIII was increased in all three patient groups compared with controls (PD, 33% +/- 29% [mean +/- SD]; P < 0.005; HD, 30% +/- 22%; P < 0.01; predialysis, 26% +/- 26%; P < 0.01; all versus controls, 14% +/- 10%). Plasma LDLIII concentration was increased only in PD patients (median, 84 mg/dL; interquartile range [IQR], 29 to 160 mg/dL versus controls; median, 31 mg/dL; IQR, 26 to 54 mg/dL). In other patient groups, total LDL level was less, with heterogeneity in LDLIII concentrations. Forty percent of PD patients and 28% of HD and predialysis patients had LDLIII concentrations greater than 100 mg/dL compared with 2.5% of controls (P = 0.002). Plasma triglyceride levels (r(2) = 38.4%; P < 0.001) and hepatic lipase activity (r(2) = 6.7%; P < 0.03) were independent predictors of LDLIII concentration. The strong association between LDLIII concentration and triglyceride level was present in all three patient groups (HD, r(2) = 47.9%; PD, r(2) = 45. 2%; predialysis, r(2) = 25.8%); plasma triglyceride levels greater than 177 mg/dL (2.0 mmol/L) had an 86% specificity and 79% sensitivity for predicting an LDLIII concentration greater than 100 mg/dL. We conclude that the atherogenic lipoprotein phenotype predominates in ESRF, with excess LDLIII particularly prominent in PD patients. Atherogenic levels of LDLIII are found in patients with triglyceride levels greater than 177 mg/dL. This is likely to represent a further cardiovascular risk factor in this population.
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PMID:Atherogenic lipoprotein phenotype in end-stage renal failure: origin and extent of small dense low-density lipoprotein formation. 1079 19

Family history is an important predictor of the cardiovascular risk factor cluster associated with insulin resistance. The dyslipidemia associated with insulin resistance may contribute to elevated blood pressure (BP). This study was undertaken to further explore the link between family history, dyslipidemia, and BP regulation. Twenty-three lean normal volunteers with a negative family history (FH-, n = 11) or positive family history (FH+, n = 12) of hypertension were evaluated under baseline conditions and during a 4-h infusion of intralipid and heparin (acute hyperlipidemia). Fasting blood was drawn for lipids including nonesterified fatty acids (NEFA). After 2 and 4 h of intralipid and heparin, blood was drawn for NEFA. The BP was measured at baseline and every 30 min after starting the intralipid and heparin infusion. Baseline triglycerides and very low density lipoprotein cholesterol concentrations were higher in FH+ than FH- subjects (P < .05). However, NEFA increased similarly in both groups during the infusion of intralipid and heparin. The BP and heart rate increased with acute hyperlipidemia in all subjects combined (P < .05). Despite the similar increase of NEFA, mean BP, pulse pressure, and pressure-rate product increased significantly in FH+ subjects but not in FH- volunteers with acute hyperlipidemia. Although systolic BP increased in both groups, the increase was greater in FH+ than in FH- volunteers during acute hyperlipidemia (14 +/- 2 v 10 +/- 2 mm Hg, P < .05). These results suggest that higher plasma lipids combined with a greater pressor response to hyperlipidemia may contribute to the development of high BP in subjects with a family history of hypertension.
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PMID:The pressor response to acute hyperlipidemia is enhanced in lean normotensive offspring of hypertensive parents. 1171 Jul 82

Hypertension, central obesity and dyslipidemia are associated with high cardiovascular risk. Estrogen therapy in women has beneficial effects on some of these metabolic cardiovascular risk factors. It is not known whether dietary estrogens have similar effects, especially in Western populations. We studied the association between dietary phytoestrogen intake and metabolic cardiovascular risk factors in postmenopausal women. For this purpose, 939 postmenopausal women participating in the Framingham Offspring Study were included in this cross-sectional study. Mean blood pressure, waist-hip ratio (WHR) and lipoprotein levels were determined in quartile categories of dietary phytoestrogen (isoflavones and lignans) intake, determined by a food-frequency questionnaire. In addition, a metabolic syndrome score was defined according to WHO criteria (range 0-6). The WHR was lower in women in the highest quartile of intake of lignans compared with the lowest [-0.017; 95% confidence interval (CI) -0.030 to -0.0016]. In the highest quartile of intake of isoflavones, plasma triglyceride levels were 0.16 mmol/L lower (95% CI, -0.30 to -0.02) compared with the lowest quartile of isoflavones; for lignan intake, this difference was 0.23 mmol/L (95% CI, -0.37 to -0.09). In the highest quartile of isoflavone intake, the mean cardiovascular risk factor metabolic score was 0.43 points lower (95% CI, -0.70 to -0.16) than the lowest quartile. The difference in this score between the extreme quartiles of intake of lignans was -0.55 points (95% CI, -0.82 to -0.28). In conclusion, high intake of phytoestrogens in postmenopausal women appears to be associated with a favorable metabolic cardiovascular risk profile.
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PMID:Dietary intake of phytoestrogens is associated with a favorable metabolic cardiovascular risk profile in postmenopausal U.S.women: the Framingham study. 1182 90


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