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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is one of the main risk factors for cerebrovascular disease (stroke), coronary artery disease (acute myocardial infarction), congestive heart failure (both systolic and diastolic dysfunction), and renal dysfunction. The risk is related to blood pressure level and to the presence of target organ damage. Together with hypertension, other cardiovascular risk factors, such as hyperlipidemia and/or diabetes, also contribute to the chain of events leading to atherosclerosis, vascular complications and death. Three-quarters of middle-aged, urban population show at least one cardiovascular risk factor and 91.3% of all hypertensives show at least one cardiovascular risk factor in addition to hypertension itself. In most populations, the risk of cardiovascular disease rises steeply with age. This powerful effect of age on disease risk has important consequences for the risk of cardiovascular disease related to blood pressure and other risk factors. At most ages the risk for cardiovascular diseases is higher in men than in women, although this difference declines with increasing age and is greater for coronary heart disease than for stroke; in the United States from age 34 to 74 the risk of death from coronary heart disease is 2- to 3-fold greater in men; the risk of death from stroke is 30% higher in men than in women; after age 75 the risk of death from stroke and from coronary heart disease is similar in men and women. Postmenopausal women share the same risk with men for cardiovascular disease. For many years the study and treatment of hypertension has been largely directed toward diastolic blood pressure; the importance of elevated systolic blood pressure in the management of cardiovascular disease is being largely underrecognized. Convincing evidence is presently available indicating that elevated systolic blood pressure is even a stronger predictor than diastolic blood pressure for progression of cardiovascular disease and adverse outcomes. The clinical and laboratory evaluation and drug treatment of the hypertension is related to age. The elderly benefit from treatment of elevated systolic blood pressure as much or even more than middle-aged hypertensive subjects. Two large clinical trials on treatment of isolated systolic hypertension, the Systolic Hypertension in the Elderly Program (SHEP) and the Systolic Hypertension in Europe Study (Syst-Eur), have demonstrated that antihypertensive drug therapy in elderly patients with isolated systolic hypertension effectively reduces the risk of stroke and other major cardiovascular events.
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PMID:[Hypertension as a function of age]. 1090 25

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.
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PMID:Renal disease as a risk factor for cardiovascular disease. 1119 57

Hypertension, a relatively uncommon problem in childhood except in certain groups of children, is an important cardiovascular risk factor that can have significant health implications, especially the tendency for an elevated blood pressure in childhood to predict the development of adult hypertension. Common causes of childhood hypertension include renal and cardiac disease, as well as essential hypertension in adolescents. Given these factors, it is usually possible to evaluate the hypertensive child in a focused manner that should reveal not only the underlying cause of hypertension, but also its severity. Treatment should incorporate non-pharmacologic approaches as well as antihypertensive medications, and should take into account other cardiovascular risk factors such as hyperlipidemia. This review highlights these and other important issues in the evaluation and management of hypertensive children, and provides practical guidance to the practitioner involved in caring for such patients.
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PMID:Evaluation and management of hypertension in childhood. 1122 45

The effect of fenofibrate (FEN), compared with placebo (PL), on total plasma homocysteine (tHcy) levels in the fasted and fed states has been examined. Twenty men with established coronary artery disease (CAD) or with at least two cardiovascular risk factors, who had elevated plasma triglyceride levels (> 2.3 mmol/l) and reduced HDL-C levels (< 0.91 mmol/l), and in whom a fibric acid derivative was clinically indicated were studied. The study was a randomized, PL controlled, double-blind study designed to test the effect of micronized FEN on postprandial lipemia. Plasma tHcy levels were investigated as a post-hoc analysis. After a 4-week dietary stabilization period, patients were randomized to PL or FEN (200 mg/day) for 8 weeks, followed by an 8-h postprandial study, consisting of 1 g fat/kg body weight (35% cream). The methionine content of cream was approximately 0.53 mg/ml. A 5-week washout period was then followed by a second 8-week treatment period (FEN or PL), at the end of which a second postprandial study was undertaken. Blood was sampled in the fasted state (0 h) and postprandially at 2, 4, 6 and 8 h. Plasma was stored at -80 degrees C for homocysteine, vitamins B(6), B(12) and folate measurements. FEN caused a marked decrease in all triglyceride-rich lipoprotein parameters, no change in LDL-C, and an increase in HDL-C levels. Fen treatment was associated with an increase in fasting tHcy (PL: 10.3+/-3.3 micromol/l to FEN: 14.1+/-3.8 micromol/l, 40.4+/-20.5%, P < 0.001) and fed tHcy levels 6 h post-fat load (PL: 11.6+/-3.3 micromol/l vs. FEN: 17.1+/-5.4 micromol/l, P < 0.001). Homocysteine levels were increased by the fat load; PL: 14% (P < 0.001) and FEN: 21%, P < 0.001 at the 2, 4, 6 and 8 h time points. Change in tHcy level on FEN was not associated with changes in plasma levels of folate, vitamins B(6) or B(12) or creatinine. Amino acid analysis revealed that methionine and cysteine were significantly increased on FEN (P < 0.005). The incidence of hyperhomocysteinemia (defined as tHcy level >14 micromol/l) was PL: 2/20 (10%) and FEN: 9/20 (45%) (chi(2) = 4.51, P = 0.034). There was no correlation between changes in plasma triglyceride levels and tHcy levels. Since tHcy is considered an emerging cardiovascular risk factor, the ability of FEN to increase plasma tHcy levels could potentially mitigate the potential of this drug to protect against cardiovascular disease.
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PMID:Fenofibrate raises plasma homocysteine levels in the fasted and fed states. 1125 17

The association of postprandial hyperlipidemia, small and dense LDL particles and low HDL cholesterol levels is a major cardiovascular risk factor, highly prevalent in insulin resistant and diabetic patients. Several recent epidemiological studies have demonstrated that an abnormal increase in the postprandial triglyceride levels is an independent cardiovascular risk factor, independent from fasting triglyceride levels. A decreased clearance of postprandial triglycerides is related to an abnormal intravascular lipoprotein metabolism, most of the time secondary to an insulin resistant state and genetic factors. This abnormal lipoprotein metabolism also induces a redistribution of LDL particles towards small and dense particles and a decrease in the HDL cholesterol levels. Small, dense LDL are associated with a 3 fold increase in the risk of ischemic heart disease, but does not remain a significant risk factor after adjustment for triglyceride levels. Decreased HDL cholesterol and apolipoprotein A-I levels are strong cardiovascular risk factors, which does not seem to be better assessed with the assay of various HDL sub-fractions (HDL(2) et HDL(3), LpA-I et LpA-I: A-II.).
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PMID:[Postprandial hyperlipidemia, small and dense LDL, HDL sub-fractions]. 1143 75

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

Psychiatrists have become particularly concerned about health issues in patients with schizophrenia because of emerging data that link some of the newer atypical antipsychotics with both significant weight gain and increases in serum triglyceride levels. Excessive weight gain during antipsychotic therapy has an adverse effect on health and medication compliance, while hyperlipidemia presents an additional cardiovascular risk factor in patients with schizophrenia who typically smoke, are inactive, and possess poor dietary habits. An understanding of appropriate monitoring for metabolic adverse effects is important for those who prescribe atypical antipsychotics, as is a working knowledge of behavioral and pharmacologic treatments for weight gain and hyperlipidemia.
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PMID:Effects of atypical antipsychotics on weight and serum lipid levels. 1180 86

The purpose of this study was to evaluate risk factors predicting restenosis and primary patency after percutaneous transluminal angioplasty. Follow-up data (including cardiovascular risk factor scores according to SCVIR criteria, preinterventional and postinterventional clinical data and patient history) of all patients who underwent successful percutaneous transluminal angioplasty for lower limb ischemia were analyzed retrospectively and patients, relatives, or referring physicians underwent a telephone interview. Patients with incomplete follow-up data were examined by means of a clinical examination, including Doppler measurements and treadmill test. Additionally all angiograms were evaluated to calculate lesion length, number of treated lesions, lesion type (SCVIR score), and runoff. The outcome was categorized into four groups: early recurrence (< 1 month, group I), mean recurrence (1-6 months, group II), late recurrence (>6 months, group III), and no recurrence (group IV). According to common concepts group I was defined as early (thrombotic) reocclusion, group II as clinically defined restenosis, and group III as progression of atherosclerosis. One hundred thirty-seven patients underwent percutaneous transluminal angioplasty of 148 extremities. The groups differ significantly only with respect to a higher diabetes score for group I in comparison to group IV (p=0.002, Kruskal-Wallis test), and a worse runoff of group I compared with group IV (p =0.008). There was a trend toward a higher diabetes score for group II in comparison to group IV (p = 0.014). There were no differences with regard to hyperlipemia, hypertension, and tobacco use between patient groups. Mean primary patency was 436 days. Predictors for lower patency rates were diabetes mellitus (p<0.001), runoff (p=0.005), and number of treated lesions (p=0.007) in a stepwise, multiple regression analysis. Patients with clinically defined restenosis showed no specific risk factor profile in this study. Predictors for lower primary patency were diabetes mellitus, number of treated lesions, and runoff.
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PMID:Cardiovascular risk factors do not predict clinically defined restenosis after percutaneous transluminal angioplasty for lower limb ischemia. 1186 5

Secondary hyperlipidemia is a major cardiovascular risk factor in individuals with type 2 diabetes. Increased hepatic production of apolipoprotein B (apoB)-containing lipoproteins contributes to the elevated plasma levels, but the mechanism is poorly understood. Recent results have established that microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apoB-containing lipoproteins. To better understand the mechanism of type 2 diabetes-associated hyperlipidemia, we quantified hepatic MTP mRNA levels, hepatic microsomal triglyceride transfer activity, and in vivo triglyceride secretion from the liver in two diabetic mouse models. Obese diabetic (ob/ob) mice had 45% higher (P = 0.006) hepatic MTP mRNA levels, 54% higher (P < 0.0001) microsomal triglyceride transfer activity, and 70% higher (P < 0.0001) in vivo triglyceride secretion rates compared with ob/+ control mice. In contrast, in lean streptozotocin-treated diabetic mice, hepatic MTP mRNA levels were unchanged, whereas microsomal triglyceride transfer activity and in vivo triglyceride secretion rates were marginally decreased. These studies suggest that obesity-induced type 2 diabetes in mice confers increases in hepatic MTP expression and secretion of triglyceride-rich lipoproteins. High blood glucose and altered hepatic expression of sterol regulatory element binding protein genes play a minor role in this diabetic response.
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PMID:Hepatic expression of microsomal triglyceride transfer protein and in vivo secretion of triglyceride-rich lipoproteins are increased in obese diabetic mice. 1191 50

Coronary heart disease is a leading cause of death in industrialized nations. Hyperlipidemia with elevated serum total cholesterol, LDL cholesterol, and triglycerides is a known major cardiovascular risk factor. HDL cholesterol is considered to be protective, so low HDL cholesterol is being recognized as an independent cardiovascular risk factor that contributes to the development of atherosclerosis and related adverse cardiovascular events. The recognition of insulin resistance and metabolic syndrome is a step further in understanding these risk factors. Attempts at reducing serum cholesterol with different strategies in the past have met with limited success until the development of statins. The advent of statins has revolutionized the management of hyperlipidemia. The post-statins era has seen major clinical trials demonstrating the benefit of cholesterol reduction in the setting of both primary and secondary prevention. In general, there appears to be a 25% to 40% relative risk reduction in major adverse cardiovascular events such as death, myocardial infarction, and stroke. The recent megatrials further suggest that aggressive management of cholesterol in patients with high cardiovascular risk may be beneficial. Though the concept of the-lower-the-better may be looming, the question of "How low is good enough?" remains controversial. The results of recent megatrials such as the Heart Protection Study go a step further than the NCEP guidelines and suggest that statin therapy may benefit patients at high risk of cardiovascular disease regardless of their baseline values. We summarize the results of the available large clinical trials in our understanding of the management of dyslipidemia in a setting of primary prevention.
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PMID:Management of dyslipidemia in the primary prevention of coronary heart disease. 1235 27


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