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

The increased risk of premature cardiovascular disease (CVD) in rheumatoid arthritis (RA) patients may depend on traditional risk factors but may also be attributable to RA-specific risk factors such as disease-related dyslipidemia, or cytokines such as tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a proinflammatory cytokine that can produce widespread deleterious effects when expressed in large amounts. It is produced in the heart by both cardiac myocytes and resident macrophages under conditions of cardiac stress, and is thought to be responsible for many of the untoward manifestations of cardiac disease. TNF-alpha may play a role in the triggering and perpetuation of atherosclerosis. Treatment with biologic agents directed against TNF-alpha has significant clinical benefits in inflammatory diseases such as RA and may be able to reduce cardiovascular risk. The disappointing results of the recent studies to antagonize TNF-alpha in CVD may have various explanations. However, the effects of TNF-alpha blockers on incident cases of congestive heart failure (CHF) in RA remains controversial. Due to the lack of evidence of a beneficial effect of anti-TNF-alpha agents in treatment of CHF, they should not be used to treat patients with New York Heart Association (NYHA) class III or IV heart failure.
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PMID:Tumor necrosis factor-alpha, biologic agents and cardiovascular risk. 1621 87

The thiazolidinediones have been in clinical use for the management of type 2 diabetes for the past five years. These agents reduce insulin resistance by acting as ligands that regulate gene expression related to the proliferation and differentiation of adipose tissue. Overall, data from several clinical studies suggest that their hypoglycaemic efficacy is slightly less than sulphonylureas and metformin but greater than acarbose and the glinides. In the short term, treatment with thiazolidinediones is associated with weight gain, expansion of plasma volume, fluid retention, peripheral oedema, an increased risk of congestive heart failure when combined with insulin, and an idiosyncratic hepatotoxic reaction to troglitazone. The long term consequences of these effects are not known. Contrary to expectations, despite being insulin sensitisers these agents do not favourably influence the other components of the metabolic syndrome that are believed to be aggravated by insulin resistance. Dyslipidaemia and elevated blood pressure, which are major risk factors of cardiovascular disease in type 2 diabetes, are not favourably improved with thiazolidinedione treatment. Unlike the sulphonylureas and metformin, which have been shown in recent long term randomised studies to reduce cardiovascular risk substantially, there is no data on the long term cardiovascular safety of the thiazolidinediones. At present, in the absence of long term data, the thiazolidinediones in clinical use are moderately effective hypoglycaemic drugs with no particular advantage over existing treatments in type 2 diabetes.
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PMID:Thiazolidinediones in type 2 diabetes--have they lived up to expectations? 1622 62

Epidemiologic data from the Framingham Study provide insights into the population burden of heart failure (CHF), its prognosis and modifiable risk factors that promote it. In the general population CHF is chiefly the end stage of hypertensive, coronary and valvular cardiovascular disease. It is a major and growing problem in most affluent countries because of aging populations of increased size, and the prolongation of the lives of cardiac patients by modern therapy. Once clinically manifest, CHF, despite recent innovations in therapy, carries an unacceptably high mortality rate. In the Framingham Study, median survival is only 1.7 y for men and 3.2 y for women, with only 25% of men and 38% of women surviving 5 y. This is a mortality rate 4-8 times that of the general population of the same age. This poor outlook is observed for all etiologies of CHF and sudden death is a prominent feature of the mortality. Based on population attributable risks, hypertension has the greatest impact, accounting for 39% of CHF events in men and 59% in women. Despite its much lower prevalence in the population (3-10%) myocardial infarction also has a high attributable risk in men (34%) and women (13%). Valvular heart disease only accounted for 7-8% of CHF. Hypertension increased the age and risk factor adjusted hazard of CHF 2-fold in men and 3-fold in women, with a greater impact of the systolic than diastolic blood pressure. Diabetes increased CHF risk 2-8 fold with risk ratios twice as large in women as men. About 19% of CHF cases have diabetes. It accounted for 6-12% of the CHF in the Framingham Study cohort. Dyslipidemia characterized by a high total/HDL cholesterol ratio, but not the total cholesterol alone was a risk factor for CHF. An enlarged heart on X-Ray, ECG-LVH, a reduced vital capacity and rapid heart rate usually signified deteriorating cardiac function. CHF risk associated with ECG-LVH was independent of X-Ray cardiomegaly but risk was further augmented when both coexist. Echocardiographic left ventricular hypertrophy signifies a high risk of CHF proportional to the degree of increase in left ventricular mass without a critical value that delineates compensatory from pathological hypertrophy. Risk of CHF in persons predisposed by hypertension, diabetes or cardiac conditions varies over a 10-fold range depending on the aforementioned modifiable risk factors and indicators of deteriorating left ventricular function. Using multivariate risk formulations it is possible to identify 20% of the population from which 70% of the CHF will evolve. Those in the upper quintile of multivariate risk are good candidates for echocardiographic testing to delineate those needing aggressive preventive measures to delay the onset of CHF. Therapy of CHF must begin with treatment of presymptomatic left ventricular dysfunction to reverse the dysfunctional maladaptive changes.
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PMID:Incidence and epidemiology of heart failure. 1622 42

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. The activation of PPAR-gamma, an isotype of PPARs, can either increase or decrease the transcription of target genes. The genes controlled by this form of PPAR have been shown to encode proteins or peptides that participate in the pathogenesis of insulin resistance. Insulin resistance is defined as a state of reduced responsiveness to normal circulating concentrations of insulin and it often co-exists with central obesity, hypertension, dyslipidemia, and atherosclerosis. There is substantial evidence that links obesity with insulin resistance and type-2 diabetes. The early phase of obesity-related insulin resistance has 2 components: (a) interruption of lipid homeostasis leading to the increased plasma concentration of fatty acids that is normally suppressed by the activation of PPAR-gamma, and (b) activation of factors such as cytokines depressed by PPAR-gamma that cause insulin resistance. Therefore, it is logical to suggest that activation of PPAR-gamma may partially reverse the state of insulin resistance. Evidently, activation of the nuclear receptor, PPAR-gamma, by thiazolidinediones has been reported to ameliorate insulin resistance. Although hepatotoxity and possibility to induce congestive heart failure (CHF) limit the widely use of thiazolodinediones, they are still powerful weapon to fight against insulin resistance and type-2 diabetes if use properly. This article reviews the physiology of PPAR-gamma and insulin-signaling transduction, the pathogenesis of insulin resistance in obesity-related type-2 diabetes, the pharmacological role of PPAR-gamma in insulin resistance, and additional effects of thiazolidinediones.
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PMID:Peroxisome proliferator-activated receptor gamma as a drug target in the pathogenesis of insulin resistance. 1630 9

The cardiometabolic syndrome (CMS) is associated with cardiovascular disease (CVD) and includes a constellation of risk factors such as central obesity, hypertension, insulin resistance, dyslipidemia, microalbuminuria, and hypercoagulability. Collectively, these risk factors increase CVD endpoints such as stroke, congestive heart failure, chronic kidney disease (CKD), and overall mortality. The CMS is associated with endothelial dysfunction, inflammation, abnormal thrombolysis, and increased oxidative stress that accentuate progression of CVD. We will review how the varying components of the CMS relate to an increased CVD and renal disease risk.
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PMID:The cardiometabolic syndrome as a cardiovascular risk factor. 1635 16

The objective of our study was to estimate the prevalence of not-diagnosed hypertension and to determine 10-year risk of coronary heart disease in a random sample of individuals in ASL 3 of Lagonegro (PZ). The sample was based on the whole population assisted by 21 General Practitioners. All General Practitioners filled a form for each patient containing social-demographic, anthropometric and clinical data. The study included only patients aged 35 to 74 years, without a previous diagnosis of myocardial infarction, congestive heart failure and that were not taking antihypertensive drugs (N=335). The directly standardized prevalence of prehypertension was 0.54 (IC95%: 0.47-0.59) and that of hypertension was 0.33 (IC95%: 0.28-0.38). The prevalence of both, prehypertension and hypertension was higher in males than in females, as well as in old compared to young adults. Cardiovascular risk factors as Body Mass Index (BMI), diabetes, a family history of dyslipidemia and diabetes were more frequent among prehypertensive and hypertensive individuals, than in normotensive ones. We also estimated the risk of an acute coronary event in patients whit blood pressure higher than 140/90 mmHg. The calculation, carried out through Framingham algorithm, showed that 1 out of 10 hypertensive subject had a 10-years risk of developing coronary heart disease and that males had a higher risk compared to females. Our study highlights the fundamental role of General Practitioners may play in earlier diagnosis prehypertension and hypertension in the general population, thus adopting practices oriented to healthy promotion and prevention.
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PMID:["Initiative" in primary care: survey on hypertension prevalence and definition of cardiovascular risk profile in ASL 3 of Lagonegro (PZ)]. 1664 11

Lipid metabolism can modulate structural and functional characteristics of the vascular system. Recent studies suggested that dyslipidemia may also affect the hemodynamic response to salt intake through the impairment of intravascular volume regulation and cellular sodium handling. Indeed, dyslipidemia may affect sodium homeostasis through several pathways, including defective nitric oxide and eicosanoid production, enhanced renin-angiotensin system activity and increased sympathetic response. Moreover, dyslipidemia directly affects cellular membrane viscosity and modifies membrane ion transport activity. In line with this evidence, attenuation of the above mentioned mechanisms has been demonstrated after lipid-lowering treatment. From the clinical point of view, such interaction between plasma lipids and sodium homeostasis may adversely affect the clinical presentation of diseases such as salt-sensitive hypertension, congestive heart failure, renal diseases with proteinuria or sodium retention. This review considers the interplay between plasma lipids and sodium homeostasis and its potential clinical implication.
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PMID:Lipid modulation of intravascular and cellular sodium handling: mechanistic insights and potential clinical implications. 1707 5

Type 2 diabetes is a global epidemic contributing to significant cardiovascular morbidity and mortality. The high prevalence of cardiovascular disease can largely be attributed to the metabolic syndrome with its multiple cardiovascular risk factors, including central obesity, hypertension, glucose intolerance, chronic inflammation, and dyslipidemia. The peroxisome proliferator-activated receptor-gamma agonists, the thiazolidinediones, may potentially correct the inflammatory disarray, endothelial dysfunction, dyslipidemia, and plaque vulnerability associated with diabetic cardiovascular disease through their effects on insulin resistance and fat metabolism, yet they can also exacerbate congestive heart failure. This review summarizes basic science, animal, and human data on the effects of thiazolidinediones on cardiovascular disease.
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PMID:Are thiazolidinediones good or bad for the heart? 1707 99

Cardiovascular disease has been well documented in patients with Human Immunodeficiency Virus infection, especially after the introduction of highly active antiretroviral therapy. At present, HIV infection is one of the leading causes of acquired cardiovascular disease including heart failure. Some of the changes observed in these patients include left ventricular systolic dysfunction, dilated cardiomyopathy, congestive heart failure, myocarditis, lipodystrophy, dyslipidemia, insulin resistance, accelerated atherosclerosis including myocardial infarction, prothrombotic state, pericardial effusion, pulmonary hypertension, autonomic dysfunction, and malignancy. This article summarizes the main findings in the principal HIV-associated cardiovascular manifestations in order to stimulate its early recognition so helping in early intervention and therapy.
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PMID:Cardiovascular disease in HIV infection. 1720 95

This cross-sectional, multicenter study investigated the prevalence of chronic kidney disease and associated disorders, in an adult population sample (> 18 years old) attending Primary Care services in Spain. Estimated glomerular filtration rate (Modification Diet in Renal Disease equation) was used for analysis of kidney disease prevalence according to NFK-KDOQI (The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative) stages. Data were collected on serum creatinine, other laboratory parameters blood pressure, and medical history of cardiovascular risk factors or disease (hypertension, dislypidemia, diabetes, congestive heart failure, coronary artery disease, stroke or peripheral arteriopathy) in 7,202 patients attending Primary Care Centers. 47.3% were males, mean age 60,6 +/- 14,3 years, BMI 28.2 +/- 5.3, with 27,6% overweight (27-30 kg/m2) and 32,1% obese (BMI>or=30 kg/m2), The prevalence of cardiovascular risks factors were: absence in 17.3%, one factor 26.9% two 31.2%, and 23.6% presented three or more The frequency of CV risk factors was: hypertension (66.7%), dyslipidemia (48%) and diabetes (31.5%). Congestive heart failure, coronary artery disease, stroke or peripheral vascular disease frequency was lower than 10% The prevalence of eGFR < 60 ml/min x 1.73 m2 was: stage 3 (30-59 ml/min/1.73 m2) 19.7%; stage 4 (15-29 ml/min/1.73 m2) 1.2%; stage 5 no dialysis (GFR < 15 ml/min) 0.4%. This prevalence increased with age in both sexes and 33,7% of patients attending Primary Care services over 70 years presented a eGFR < 60 ml/min. Of the total patients with eGFR < 60 ml/min 37.3% had normal serum creatinine levels. This study documents the substantial prevalence of significantly abnormal renal function among patients at Primary Care level. Early identification and appropriate nephrological management of these patients with renal disease is an important opportunity for an adequate prescription of drugs that interfere with renal function, to delay the progression of renal disease and modify CV risk factors.
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PMID:[Prevalence of kidney insufficiency in primary care population in Spain: EROCAP study]. 1772 49


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