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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic and non metabolic cardiovascular risk factors tend to cluster in the same individual. The association of the cardiovascular risk factors is referred as metabolic syndrome (MS). This syndrome is associated with an increased risk of accelerated atherosclerosis and cardiovascular events. The cluster of cardiovascular risk factors of the MS includes: insulin resistance with or without glucose intolerance or diabetes, abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, a proinflammatory and prothrombotic state. MS is one of the major issues in the management of cardiovascular disease because of its epidemic proportion and its impact on increasing risk of developing both cardiovascular disease and type 2 diabetes. The main therapeutic goal in the management of patients with the MS is to reduce risk for clinical cardiovascular events and to prevent type 2 diabetes. In particular, for individuals with established diabetes, risk factors management must be intensified to reduce their higher cardiovascular risk. Lifestyle changes have a critical role in the clinical management of the risk factors predisposing to MS, such as overweight/obesity, physical inactivity. A large body of evidence suggests the use of Metformin and Acarbose for the treatment of the syndrome as these drugs have consistently shown to reduce cardiovascular events and mortality. Most anti-hypertensive drugs have unfavorable metabolic profile while b-blockers, centrally acting agents and drugs targeting the renin angiotensin system should always be considered for the treatment of hypertension in patients with MS.
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PMID:Metabolic syndrome. 1685 17

To investigate the effect of metabolic syndrome (MS) components on early atherosclerosis markers, i.e., urinary albumin excretion rate (UAE), pulse wave velocity (PWV), and carotid intima-media thickness (IMT), we studied 536 Japanese patients with type 2 diabetes without cardiovascular disease or nephropathy. The MS definition by ATP III was employed. UAE, PWV, and IMT increased significantly with increasing the number of components even before fulfilling the diagnosis of MS. UAE was significantly influenced by high blood pressure, high triglycerides, and low HDL cholesterol. PWV was significantly increased by high blood pressure. IMT was significantly increased by high blood pressure and abdominal obesity. Multiple regression analysis, including MS components and putative risk factors, indicated that the number of MS components, age and glycosylated HbA1C were independent determinants of UAE, PWV, and IMT. LDL cholesterol and male gender were independent determinants of IMT. In conclusion, UAE, PWV, and IMT increased according to increasing the number of MS in type 2 diabetic patients without cardiovascular disease or diabetic nephropathy. The current observation considering the modifiable factors may help to identify patients who are at high risk of experiencing cardiovascular disease.
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PMID:Relationship between metabolic syndrome components and vascular properties in Japanese type 2 diabetic patients without cardiovascular disease or nephropathy. 1686 Apr 30

Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with cardio-metabolic risk factors such as abdominal obesity, type 2 diabetes and other components of the metabolic syndrome (MetS). Currently, the importance of NAFLD and its relationship to the MetS is increasingly recognized, and this has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Indeed, the impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening/surveillance strategies in this growing number of patients. Recent evidence suggests that the severity of liver histology in NAFLD patients is closely associated with markers of early atherosclerosis such as greater carotid artery wall thickness and lower endothelial flow-mediated vasodilation independently of classical risk factors and components of the MetS. Moreover, NAFLD is associated with greater overall mortality and independently predicts the risk of future CVD events. Overall, the current body of evidence strongly suggests that NAFLD is likely to be associated with increased CVD risk, and raises the possibility that NAFLD may be not only a marker but also an early mediator of atherosclerosis.
Atherosclerosis 2007 Apr
PMID:Non-alcoholic fatty liver disease and increased risk of cardiovascular disease. 1733 26

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21

Up-to-date therapy has in recent years substantially modified the clinical course of HIV infections and AIDS. The progress of the disorder has changed-today it is a chronic disease of many years. Already in 1997 and 1998 it transpired that long-term HAART, highly active antiretroviral therapy, produced adverse metabolic changes, which significantly affect the subsequent progress of the disease. The mechanism responsible for these metabolic changes has not, as yet, been fully clarified-in all probability its etiology is multifactorial. Even prior to the introduction of HAART, some metabolic changes were observed in HIV-infected subjects. These changes are, however, not specific for the pathogen concerned, they are generally seen in acute inflammatory reactions. Since the introduction of HAART in 1996 the range of metabolic changes has expanded. Gradually we detect more and more anthropometric, metabolic and coagulation changes, closely resembling changes seen in the metabolic syndrome (SIR, syndrome of insulin resistance), well known from cardiology and internal medicine-dyslipoproteinaemia, insulin resistance, abdominal obesity. A combination of these disorders is clinically significant due to their role in the development of atherosclerosis and their by no means negligible involvement in the onset of ischaemic heart disease. In view of the much lower mean age of HIV-positive subjects the earlier mentioned complications should be expected in much lower age categories than with HIV-negative individuals. The paper discusses the possible pathogenesis and potential mechanisms of metabolic complications related to HAART, its impact on the cardiovascular risk and the possibilities of hypolipidaemic therapy in HIV-positive patients.
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PMID:[Metabolic syndrome and HIV/AIDS disorder]. 1705 72

Familial hypercholesterolemia (FH) is characterized by increased risk for premature coronary artery disease (CAD). This risk is exacerbated in the presence of abdominal obesity and insulin resistance. Low adiponectin is part of the clustering of metabolic abnormalities associated with abdominal obesity and insulin resistance. The present study, therefore, aims to examine the relationship between plasma adiponectin and age at CAD diagnosis in FH patients. Plasma adiponectin was measured by ELISA in 568 non-diabetic FH individuals of French-Canadian origin. CAD was defined according to strict clinical criteria. Prior to analyses, patients were grouped according to age and gender-specific tertiles of plasma adiponectin levels. Multivariate Cox proportional hazards regression was used to estimate the association between plasma adiponectin levels and age at diagnosis of CAD. Overall, FH patients in the lowest tertile of plasma adiponectin exhibited CAD at a significantly younger age (hazard ratio=1.73, confidence interval 95%: [1.19-2.53]; p=0.004). These results suggest that low plasma adiponectin is associated with an increased risk of premature CAD over and above the already exaggerated risk seen in FH patients.
Atherosclerosis 2008 Jan
PMID:Low plasma adiponectin exacerbates the risk of premature coronary artery disease in familial hypercholesterolemia. 1712 36

Metabolic syndrome (MS) consists of a cluster of metabolic and hemodynamic disorders that promote the development of atherosclerosis and increase cardiovascular morbidity/mortality. We evaluated the prevalence and characteristics of MS after acute coronary syndrome (ACS) and the effect of intensive risk factor management on the morbidity/mortality associated with MS in a therapeutic cohort; 480 consecutive patients were summoned 3 months after an ACS for cardiovascular evaluation and management. Follow-up was carried out 16 months later. At 3 months after ACS, prevalence of MS was 20.8%, as assessed by criteria of the National Cholesterol Education Program Adult Treatment Panel III and 27.7% according to the definition of the International Diabetes Federation. The most common metabolic disorders were abdominal obesity, hypertriglyceridemia, and fasting hyperglycemia. Characteristics of the initial ACS showed no significant difference between the MS and non-MS groups. Atherosclerotic extent was greater in the MS group according to Adult Treatment Panel III. At follow-up, the MS and non-MS groups achieved optimal low-density lipoprotein cholesterol and blood pressure levels. During follow-up, there was an increase in total mortality in the MS group compared with the non-MS group (5.2% vs 1.4%, p <0.01) as assessed by International Diabetes Federation criteria; however, no difference in minor or major cardiovascular events was found between the 2 groups. In conclusion, MS was highly prevalent after an ACS, notably in young patients, and was not associated with a specific ACS presentation.
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PMID:Prevalence of metabolic syndrome after acute coronary syndrome and its prognostic significance. 1712 44

The endothelium plays a crucial role in modulating vascular function and structure. In healthy conditions, nitric oxide produced by endothelial cells exerts not only vasodilating properties, but also several other protective actions toward the vessel wall against the development of atherosclerosis and thrombosis. Traditional cardiovascular risk factors are characterized by endothelial dysfunction caused by an enhanced production of oxidative stress leading to destroy nitric oxide, thus reducing its availability. Abdominal obesity is associated with endothelial dysfunction, through direct mechanisms, such as insulin resistance and the association with risk factors (including diabetes mellitus, hypertension and dyslipidemia), and direct, by the production of adipokines and pro-inflammatory cytokines, which in turn induce oxidative stress leading to a reduced nitric oxide availability. A reduced endothelium-dependent relaxation is a predictor of cardiovascular events in high-risk patients and represents a putative clinical parameter to stratify the cardiovascular risk and a useful marker for therapy efficacy. Weight loss and a modification of lifestyle ameliorate endothelial function in obese patients, an effect due not only to a better glycemic profile, but also secondary to reduced plasma levels of inflammatory markers and adipokines. At present, whether an improvement of endothelial dysfunction secondary to weight loss is significantly associated with a better cardiovascular prognosis is still unknown. (G Ital Cardiol 2006; 7 (11): 715-723)
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PMID:[Obesity and endothelial dysfunction]. 1721 13

Metabolic syndrome consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart disease. One of the defects in metabolic syndrome and its associated diseases is excess cellular oxidative stress (mediated by reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to mitochondrial components, resulting in reduced efficiency of the electron transport chain. Recent evidence indicates that reduced mitochondrial function caused by ROS/RNS membrane oxidation is related to fatigue, a common complaint of MS patients. Lipid replacement therapy (LRT) administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial and other cellular membrane functions and reduce fatigue. Recent clinical trials have shown the benefit of LRT plus antioxidants in restoring mitochondrial electron transport function and reducing moderate to severe chronic fatigue. Thus LRT plus antioxidant supplements should be considered for metabolic syndrome patients who suffer to various degrees from fatigue.
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PMID:Metabolic syndrome and mitochondrial function: molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function. 1724 17

The inflammatory component of atherogenesis has been increasingly recognized over the last decade. Inflammation participates in all stages of atherosclerosis, not only during initiation and during evolution of lesions, but also with precipitation of acute thrombotic complications. The metabolic syndrome is associated with increased risk for development of both cardiovascular disease and type-2 diabetes in humans. Central obesity and insulin resistance are thought to represent common underlying factors of the syndrome, which features a chronic low-grade inflammatory state. Diagnosis of the metabolic syndrome occurs using defined threshold values for waist circumference, blood pressure, fasting glucose and dyslipidemia. The metabolic syndrome appears to affect a significant proportion of the population. Therapeutic approaches that reduce the levels of proinflammatory biomarkers and address traditional risk factors are particularly important in preventing cardiovascular disease and, potentially, diabetes. The primary management of metabolic syndrome involves healthy lifestyle promotion through moderate calorie restriction, moderate increase in physical activity and change in dietary composition. Treatment of individual components aims to control atherogenic dyslipidemia using fibrates and statins, elevated blood pressure, and hyperglycemia. While no single treatment for the metabolic syndrome as a whole yet exists, emerging therapies offer potential as future therapeutic approaches.
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PMID:Metabolic syndrome, inflammation and atherosclerosis. 1732 25


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