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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 2007 European Guidelines on Hypertension are jointly sponsored by the European Society of Cardiology and the European Society of Hypertension. Changes with respect to the previous 2003 Guidelines are few but some are significant. Perhaps the most significant change is inclusion of metabolic syndrome as a cardiovascular risk factor similar in importance to diabetes mellitus or target-organ damage. Also striking is the recognition of chronic kidney disease as a very high risk condition in hypertensive patients. Masked arterial hypertension (AHT) is included for the first time as a new entity that is present in 10-15% of cases and associated with increased cardiovascular risk. The eye fundus examination is no longer considered necessary in the diagnostic evaluation. The decision to start treatment should be based on systolic and diastolic BP values and on assessment of total cardiovascular risk. Drug therapy should be started early. The delay to check the response to nonpharmacological measures should be only some weeks and not months as was previously established. Any of the five large groups (diuretics, beta-blockers, calcium antagonists, ACE inhibitors and angiotensin II blockers) is valid for the first stage of treatment, although the choice should be individualized based on the possible risk factors and associated cardiovascular and renal disease. The guidelines place strong emphasis on drug combinations because most patients will require more than one drug for their control.
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PMID:[Novelties in the European Hypertension Guide 2007. European Society of Cardiology. European Society of Hypertension]. 1884 31

Metabolic syndrome is increasingly recognized as an important cardiovascular risk factor in hypertension, but its influence on the cardiovascular risk profile in hypertensive postmenopausal women has not been studied. The aim of the present study was to investigate the impact of metabolic syndrome on the cardiovascular risk profile and the response to treatment. We enrolled 350 hypertensive postmenopausal women, 55+/-6 years of age (range 47 to 60 years of age). Patients were divided into 2 groups according to the presence of metabolic syndrome. Compared with those without, women with metabolic syndrome had higher waist circumference, body mass index, and levels of glucose, triglycerides, and HDL cholesterol, as would be expected, based on definition. In addition, patients with metabolic syndrome had a cardiovascular risk profile less favorable, characterized by a significantly higher highly sensitive C-reactive protein (2.2+/-0.6 versus 1.7+/-0.7 ng/L; P<0.01), a more compromised endothelial function (flow-mediated vasodilation 2.4+/-2.2 versus 4.4+/-2.5%; P=0.01), and a significantly higher left ventricular mass (44+/-15 versus 41+/-16 g/m(2.7)). Also, antihypertensive treatment induced a more modest improvement of both endothelial dysfunction and subclinical inflammation in women with metabolic syndrome. The results of our study show that in postmenopausal women, there are 2 different forms of hypertension: that which is isolated, and that which is associated with metabolic syndrome. This last form is related to a more severe risk profile, and response to therapy is less favorable.
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PMID:Metabolic syndrome affects cardiovascular risk profile and response to treatment in hypertensive postmenopausal women. 1885 86

Low levels of high-density lipoprotein cholesterol (HDL-C) represent a major cardiovascular risk factor, with a stronger relationship to coronary heart disease than that seen with elevated levels of low-density lipoprotein cholesterol (LDL-C). HDL-C has important antiatherogenic effects, including reverse cholesterol transport, inhibition of LDL-C oxidation, and antiplatelet and anti-inflammatory actions. Patients with low HDL-C are also at an amplified risk of coronary heart disease due to the common coexistence of other risk factors, including excess adiposity, metabolic syndrome, type 2 diabetes mellitus, hypertriglyceridemia, and the atherogenic dyslipidemia characterized by small dense LDL-C. First-line therapy of low HDL-C generally consists of nonpharmacologic measures such as improved fitness and weight loss. Current pharmaceutical options include statins, fibrates, and nicotinic acid. A host of novel approaches involving HDL-C and reverse cholesterol transport hold the promise of fundamentally changing the natural history of atherosclerosis, the most common and important chronic disease in humans.
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PMID:The importance of recognizing and treating low levels of high-density lipoprotein cholesterol: a new era in atherosclerosis management. 1912 82

Whether intensive pharmacologic cardiovascular risk factor management reduces metabolic syndrome (MetS) prevalence is unknown. The authors compared the number of secondary prevention medications and National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III)-defined MetS prevalence in coronary artery disease patients entering cardiac rehabilitation from 1996 to 2001 (period 1, n=516) with those entering from 2002 to 2006 (period 2, n=609). Age, sex, and ethnicity were similar in both periods. From period 1 to period 2, participants took more secondary prevention medications (2.8+/-1.3 vs 3.5+/-1.0, P<.001). Prevalence of low high-density lipoprotein cholesterol (66% vs 66%), diabetes (37% vs 38%), and hypertension (81% vs 81%) were unchanged. The prevalence of hypertriglyceridemia decreased (48% vs 36%, P<.001), but the proportion meeting criteria for elevated waist circumference increased (51% vs 58%, P<.05), resulting in no change in overall MetS prevalence (60% vs 59%, P=NS). More emphasis on therapeutic lifestyle change in addition to intensive pharmacologic therapy is needed to reduce MetS prevalence in patients with coronary artery disease.
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PMID:Drugs are not enough: the metabolic syndrome--a call for intensive therapeutic lifestyle change. 1924 12

The Turkish Cardiovascular Risk Platform (TCRP) calls for the diagnosis of the metabolic syndrome (MS) if insulin resistance, impaired fasting glucose, impaired glucose tolerance, or diabetes mellitus and >or=2 other established criteria are present. TCRP defines insulin resistance as a homeostasis model assessment >2.7. The aim of this cross-sectional study was to compare TCRP guidelines with the United States National Cholesterol Education Program Adult Treatment Panel III (NCEP) definition of MS in Turkish adults (N=1690). The age- and sex-adjusted prevalence of MS was 25% with the TCRP and 40% for the NCEP definition. Patients with MS identified by the NCEP definition but not by the TCRP definition had lower body mass index and less insulin resistance, but had a similarly adverse cardiovascular risk factor profile to those with TCRP-identified MS, with high blood pressure, waist circumference, triglycerides, and total cholesterol/high-density lipoprotein cholesterol ratio. Other national health organizations should avoid using homeostasis model assessment as a prerequisite for diagnosing MS. Modification of the NCEP definition would be more appropriate for ethnic groups with different body sizes.
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PMID:Comparison between Turkish Cardiovascular Risk Platform and United States National Cholesterol Education Program Adult Treatment Panel III definitions of the metabolic syndrome in Turkish adults. 1924 13

Patients classified as having a "poor lung function" in large populations studies are at increased risk of atherothrombosis, but potential mechanisms are unclear. A large proportion of these people are affected by chronic obstructive pulmonary disease (COPD), a recognized risk factor for vascular events. Systemic inflammation is the main atherothrombotic abnormality in COPD, but hypoxia-related platelet activation, pro-coagulant status and oxidative stress may play a role. Systemic inflammation is presumably a leading mechanism of atherothrombosis also in people who have a "restrictive" spirometric dysfunction, rather than the classic obstructive pattern of COPD. Many persons with "poor lung function" are affected by diabetes and their cardiovascular risk is therefore linked to the diabetic status. Patients affected by diabetes tend to have a "restrictive" dysfunction, rather than COPD. Recent studies show that restriction at spirometry precedes the onset of diabetes, thereby representing a marker of mechanisms involved in the pre-diabetic, insulin-resistant state. This is also proved by the fact that most patients with metabolic syndrome, a pre-diabetic condition, have a restrictive ventilatory pattern at spirometry. A significant proportion of people with "poor lung function" have visceral obesity, a cardiovascular risk factor. By hampering lung expansion, visceral obesity causes a restrictive ventilatory pattern. In conclusion, the term "poor lung function" includes various chronic illnesses with different mechanisms of atherothrombosis. Research is needed for better understanding why persons with lung dysfunctions have higher cardiovascular risk, and for identifying adequate preventive strategies.
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PMID:Why are people with "poor lung function" at increased atherothrombotic risk? A critical review with potential therapeutic indications. 1948 25

The objective of this study was to verify the clustering of anthropometric and metabolic variables related to metabolic syndrome, by sex. Data were collected from 579 subjects aged 18-94 years living in two rural areas of Brazil. Factor analysis was performed using principal components analysis with varimax orthogonal rotation. The study reduced a complex set of cardiovascular risk factor into 3 independent factors, each reflecting a different aspect of metabolic syndrome. In both sexes, factor 1 related to obesity and dyslipidemia, factor 2 to obesity and blood pressure, and factor 3 to obesity and insulin resistance. The total variance explained for men and women was, respectively, 66.61% and 68.98%. The findings corroborate the hypothesis that at least 3 pathophysiological domains act in the clustering of cardiovascular risk factors related to metabolic syndrome in this population.
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PMID:[A multidimensional exploration of metabolic syndrome components]. 1948 92

Male hypogonadism now has a new spectrum of complications. They are mainly cardiometabolic in nature. Low serum testosterone levels are a risk factor for diabetes, metabolic syndrome, inflammation and dyslipidemia. These metabolic and inflammatory complications are not without consequences. Recent studies have shown low serum testosterone levels to be an independent risk factor of cardiovascular and all-cause mortality. It is time to welcome low serum testosterone levels as a cardiovascular risk factor.
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PMID:Welcoming low testosterone as a cardiovascular risk factor. 1953 27

Non-alcoholic fatty liver disease (NAFLD) is the most frequent cause of liver damage and alteration of hepatic enzymes. NAFLD is strongly associated with metabolic syndrome and obesity. It is characterized by fat accumulation in the liver that may progress throughout hepatic steatosis and inflammation (non-alcoholic steatohepatitis [NASH]) toward cirrhosis and liver failure. In the last decade several studies suggested that NAFLD is an independent cardiovascular risk factor that increases cardiovascular mortality. At present, several studies investigating possible therapeutic approaches are ongoing. The present review is focused on the current and promising treatments of NAFLD.
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PMID:Update on the treatments of non-alcoholic fatty liver disease (NAFLD). 1975 Nov 86

The metabolic syndrome (MS) is a known cardiovascular risk factor in the general population and a common problem among renal transplant recipients. This study investigated whether MS after renal transplantation affected long-term graft function. We included 112 transplants at our center between 2000 and 2002. We excluded patients with the presence of pretransplant diabetes or nonstable renal function at 1 year after transplantation. We evaluated parameters such as demographic features, medications, smoking history, body mass index, daily proteinuria, blood pressure, number of HLA mismatches, number of acute rejection episodes, delayed graft function, and laboratory parameters. Patients were followed for a mean of 69.86 +/- 21.94 months. The prevalence of MS was determined using the National Cholesterol Education Program-Adult Treatment Panel III criteria. At 1 year after transplant, 28.6% of subjects had MS, whereas only 10.7% had MS before transplantation. Among 27.7% of patients graft failure had occurred during the follow-up; MS was more frequent among these individuals compared with those displaying stable renal function (51.6% vs 19.8%; P = .002). Older donor age, delayed graft function, acute rejection episodes, smoking history, MS, proteinuria, serum creatinine level, and C-reactive protein were associated with graft failure. Upon multivariate Cox regression analysis, patients with MS at 1 year after transplantation showed an increased risk for graft failure (relative risk, 0.22; 95% confidence interval, 0.06-0.75; P = .016). Older donor age and proteinuria level were other independent risk factors for graft failure. The MS was a prominent risk factor for graft failure. Because MS is a cluster of modifiable risk factors, early identification of patients at risk and intervention in due time may improve graft survival.
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PMID:Metabolic syndrome is related to long-term graft function in renal transplant recipients. 1976 41


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