Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The growing "epidemic" of non-valvular atrial fibrillation (NVAF) with its associated morbidity and mortality intersects with a number of conditions including aging, thromboembolism, stroke, congestive heart failure, hypertension, and perhaps the metabolic syndrome and inflammation.In the USA approximately 2.3 million people currently have NVAF and estimates based upon the United States census and the aging of the population suggests that this will be 3.3 million by 2020 and 5.6 million by 2050. This may be a serious underestimate since recent data from Rochester, Minnesota have demonstrated an almost threefold increase in the prevalence over the last three decades after adjustment for age. The explanation is probably multifactorial but the socioeconomic implications of this phenomenon are enormous and sobering.Ongoing efforts towards understanding atrial fibrillation are driven, in part, by the concept that atrial fibrillation may in most patients be the consequence of a systemic condition, in which reduced vascular compliance, atherosclerosis, obesity, and inflammation are primary causal factors. These epidemiological investigations need to be carried out in association with studies aimed at defining the molecular genetics of atrial fibrillation which hopefully will provide more insights into the structural and electrical phenotypes resulting from genetic mutations and their interactions with the environment.
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PMID:The changing epidemiology and natural history of nonvalvular atrial fibrillation: clinical implications. 1706 Sep 64

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

Congestive heart failure is characterized by sympathetic activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure sympathetic activation is closely related to mortality. We studied 48 control subjects (age: 58.4+/-1.6 years, mean+/-SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7+/-3.2 versus 45.8+/-2.9 bursts/100 heartbeats; P<0.01), a further pronounced increase being detected in those with metabolic syndrome (80.9+/-3.2 bursts/100 heartbeats; P<0.01). In the multivariate analysis, waist circumference and body mass index were the variables most closely related to sympathetic activation. Compared with control subjects, baroreflex responses were significantly attenuated in the 2 heart failure groups, the impairment being more marked in the group with than without metabolic syndrome. Thus, obesity and metabolic syndrome potentiate the sympathetic activation characterizing heart failure. This potentiation is likely to mainly depend on metabolic and baroreflex mechanisms.
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PMID:Excessive sympathetic activation in heart failure with obesity and metabolic syndrome: characteristics and mechanisms. 1743 3

Obesity and overweight, as a part of the metabolic syndrome, are well known risk factors for the development of diabetes, hypertension, coronary heart disease, hyperlipidemia, stroke, sleep apnea syndrome, osteoarthritis and certain forms of cancer. Cardiovascular disease remains the leading killer in industrialized countries, where it accounts for 40% of deaths. Obesity is defined either by increased waist circumference, waist to hip ratio, or body mass index. Obesity results from an interaction of genes and lifestyle. As people in both developed and developing countries eat more and more energy dense food, and have ever less physical activity, the number of overweight and obese people increases to epidemic proportions. Abdominal obesity plays a key role in the pathophysiology of metabolic disorders, is associated with insulin resistance, and predicts the development of type 2 diabetes and subsequent coronary artery disease. In the general population, obesity is associated with an increased mortality, but paradoxically, a positive correlation between body mass index and survival in congestive heart failure has been reported. In secondary prevention, obesity is underrecognized, underdiagnosed and undertreated in persons with cardiovascular diseases. Weight loss and prevention of weight gain have to be considered one of the most important strategies to reduce the incidence of cardiovascular disease. Increased physical activity and appropriate diet are the cornestones of treatment. Considering the high prevalence of overweight and obesity in Croatia, there is urgent necessity to improve the level of knowledge and skills in understanding obesity by health care services, and to implement appropriate professional strategy to achieve the desired lifestyle modifications.
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PMID:[Obesity--a global public health problem]. 1758 71

Urotensin II is a potent vasoconstrictive peptide that mediates both endothelium-independent vasoconstriction and endothelium-dependent vasodilatation. Its plasma level correlates positively with body weight and is raised in diabetes, renal failure, hypertension, and other cardiovascular diseases including congestive heart failure and carotid atherosclerosis. It can inhibit glucose-induced insulin secretion, and genetic variants in urotensin II gene are associated with insulin resistance and type 2 diabetes. Urotensin II also affects lipid metabolism in fish and food intake in mice. Recent studies have also demonstrated a role of urotensin II in inflammation and endothelial dysfunction. These findings suggest a close relationship between urotensin II and at least some components of the metabolic syndrome, including hypertension, insulin resistance, hyperglycemia, and inflammation.
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PMID:The role of urotensin II in the metabolic syndrome. 1761 Sep 98

This paper presents data evidence supporting the value of diagnosing and treating obstructive sleep apnea (OSA) in reducing morbidity and mortality, improving comorbid disease processes, and improving patient quality of life. These data are derived from a PubMed-based meta-analysis of recent cost effectiveness, standards of practice, and epidemiological studies of OSA, which are ranked using a hierarchical strength of recommendation taxonomy. Cost and health care utilization data have been calculated for OSA and hypersomnolence as well as for diagnostic testing. Strong evidence (which is indicated by a strength of recommendation rating of "A") exists for the association of adult OSA with obesity, daytime sleepiness, hypertension, and motor vehicular accidents. Strong evidence also exists for requiring full-night or split-night attended polysomnography (PSG) for the diagnosis and treatment of adult OSA and for patients with systolic or diastolic heart failure not responding to optimal medical management. Good evidence (B) exists for the association of adult OSA with congestive heart failure, coronary artery disease, cerebral vascular accidents, metabolic syndrome, and increased mortality. Good evidence also exists to indicate that the nonattended PSG can be used to diagnose sleep breathing disorders, that autotitration systems can be used to titrate continuous positive airway pressure (CPAP) therapy, and that the multiple sleep latency test can be used in the assessment of daytime sleepiness.
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PMID:Obstructive sleep apnea (OSA) in primary care: evidence-based practice. 1761 20

Aldosterone concentrations are inappropriately high in many patients with hypertension, as well as in an increasing number of individuals with metabolic syndrome and sleep apnoea. A growing body of evidence suggests that aldosterone and/or activation of the MR (mineralocorticoid receptor) contributes to cardiovascular remodelling and renal injury in these conditions. In addition to causing sodium retention and increased blood pressure, MR activation induces oxidative stress, endothelial dysfunction, inflammation and subsequent fibrosis. The MR may be activated by aldosterone and cortisol or via transactivation by the AT(1) (angiotenin II type 1) receptor through a mechanism involving the EGFR (epidermal growth factor receptor) and MAPK (mitogen-activated protein kinase) pathway. In addition, aldosterone can generate rapid non-genomic effects in the heart and vasculature. MR antagonism reduces mortality in patients with CHF (congestive heart failure) and following myocardial infarction. MR antagonism improves endothelial function in patients with CHF, reduces circulating biomarkers of cardiac fibrosis in CHF or following myocardial infarction, reduces blood pressure in resistant hypertension and decreases albuminuria in hypertensive and diabetic patients. In contrast, whereas adrenalectomy improves glucose homoeostasis in hyperaldosteronism, MR antagonism may worsen glucose homoeostasis and impairs endothelial function in diabetes, suggesting a possible detrimental effect of aldosterone via non-genomic pathways.
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PMID:Aldosterone and end-organ damage. 1768 82

High triacylglycerol (TAG) levels may predict vascular risk. The effect of a statin-induced reduction in TAG levels, irrespective of HDL-C increase, on clinical outcome has not yet been addressed by an endpoint study in patients with coronary heart disease (CHD). The GREACE study compared usual with structured care aimed at achieving LDL-C = 100 mg/dL (2.6 mmol/L) by dose titration with atorvastatin. All patients had CHD and were followed for 3 years. This post hoc analysis of GREACE examines the effect of statins on TAG levels and their relation with cardiovascular disease (CVD) events in all patients and in the subgroup of patients with metabolic syndrome (MetS). Baseline TAG levels >150 mg/dL (1.7 mmol/L) were predictive of subsequent CVD events [cardiac mortality, non-fatal myocardial infarction (MI), unstable angina (UA), revascularisation, congestive heart failure (CHF), and stroke] only in statin untreated patients. Stepwise regression analysis showed that with every 20% statin-related TAG reduction there was a decrease in CVD risk by 12% (HR 0.88, 95% CI 0.75-0.95, P = 0.007) in the structured care group vs. the usual care group, by 8% (HR 0.92, 95% CI 0.81-0.97, P = 0.02) in all statin treated patients vs. the untreated ones and by 15% (HR 0.85, 95% CI 0.65-0.94, P = 0.005) in those with MetS treated with a statin vs. those untreated. Using the same analysis but only taking into consideration vascular events (cardiac mortality, non-fatal MI, UA, revascularisation, and stroke) there was a 18% (HR = 0.82, 95% CI 0.57-0.96, P = 0.03) decrease in risk in the MetS (+) patients treated with a statin vs. those not on a statin, and a decrease in risk by 16% (HR = 0.84, 95% CI 0.53-1.07, P = 0.08), when only hard vascular endpoints (cardiac mortality, non-fatal MI, and stroke) were considered. TAG levels are predictive of subsequent CVD events in statin untreated CHD patients. Statin (mainly atorvastatin)-induced decrease in TAG levels was related to a significant reduction in subsequent CVD events. This benefit was more pronounced in CHD MetS (+) patients.
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PMID:Atorvastatin decreases triacylglycerol-associated risk of vascular events in coronary heart disease patients. 1771 3

The objective of this paper is to estimate the cost of obesity's contribution to the metabolic syndrome diseases in Taiwan. We used individual data from the Cardiovascular Disease Risk Factors Two-Township Study survey and medical use and expenditures data from the Bureau of National Health Insurance (NHI) of Taiwan. By adopting the prevalence-based and population attributable risk (PAR) approaches, direct costs of obesity for six kinds of obesity related metabolic syndrome diseases have been estimated. Comorbidities used in our analysis included ischemic heart diseases, congestive heart failure, cerebrovascular disease accident, diabetes, hyper-cholesterolaemia and hypertension. The results indicate that overweight and obesity are associated with a higher prevalence and costs of the metabolic syndrome related diseases. PAR increases as the obese [body mass index (BMI)] prevalence increases. About 4-9% of the costs of those diseases can be attributed to overweight (24 < or = BMI < 27) and about 7-13% and 8-19% of such costs are attributable to the first and second degree obesity (27 < or = BMI < 30 and BMI > or = 30). The cost of obesity derived from the PAR and medical costs of metabolic syndrome diseases accounts for 2.9% of the national total healthcare expenditure. We therefore conclude that overweight and obesity have increased health costs and resulted in higher prevalence of and greater costs from metabolic syndrome related diseases in Taiwan. These findings provide important support for implementing obesity prevention programs in Taiwan.
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PMID:Costs of metabolic syndrome-related diseases induced by obesity in Taiwan. 1830 2

Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Large-scale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed.
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PMID:Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components. 1859 41


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