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

Metabolic syndrome is associated with elevated morbidity and mortality for overt coronary artery disease (CAD). In diabetic patients, CAD is often silent. The relation between metabolic syndrome and silent CAD has never been studied. We investigated whether metabolic syndrome is associated with silent CAD in patients with type 2 diabetes mellitus. We evaluated the prevalence of metabolic syndrome in 169 patients with uncomplicated diabetes and angiographically verified silent CAD and in 158 diabetic patients without myocardial ischemia on exercise electrocardiography, 48-hours ambulatory electrocardiography, and stress echocardiography. The groups were comparable for gender, age, glycemic control, and diabetes duration. Metabolic syndrome was defined according to the National Cholesterol Education Program criteria. To estimate insulin resistance in patients treated with diet alone or oral agents (122 patients with CAD and 115 patients without CAD), the Homeostasis Model Insulin-Resistance Assessment (HOMA) was used. The prevalence of metabolic syndrome (59.8% vs 44.3%, p = 0.005) and HOMA (5.4 +/- 2.1 vs 4.9 +/- 2.8, p = 0.044) were significantly higher in those with CAD than in those without CAD. Multiple logistic regression analysis showed that the metabolic syndrome was associated with silent CAD (odds ratio 2.44, 95% confidence interval 1.19 to 5.02, p = 0.015). Among patients on diet alone or oral agents, the HOMA was the strongest predictor of silent CAD (odds ratio 10.16, 95% confidence interval 2.60 to 39.63, p < 0.001). In conclusion, our data have shown an independent association of metabolic syndrome and insulin resistance with silent CAD in patients with type 2 diabetes mellitus. Other studies are needed to establish whether metabolic syndrome and HOMA are reliable markers to identify diabetic patients for additional screening for silent CAD.
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PMID:Association of the metabolic syndrome and insulin resistance with silent myocardial ischemia in patients with type 2 diabetes mellitus. 1644 69

Development of coronary collaterals (CCs) is triggered by the gradient between arteries due to obstruction and myocardial ischemia. Presence of CCs that feed the jeopardized myocardial area may limit the infarct size after coronary occlusion and may even provide a survival benefit. However, some patients develop good CCs, whereas others do not. The metabolic syndrome (MS) has been identified as a secondary target to decrease cardiovascular risk, although the effect of MS on development of CCs has not been investigated. We prospectively enrolled 596 consecutive patients (337 men and 259 women; mean age 56 +/- 8 years) who underwent coronary angiography at our center and were found to have total occlusion of the right coronary artery. Patients were then classified as having good CCs (Rentrop's grades 2 to 3) or poor CCs (Rentrop's grades 0 to 1). There were significant differences in terms of body mass index (kilograms of body weight divided by square meters of height), glucose levels, triglyceride levels, and years with angina pectoris between those with good and poor CCs. Prevalences of diabetes mellitus were 27.1% among patients with good CCs and 44% among those with poor CCs (p <0.001). Presence of MS was significantly higher in patients with poor CCs than in those with good CCs (78.4% vs 49.2%, p <0.001). In regression analysis, duration of angina pectoris (beta = 0.347, 95% confidence interval [CI] 0.266 to 0.453, p <0.001), presence of diabetes mellitus (beta = 1.829, 95% CI 1.021 to 3.279, p = 0.042), wall score (beta = 2.379, 95% CI 1.356 to 4.173, p = 0.003), and presence of MS (beta = 2.993, 95% CI 1.541 to 5.813, p = 0.001) were independent predictors of angiographically determined poor CCs. In conclusion, MS seems to be independently associated with poor CCs in patients with an occluded right coronary artery.
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PMID:Relation of coronary collateral vessel development in patients with a totally occluded right coronary artery to the metabolic syndrome. 1649 Apr 28

There is ample evidence from many epidemiological studies that lower urinary tract symptoms (LUTS) and sexual dysfunction are strongly linked, independently of age and comorbidities such as hypertension, diabetes, dyslipidaemia and coronary heart disease. However, a causal link between both conditions is not yet established. Four pathophysiological mechanisms currently support the relationship between LUTS and erectile dysfunction (ED): (i) The nitric oxide synthase (NOS)/NO theory; there is a reduction in NOS-containing nerves in the prostate and bladder/urethra in patients with bladder outlet obstruction (BOO), and that lack of NO or loss of protein kinase G causes ED; (ii) The autonomic hyperactivity and metabolic syndrome hypothesis: benign prostatic hyperplasia (BPH) may be part of the metabolic syndrome, which includes cardiovascular diseases (e.g. hypertension, ischaemic heart disease) and diabetes mellitus, known risk factors for ED. Hypertension, obesity, and hyperinsulinaemia have all been claimed to be associated with an increased sympathetic activity. Increased sympathetic activity is involved in LUTS/BPH and may have a role in ED/sexual dysfunction, with noradrenaline and alpha1-adrenoceptors representing a common link; (iii) the Rho-kinase activation/endothelin pathway; there can be increased Rho-kinase activity, and consequently calcium sensitivity of the contractile machinery, in prostate smooth muscle in BPH, the detrusor in BOO, corpora cavernosa in ED, and in the resistance vessels in hypertension. The actions of several factors beside noradrenaline (e.g. endothelin-1, angiotensin II), possibly involved in the increased smooth muscle activity found in both LUTS/BPH and sexual dysfunction, are dependent on Rho-kinase activity. Thus increased Rho-kinase activity might represent a common link between LUTS and sexual dysfunction; (iv) Pelvic atherosclerosis; animal models mimicking pelvic ischaemia and hypercholesterolaemia show similar smooth muscle alterations of the detrusor and corpora. Pelvic ischaemia may induce the biological modifications described above and may thus represent as well a common link between LUTS and sexual dysfunction. Studies treating one condition (e.g. ED) and measuring the impact on the other (e.g. LUTS) should further contribute to support this common link.
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PMID:Lower urinary tract symptoms and sexual dysfunction: epidemiology and pathophysiology. 1650 50

Patients with ischaemic heart disease commonly have an impaired glucose tolerance. On the 2004 congress of the ESC, the 75-75-rule was announced, indicating that 75% of all diabetics die of cardiovascular complications, and that 75% of all patients with myocardial infarction have diabetes or an (often undiagnosed) impaired glucose tolerance. Data of our "Esslinger Koronarregister" confirm that diabetics and in particular women with diabetes have a higher mortality both after STEMI and NSTEMI. During acute myocardial infarction, a higher blood glucose level strongly correlates with increased mortality. This increased blood glucose level on the one hand is due to preexisting diabetes mellitus or metabolic syndrome, but on the other hand may be a marker of larger myocardial damage with excess katecholamine release. Recent data indicate that intensive glucose control results in a reduction of cardiovascular risk, e. g. the risk of sudden cardiac death. The data presented show that an early intervention in preclinical diabetics aiming at normalization of blood glucose control is necessary in order to reduce cardiovascular mortality.
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PMID:[Impaired glucose metabolism in patients with ischaemic heart disease]. 1659 58

There is a considerable body of evidence supporting an association between hypertriglyceridaemia, a hypercoagulable state and atherothrombosis. A disorder of triglyceride metabolism is a key feature of the metabolic syndrome that increases risk of both ischaemic heart disease and type 2 diabetes approximately 3-fold. An increasing prevalence of obesity and metabolic syndrome is likely to contribute markedly to the prevalent ischaemic heart in the foreseeable future, and therefore it is crucial to understand mechanisms linking hypertriglyceridaemia and a hypercoagulable state. Activation of platelets and the coagulation cascade are intertwined. VLDL and remnant lipoprotein concentrations are often increased with the metabolic syndrome. These lipoproteins have the capacity to activate platelets and the coagulation pathway, and to support the assembly of the prothrombinase complex. VLDL also upregulates expression of the plasminogen activator inhibitor-1 gene and plasminogen activator inhibitor-1 antigen and activity, a process accompanied by platelet aggregation and clot formation. The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. Fibrinolysis is also less efficient when thrombin is generated. Thrombin induces thrombin activatable fibrinolysis inhibitor. Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. Thus the evidence is supportive of dysregulated coagulation, and impaired fibrinolysis with a predisposition to atherothrombosis, in conditions such as the metabolic syndrome, in which there are increased concentrations of VLDL and remnant lipoproteins. The purpose of this review is to describe the current evidence supporting a procoagulant state induced by VLDL and remnant lipoproteins. The role of these lipoprotein classes in (1) platelet activation; (2) the intrinsic coagulation cascade, and (3) clot formation and fibrinolysis is discussed.
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PMID:Effects of VLDL and remnant particles on platelets. 1687 77

The risk factors, such as hypertension and metabolic syndrome, tend to promote heart pathology. These risk factors can aggravate concomitant heart insults as well. Diabetes mellitus represents one of the most important risk factors for the development of heart pathology. By itself it represents a source of vascular and heart dysfunction through formation of reactive oxygen species (ROS) and can compromise the recovery from cardiovascular diseases. This review focuses on the evidence that cellular oxidative stress is the leading cause of the worst outcome of myocardial infarction (MI) in diabetics. Hyperglycemia is viewed in this article as the primary mediator of a cascade of heart damaging events, starting from ROS formation and leading to myocardial ischemia, inflammation and death of myocytes. This article also provides insights into why diverse therapeutic interventions, which have in common the ability to reduce oxidative stress and inflammation, can impede or delay the onset of complications of myocardial infarction in diabetic patients.
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PMID:Oxidative stress as the leading cause of acute myocardial infarction in diabetics. 1696 22

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

To explore the association of job strain with CHD and metabolic syndrome in municipal workers. A cross-sectional study was completed of 450 male workers. Coronary heart disease was defined as: physician diagnosed ischemic heart disease; and/or, ischemic findings in the ECG. Metabolic syndrome was defined according to the criterion set by the National Cholesterol Education Panel. The demand-control model was used to assess job strain. Self administered questionnaires were completed after a face to face interview. Logistic regression models were constructed to assess the association of job strain with CHD and metabolic syndrome. The prevalence of metabolic syndrome and CHD were 17.8% and 8.0% respectively. Both CHD and metabolic syndrome were found to be significantly higher in higher income groups. Job demand and job control were not found to be associated with either CHD or metabolic syndrome. Metabolic syndrome was significantly more prevalent among the high job strain workers, but the significance was lost when controlled for age. The findings suggest that there is no significant association between job strain and metabolic syndrome and CHD in this sample of Turkish workers. Job strain may possibly be perceived differently in different cultures and occupations. Future studies may benefit from using a combination of different stress models and more diverse study populations.
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PMID:The association of job strain with coronary heart disease and metabolic syndrome in municipal workers in Turkey. 1705 99

Using non-cholesterol sterols investigation several authors postulated a hypothesis that in the metabolic syndrome cholesterol endogenous synthesis is increased and its absorption decreased. Our study is the first attempt to evaluate the direct relation of cholesterol metabolism to the principal pathogenetic phenomenon of the metabolic syndrome--namely to insulin resistance. We have measured insulin sensitivity by two methods--Quicki (Quantitative Sensitivity Check Index) and intravenous insulin tolerance test (Kitt) and 3 indirect markers--fasting insulin level, fasting C-peptide level and SHBG (sex hormone binding globulin). The investigation was performed in three groups of subjects with a different prevalence of insulin resistance: 72 non-diabetics with ischemic heart disease, 117 young blood donors and 63 type 2 diabetics on diet therapy only. Analyzing altogether 60 relationships--between four sterols (lathosterol, squalene, sitosterol and campesterol) and five markers of insulin resistance in three groups of subjects--we have found only six significant relations between cholesterol synthesis and absorption and insulin resistance in all groups of patients. Our results indicate that there exists a significant relationship between insulin sensitivity and indices of either increased cholesterol synthesis or decreased cholesterol absorption. Insulin resistance explains only a part of both abnormalities mentioned above.
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PMID:Relation of cholesterol metabolism and non-cholesterol sterols to insulin resistance. 1708

The aim of the present study was to evaluate the relation among alcohol consumption, the metabolic syndrome, and the risk of ischemic heart disease (IHD). The study was conducted in a cohort of 1966 men from the Quebec Cardiovascular Study. All men were initially free of IHD and, during the follow-up period of 13 y, 219 first cases of IHD were diagnosed. Alcohol consumption was determined by calculating the g/d intake based on standard portions of beer, wine, and spirits. Metabolic syndrome was diagnosed according to a modification of the National Cholesterol Education Program Adult Treatment Panel III definition. Men who consumed >or=15.2 g of alcohol/d (4th quartile of the distribution) were younger (P < 0.001), had elevated plasma HDL-C concentrations (P < 0.001), and lower plasma concentrations of insulin (P = 0.01), CRP (P = 0.01), and fibrinogen (P < 0.001) than men in the 1st quartile (<1.3 g of alcohol/d). After adjustment for a series of coronary risk factors, alcohol consumption >or=15.2 g/d was associated with a 39% reduction in the 13-y risk of IHD [relative risk (RR) of IHD = 0.61, P = 0.02]. Finally, an alcohol consumption <15.2 g/d was associated with an increase of the risk of IHD in men with the metabolic syndrome (RR = 2.24, P < 0.001) but not in men without the metabolic syndrome (RR = 1.31, P = 0.22). These results confirm that moderate daily alcohol consumption has cardioprotective properties and suggest that the effects may be more important in subjects with a deteriorated risk profile, such as those with the metabolic syndrome.
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PMID:Moderate alcohol consumption is more cardioprotective in men with the metabolic syndrome. 1711 15


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