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)

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

To assess the prevalence of metabolic syndrome (MS) and estimates of global risk by Framingham Risk Score in young subjects with acute myocardial infarction (MI), we assessed metabolic parameters and global risk assessment in 165 consecutive subjects who presented with myocardial infarction prior to 45 years of age. Nearly 80% of subjects were overweight or obese and at least one cardiovascular risk factor was present in 96% of patients. MS with or without overt diabetes was present in nearly two thirds of subjects. Excluding subjects with diabetes, the mean 10-year Framingham Risk Score estimate in the total cohort was 9.3%, with only 17.1% of subjects having a 10-year risk greater than 20%. Only 28% of subjects with MS had a Framingham Risk Score greater than 20%. Although MS is present in nearly two thirds of young patients with premature myocardial infarction, the Framingham Risk Score appears to underestimate global cardiovascular risk in this population.
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PMID:Prevalence of metabolic syndrome in young patients with acute MI: does the Framingham Risk Score underestimate cardiovascular risk in this population? 1705 30

Atherothrombotic vascular disease is a complex disorder in which inflammation and coagulation play a pivotal role. Rupture of high-risk, vulnerable plaques with the subsequent tissue factor (TF) exposure is responsible for coronary thrombosis, the main cause of unstable angina, acute myocardial infarction, and sudden cardiac death. Tissue factor (TF), the key initiator of coagulation is an important modulator of inflammation. TF is widely expressed in atherosclerotic plaques and found in macrophages, smooth muscle cells, extracellular matrix and acellular lipid-rich core. TF expression can be induced by various stimulants such as C-reactive protein, oxLDL, hyperglycemia and adipocytokines. The blood-born TF encrypted on the circulating microparticles derived from vascular cells is a marker of vascular injury and a source of procoagulant activity. Another form of TF, called alternatively spliced has been recently identified in human and murine. It is soluble, circulates in plasma and initiates coagulation and thrombus propagation. Evidence indicates that elevated levels of blood-borne or circulating TF has been associated with metabolic syndrome, type 2 diabetes and cardiovascular risk factors and is a candidate biomarker for future cardiovascular events. Therapeutic strategies have been developed to specifically interfere with TF activity in the treatment of cardiovascular disease.
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PMID:Atherothrombosis: role of tissue factor; link between diabetes, obesity and inflammation. 1724 34

Little information is available regarding the clinical effect of metabolic syndrome (MS) or its combined effect with smoking on subsequent cardiac events after acute myocardial infarction (AMI). To examine whether MS independently predicts cardiac events (cardiac death and nonfatal reinfarction) and to assess the combined effect of MS and smoking on cardiac events after AMI, we studied 3,858 survivors of AMI registered in the Osaka Acute Coronary Insufficiency Study (OACIS). During a median follow-up of 725 days, the incidence of cardiac events was higher in patients with MS than in those without MS (p=0.021). After adjustment for baseline characteristics, MS was an independent predictor of cardiac events after AMI (hazard ratio [HR] 1.480, 95% confidence interval [CI] 1.128 to 1.942, p=0.005). Compared with patients who did not have MS and were nonsmokers, the adjusted HR for cardiac events was 2.868 (95% CI 1.573 to 5.227, p=0.001) in patients with MS who continued smoking after AMI. Cessation of smoking after AMI was associated with a significantly lower risk of cardiac events in patients with MS (HR 0.485, 95% CI 0.281 to 0.837, p=0.009) but not in patients without MS (HR 0.618, 95% CI 0.330 to 1.157, p=0.132). In conclusion, MS is independently associated with an increased risk of cardiac events after AMI. Smoking has an additive adverse effect on cardiac events after AMI, and cessation of smoking is beneficial and strongly recommended for AMI, especially in patients with MS.
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PMID:Clinical impact of metabolic syndrome and its additive effect with smoking on subsequent cardiac events after acute myocardial infarction. 1739 77

Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. Cholesterol and vitamin D share the 7-dehydrocholesterol metabolic pathway. This study evaluated the possible effect of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. After diagnosis, patients received atorvastatin as secondary prevention. Serum vitamin D was measured by high-performance liquid chromatography at baseline and at 12 months. Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels (41+/-19 vs 47+/-19 nmol/L, p=0.003). Vitamin D deficiency was decreased by 75% to 57% at 12 months. In conclusion, atorvastatin increases vitamin D levels. This increase could explain some of the beneficial effects of atorvastatin at the cardiovascular level that are unrelated to cholesterol levels.
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PMID:Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease. 1792 Mar 83

Despite optimal therapy, the morbidity and mortality of coronary heart disease (CHD) remains significant, particularly in patients with diabetes or the metabolic syndrome. New strategies for cardioprotection are therefore required to improve the clinical outcomes in patients with CHD. Ischaemic preconditioning (IPC) as a cardioprotective strategy has not fulfilled it clinical potential, primarily because of the need to intervene before the index ischaemic event, which is impossible to predict in patients presenting with an acute myocardial infarction (AMI). However, emerging studies suggest that IPC-induced protection is mediated in part by signalling transduction pathways recruited at time of myocardial reperfusion, creating the possibility of harnessing its cardioprotective potential by intervening at time of reperfusion. In this regard, the recently described phenomenon of ischaemic postconditioning (IPost) has attracted great interest, particularly as it represents an intervention, which can be applied at time of myocardial reperfusion for patients presenting with an AMI. Interestingly, the signal transduction pathways, which underlie its protection, are similar to those recruited by IPC, creating a potential common cardioprotective pathway, which can be recruited at time of myocardial reperfusion, through the use of appropriate pharmacological agents given as adjuvant therapy to current myocardial reperfusion strategies such as thrombolysis and primary percutaneous coronary intervention for patients presenting with an AMI. This article provides a brief overview of IPC and IPost and describes the common signal transduction pathway they both appear to recruit at time of myocardial reperfusion, the pharmacological manipulation of which has the potential to generate new strategies for cardioprotection.
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PMID:Preconditioning and postconditioning: new strategies for cardioprotection. 1782 79

The prevalence of metabolic syndrome (MS) was determined in patients aged < or =45 years who presented with acute myocardial infarction and underwent primary percutaneous coronary intervention. Two hundred twenty-three consecutive patients aged 18 to 45 years who underwent cardiac catheterization for acute myocardial infarction from June 2001 to December 2004 were reviewed. MS was diagnosed by National Cholesterol Education Program Adult Treatment Panel III guidelines (modified by substituting body mass index > or =28.8 kg/m2 for waist circumference). One hundred sixty-one patients met all 5 criteria for MS available for evaluation. Seventy-six of these patients (47%) met > or =3 of the 5 criteria for MS. Sixteen patients with MS (21%) and 5 patients without MS (6%) had diabetes mellitus. The prevalence of each criterion was significantly higher (p <0.05) in the MS group. Average Framingham risk scores were 7.0 and 4.5 for patients with and without MS, respectively. The prevalence of smoking, male gender, and family history of premature coronary artery disease were the same for the 2 groups. In conclusion, MS was highly prevalent in this population of young patients with acute myocardial infarction.
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PMID:Prevalence of metabolic syndrome in patients < or =45 years of age with acute myocardial infarction having percutaneous coronary intervention. 1788 60

Several large-scale clinical trials have assessed the efficacy of atorvastatin in the primary and secondary prevention of cardiovascular events in patients with diabetes mellitus and/or metabolic syndrome. In primary prevention, CARDS (Collaborative Atorvastatin Diabetes Study) showed that atorvastatin 10 mg/day (vs placebo) reduced relative risk of the composite primary endpoint (acute coronary heart disease [CHD] events, coronary revascularisation, or stroke) by 37% (p = 0.001). This decrease was similar to decreases in major cardiovascular events in the ASCOT-LLA (Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm) trial and HPS (Heart Protection Study). However, in CARDS, atorvastatin efficacy was evident as early as 6 months after starting treatment, whereas in HPS, simvastatin efficacy was noticeable only from about 15-18 months after starting treatment. In the ASCOT-LLA trial, in 2226 hypertensive diabetic patients without previous cardiovascular disease, atorvastatin (vs placebo) reduced the relative risk of all cardiovascular events and procedures by 25% (p = 0.038). In secondary prevention, substudies of the GREACE (GREek Atorvastatin and Coronary-heart-disease Evaluation), TNT (Treating to New Targets) and PROVE-IT (PRavastatin Or atorVastatin Evaluation and Infection Therapy) trials reported results for the approximately 15-25% of study participants who had diabetes. In the GREACE substudy, atorvastatin (vs physicians' standard care) significantly reduced the relative risk of total mortality by 52% (p = 0.049), coronary mortality by 62% (p = 0.042), coronary morbidity by 59% (p < 0.002) and stroke by 68% (p = 0.046). In the TNT substudy, incidence of the primary endpoint was significantly lower in diabetic patients treated with atorvastatin 80 mg/day rather than 10 mg/day (13.8% vs 17.9%; relative risk 0.75; p = 0.026). In the PROVE-IT substudy, a significantly lower incidence of acute cardiac events was reported for atorvastatin versus pravastatin recipients (21.1% vs 26.6%; p = 0.03) and, therefore, an absolute risk reduction of 5.5% was associated with atorvastatin therapy. ASPEN (Atorvastatin Study for Prevention of coronary heart disease Endpoints in Non-insulin-dependent diabetes mellitus) - a mixed primary and secondary prevention trial in diabetic patients - found that a 29% lower low-density lipoprotein-cholesterol level was seen with atorvastatin than placebo at endpoint (p < 0.0001); however, the reduction in composite primary endpoint of major cardiovascular events (cardiovascular mortality, nonfatal major cardiovascular event or stroke, and unstable angina requiring hospitalisation) with atorvastatin (13.7% vs 15.0% with placebo), and reduction in acute myocardial infarction relative risk of 27% with atorvastatin were not statistically significant. In CHD patients with metabolic syndrome (n = 5584) in a sub-analysis of the TNT trial, intensive versus lower-dosage atorvastatin therapy reduced the relative risk of major cardiovascular and cerebrovascular events by 29% (p < 0.0001). The analysis also revealed that CHD patients with, rather than those without, metabolic syndrome had a 44% greater level of absolute cardiovascular risk, thus clearly underscoring the clinical feasibility of administering intensive lipid-lowering therapy to CHD patients with metabolic syndrome. In summary, several patient populations, from definitive, large-scale studies, are now available to corroborate the integral place of atorvastatin--in line with various regional and internationally accepted disease management guidelines--in the primary and secondary prevention of cardiovascular events in patients with diabetes and/or metabolic syndrome.
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PMID:Atorvastatin efficacy in the prevention of cardiovascular events in patients with diabetes mellitus and/or metabolic syndrome. 1791 May 20

The -1131C is a naturally occurring variant of the apolipoprotein A5 (ApoA5) gene, which has been shown to associate with increased triglyceride levels. This variant has also been shown to confer risk for development of ischemic heart disease and stroke. The gene is in linkage disequilibrium with factors known to correlate with impaired glucose homeostasis. These observations prompted us to study the prevalence of the ApoA5 -1131C allele in patients with metabolic syndrome. A total of 201 metabolic syndrome patients and 210 controls were studied. In both groups the triglyceride levels of patients with -1131C allele were significantly increased compared to the subjects with -1131T allele (3.22+/-0.43 mmol/l vs. 2.24+/-0.12 mmol/l, p<0.01 in the metabolic syndrome patients; 2.10+/-0.19 mmol/l vs. 1.22+/-0.05 mmol/l, p<0.01 in the controls). In metabolic syndrome patients the prevalence of the ApoA5 -1131C variant was increased compared to the healthy controls (11% vs. 6.20%). Multiplex regression analysis model adjusted for age, gender, serum total cholesterol levels, acute myocardial infarction and stroke events revealed that the examined ApoA5 variant confers risk for the development of metabolic syndrome: the odds ratio at 95% confidence interval was 3.622 (1.200-10.936), p=0.02. Our findings strongly suggest that this variant is a risk factor for the development of hypertriglyceridemia and metabolic syndrome.
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PMID:Apolipoprotein A5 T-1131C variant confers risk for metabolic syndrome. 1792 54

Metabolic syndrome (MS) induces an increase in oxidative stress and may be an important contributory factor for coronary artery disease (CAD). Telomere shortening of endothelial progenitor cells (EPCs) may be the key factor in endothelial cell senescence. The rate of telomere shortening is highly dependent on cellular oxidative damage. This study analyzed the relationship between telomere shortening and oxidative DNA damage in EPCs obtained from CAD patients with MS and without MS. We analyzed circulating EPCs in peripheral blood obtained from 57 patients with CAD (acute myocardial infarction [AMI], n=26; stable angina pectoris [AP], n=31) and 21 age-matched healthy subjects (control). Telomere length and telomerase activity were significantly lower in CAD patients than in controls, and were lower in AMI patients than in AP patients. Oxidative DNA damage was higher in CAD patients compared with controls, and oxidative DNA damage in AMI patients was also higher than in AP patients. There was a negative correlation between telomere length and oxidative DNA damage. Telomere length and telomerase activity were lower in CAD patients with MS than in those without MS. Oxidative DNA damage in CAD patients with MS was higher than in those without MS. In our in vitro study, oxidative treatments induced telomere shortening and decrease in telomerase activity of EPCs. These results suggest that EPC telomere shortening via increased oxidative DNA damage may play an important role in the pathogenesis of CAD. In addition, MS may be related to increased oxidative DNA damage and EPC telomere shortening.
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PMID:Association between oxidative DNA damage and telomere shortening in circulating endothelial progenitor cells obtained from metabolic syndrome patients with coronary artery disease. 1798 21


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