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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 levels (MSLs) were compared in caregivers (CGs) of spouses with Alzheimer's disease who had diagnoses of coronary heart disease (CHD; n = 27) with non CGs with CHD diagnoses (n = 18), and CGs (n = 44) to non CGs (n = 52) free of CHD. MSLs were greater for CGs than non CGs, but only in persons with CHD (CHD, B for CG status = -.41; non CHD, B = .12; p < .05) at study entry (Time 1 = T1) and CHD, B = -.32; non CHD, B = .14; p < .05) 15-18 months later (Time 2 = T2). In the CHD group, MSLs were associated with poorer health habits at T1 (r = .39, p < .01), uplifts (r = -.37, p < .01) at T2, and CG status (p < .05) at T1 and T2. Relationships of CG status and MSLs declined in the presence of poor health habits at T1 and uplifts at T2. Poorer health habits and fewer uplifts may be associated with elevated MSLs in CGs with CHD.
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PMID:Coronary heart disease moderates the relationship of chronic stress with the metabolic syndrome. 984 2

Obesity is an essential risk factor for hypertension, coronary heart disease and stroke as well as for metabolic disturbances, especially for type 2 diabetes, hyper- and dyslipidemia, and it is responsible for the metabolic syndrome with insulin resistance and hyperinsulinemia. Disturbances in the lung function are also induced by obesity, as a higher risk for arthrosis on the lower extremities. Some oncological diseases like breast-, endometrial-, and prostatic cancer are associated with obesity. It is evident, that the fat distribution plays an important role in the development of obesity associated diseases: the accumulation of visceral fat has a higher risk as the peripheral fat, probably due to the different metabolism.
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PMID:[Obesity: entrance port to multimorbidity]. 988 99

Treatment of arterial hypertension is known to reduce cardiovascular morbidity and mortality and has a positive effect against stroke, where benefit is strongly linked to reduction in blood pressure per se. The protective effects against coronary heart disease (CHD) have also been significant but numerically less impressive than the effect against stroke. It is conceivable that this due to the fact that not just blood pressure, but also a number of metabolic variables need to be considered in this context. The insight that hypertension is often just one of the components of the so-called metabolic syndrome suggests that a modern antihypertensive drug should not only lower blood pressure; to exert optimal cardioprotective properties it should also have a neutral or even positive metabolic profile as regards its effects on lipids, glucose and insulin in order to achieve a better protection against CHD. Against this background the centrally acting selective imidazoline receptor (I1) agonist moxonidine is of considerable interest. Moxonidine has been shown to improve glucose tolerance in man, probably by two different mechanisms, i.e. by augmenting insulin sensitivity in peripheral tissues and by enhancing glucose-stimulated insulin release from the pancreas. By employing a therapeutic intervention against hypertension that not only lowers elevated arterial pressure but also positively affects some of the frequently occurring concomitant metabolic disturbances, it appears that today's standard of antihypertensive therapy may be surpassed in tomorrow's perspective.
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PMID:Therapy of hypertension and metabolic syndrome: today's standard and tomorrow's perspectives. 1032 50

Thrombus formation at the site of atherosclerotic lesions, especially on a ruptured plaque, plays a central role in the "atherothrombosis" hypothesis. An activation of the hemostasis and a disturbed fibrinolysis are known. These alterations are especially marked in patients with acute coronary syndromes. In stable coronary artery disease, fibrinogen is elevated. Furthermore, minor alterations of the contact phase factor VII and consecutively of the thrombin system are detectable depending on the study population. Thrombin generation and activation become marked in patients with unstable angina pectoris or acute myocardial infarction. Possible reasons for this activation are an activation of the contact phase factor XII system and the release of tissue factor both from the ruptured plaque and from stimulated monocytes. The fibrinolytic system is markedly altered already in patients with stable coronary heart disease. Increased levels of tissue-type plasminogen activator and of urokinase-type plasminogen activator/receptor are measurable in atheromas. Tissue-type plasminogen activator mass concentration is systemically elevated already at early stages of atherosclerosis. Especially in patients with increased risk for acute coronary syndromes, the plasminogen activator inhibitor activity is significantly increased. Furthermore, a hypercoagulative state with increased d-dimer levels and plasmin-antiplasmin complexes can be measured. The alterations of hemostasis and especially of fibrinolysis are detectable for prolonged time period and persist much longer than the clinical symptoms of the patients. The increased plasminogen activator inhibitor activity is associated with the metabolic syndrome and constitutes an (in part genetically determined) disturbance in patients with stable or unstable coronary heart disease. However, the large intra- und interobserver as well as diurnal variability of this marker limits its use as a routine measure for risk stratification in patients. Alterations of the hemostasis and disturbances of fibrinolysis are detectable during the chronic as well as the acute phase of atherosclerosis. These changes are best documented for coronary heart disease, whereas less data are available for other manifestations of atherosclerosis. The use of newly developed molecular markers for single reaction steps of pathways instead of global functional tests and of new molecular biological methods did considerably improve the detailed knowledge on the pathomechanisms of the development of atherosclerosis, making the development of targeted therapies, e.g., against receptors possible. Future studies will investigate the quantitative impact of the various activated pathways (cause or reaction) and the effects of interventions on these pathomechanisms in patients with acute coronary syndromes. Studies will have to focus especially on the meaning of polymorphisms, early changes in the development of atherosclerosis and interactions with inflammatory processes.
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PMID:[Blood coagulation and fibrinolysis in arteriosclerosis]. 1041 53

Of the major risk factors of coronary heart disease dyslipoproteinemia, obesity, hypertension, and diabetes are nutrition related and can be considered of metabolic origin. Dyslipoproteinemia affects 2/3 of the adult population. The risk of coronary heart disease can be decreased 2-5 fold by lowering hypercholesterinemia; atherosclerosis in the coronaries may regress and total mortality may decrease. Atherogenic dyslipidemia (i.e. hypertriglyceridaemia, low HDL cholesterol levels, elevated concentrations of small dense LDL) increases the risk as part of the metabolic syndrome. Obesity is already highly prevalent, and it is affecting ever growing proportions of the adult population. Abdominal obesity furthermore predisposes patients to complications. No effective therapy is available for obesity. 3/4 of hypertensive patients are obese and more than half of them have insulin resistance. By decreasing blood pressure, the risk of stroke decreases by about 40%, that of coronary heart disease by 14-30%. Slimming cures are the most important non-pharmacological way of treating hypertension. 5% of the population has diabetes mellitus, and a further 5% has impaired glucose tolerance. Type 2 diabetes predisposes patients to macrovascular complications. The risk of coronary heart disease can be decreased by controlling diabetes by e.g. metformin.
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PMID:[Major nutrition-related risk factors of ischemic heart disease: dyslipoproteinemia, obesity, hypertension, glucose intolerance]. 1044 32

The combination of high serum triglyceride levels and small low density lipoprotein particles, with a reduction in high density lipoprotein cholesterol levels has been named atherogenic lipoprotein phenotype or, simply, lipid triad. These lipid factors are commonly associated with peripheral resistance to the action of insulin, hyperinsulinism, central and visceral obesity, hypertension, hyperuricemia, hypercoagulability. The clustering of these nonlipid factors along with the lipid factors has been called metabolic syndrome. Insulin resistance plays a central role in the development of the lipid triad increasing the production of triglyceride-rich lipoproteins and decreasing their catabolism. There is currently great interest about the origins of the metabolic syndrome. One question under considerable research is whether genetic or acquired factors predominate in causing this syndrome. There seems to be little doubt that the metabolic syndrome taken as a whole constitutes a major risk factor for coronary heart disease. What is less certain is that each component of the syndrome is an independent risk factor. People with lipid triad are at very high risk of developing coronary heart disease, and careful management is warranted. Nonetheless, appropriate therapeutic strategies that will modify the metabolic syndrome as a whole are needed. More investigations about key metabolic steps that simultaneously affect multiple pathways will be required to yield a satisfactory therapy for high risk patients exhibiting the metabolic syndrome.
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PMID:[Atherogenic dyslipidemia, metabolic syndrome and cardiovascular risk]. 1063 48

Seroepidemiologic studies have provided information on the association of Chlamydia pneumoniae with the classical risk factors of coronary heart disease (CHD). C. pneumoniae infections are more common in smokers than in nonsmokers, suggesting that smoking predisposes to the development of chronic infection. Infections may also affect lipid metabolism. In persons with acute pneumonia caused by C. pneumoniae, high-density lipoprotein (HDL) values are lower and triglyceride values higher than seen in pneumonia caused by viruses and other bacteria. Furthermore, chronic C. pneumoniae infection is associated with elevated triglyceride and lowered HDL levels in healthy Finnish men. Recent studies also suggest that chronic C. pneumoniae infection considerably enhances the effect of the metabolic syndrome on the CHD risk. Thus, known CHD risk factors may be partly explained by their association with chronic C. pneumoniae infection. Further studies are needed to elucidate the pathogenetic mechanisms underlying these associations.
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PMID:Chlamydia pneumoniae and other risk factors for atherosclerosis. 1083 26

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear. Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered. One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.
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PMID:Visceral fat and insulin resistance--causative or correlative? 1088 95

The increased risk of coronary heart disease associated with the metabolic syndrome may be partially explained by prothrombotic deviations of the haemostatic system. Individuals with insulin resistance, dyslipidaemia and obesity are characterized by elevated plasma fibrinogen and factor VII coagulant activity levels and raised concentrations of plasminogen-activator inhibitor, the main inhibitor of endogenous fibrinolysis. These haemostatic abnormalities may be corrected with dietary treatment of the underlying clinical disorder. Dietary trials of diseased and healthy volunteers suggest that the optimal antithrombotic diet is a low-fat diet with a high content of foods rich in complex carbohydrates and dietary fibre. The dietary fatty acid composition has a profound effect on blood lipids, but seems of minor importance for the haemostatic system.
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PMID:Dietary treatment of thrombogenic disorders related to the metabolic syndrome. 1088 2

Data from the Whitehall II Study and others have demonstrated a role for the metabolic syndrome and fibrinogen underlying the association between social position and coronary heart disease. In this study, we examined the role of an additional hemostatic factor and marker of endothelial dysfunction, von Willebrand factor (vWF). Four thousand five hundred and forty-eight men and 1837 women were examined in the third phase of the study, which took place between 1991 and 1993. Employment grade was used as a measure of socioeconomic position. An inverse relation between employment grade and vWF was evident (P<0.0003). This employment grade gradient was apparent overall, and the relation persisted even when nonsmokers and participants with poor health were removed from the analyses (P=0.02). The difference between the highest (unified grades 1 to 6) and lowest (clerical/support) employment grades in vWF concentrations was 8.9 IU/dL (95% CI 6.0, 11.8; P<0.001) for men and 6.9 IU/dL (95% CI 4.0, 9.7; P=0.06) for women. vWF was associated with a number of biological factors that themselves showed an employment grade gradient, including fibrinogen (P<0.001), fasting and postload glucose (P<0.05) levels, and fasting and postload insulin (P<0.01) levels. Associations with smoking and alcohol intake were apparent. Smoking showed a threshold effect, such that only men who smoked >21 cigarettes per day produced a significantly increased vWF level (P<0.05) compared with lighter smokers. The health-related behaviors explained 25% of the grade gradient in men and 28% in women, while the biological factors accounted for 32% in men and 22% in women. We conclude that there is a grade gradient in vWF that was not fully explained by health-related behaviors and risk factors for coronary heart disease. These data are consistent with the hypothesis that endothelial dysfunction is part of the explanation for social inequalities in cardiovascular disease.
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PMID:Social determinants of von willebrand factor: the Whitehall II study. 1089 27


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