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

HYPERTENSION-ASSOCIATED ABNORMALITIES THAT PROMOTE CORONARY DISEASE: Although antihypertensive treatment has been effective in reducing premature cardiovascular mortality, the effect on various organ-specific morbid events has been unequal; the effect is much more impressive on stroke reduction than on reduction of coronary events. A student of pathophysiology would have anticipated such an outcome since blood pressure elevation is only one of multiple abnormalities in hypertension. Even in its mildest form hypertension is associated with the metabolic syndrome of dyslipidemia/insulin resistance which is conducive to early atherosclerosis. A large proportion of patients also have increased sympathetic and decreased parasympathetic tone, a constellation conducive to arrhythmias and, ultimately, to sudden death. An elevated hematocrit is also found in a substantial proportion of male patients and excessive platelet aggregability has also been described in hypertension. These hematologic abnormalities are conducive to coronary thrombosis. Angiotensin II and norepinephrine, two of the most potent trophic hormones, are frequently elevated in hypertension. The effect of these hormones on the cardiac and vascular structure further increases the predilection for negative outcomes. Left ventricular hypertrophy is a potent risk factor of coronary mortality, congestive heart failure and sudden death. Vascular hypertrophy reduces the coronary reserve and at the level of skeletal muscles contributes to the evolution of the metabolic syndrome. ORGAN-SPECIFIC HYPERTENSION TREATMENT: Because of these abnormalities we are entering a new era of treatment in hypertension. Whereas an effective fall in blood pressure remains the main goal of treatment, differential effects of various antihypertensive agents on organ-specific morbidity are being actively explored. If this research proves that certain drugs have a specific advantage in defined subgroups of patients, clinical practice will change. It is reasonable to expect that in the next century we will witness a further improvement in the impact of antihypertensive treatment on public health.
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PMID:Coronary disease in hypertension: a new mosaic. 921 91

Mortality from coronary heart disease (CHD), stroke and end-stage renal failure are high in South Asian migrants in the UK. This is associated with high prevalence of diabetes and hypertension. These seem to be manifestations of a metabolic syndrome with insulin resistance (hyperinsulinaemia) and central obesity (based on high waist-to-hip ratio rather than on conventional measures of body mass index). This is associated with sedentary lifestyle, high serum triglycerides and low HDL-cholesterol. Mortality from stroke and end-stage renal failure are high in black migrants to the UK (both Caribbeans and West Africans). However, CHD mortality is low in this group. This pattern of mortality is associated with high prevalence of hypertension and diabetes. This group tends to be obese (particularly women) according to conventional measures of body mass index and to have hyperinsulinaemia, low serum triglycerides and high HDL-cholesterol. Conventional risk factors such as cigarette smoking and hypercholesterolaemia are less prevalent in ethnic minority populations in the United Kingdom and unlikely to explain the differences seen between groups, although each risk factor is likely to contribute to the variation in vascular disease within each group. There is difficulty in reconciling the results of migration studies (eg, from rural to urban environments) pointing to major environmental influences on the changes in cardiovascular risk factors with the consistent pattern of disease of ethnic groups across the world and in subsequent generations, suggesting a certain degree of genetic susceptibility. Important environment-gene interplays might be underlying some of these processes. The detection and management of hypertension and diabetes are still unsatisfactory in inner city areas and show variations by ethnic origin. Strategies for the control of CHD and stroke adopted in European countries directed mostly to white populations may be inappropriate for ethnic minority populations.
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PMID:Ethnicity and cardiovascular risk: variations in people of African ancestry and South Asian origin. 936 74

Estradiol-17 beta has beneficial effects on a range of metabolic risk factors for coronary heart disease and the decline in estrogen concentrations at the menopause would be expected to have adverse effects. Review of the literature on effects of the menopause and of estradiol-17 beta provides evidence for the following changes occurring at or after the menopause: increased total cholesterol and triglycerides; decreased high density lipoprotein (HDL) and HDL subfraction 2; increased low density lipoprotein, particularly in the small, dense subfraction; increased lipoprotein (a); increased insulin resistance; decreased insulin secretion; decreased insulin elimination; increased android fat distribution; impaired vascular function; increased factor VII and fibrinogen, and reduced sex-hormone binding globulin. Many of these changes will themselves have adverse effects on other metabolic risk factors. This complex of inter-correlated adverse changes in metabolic risk factors justifies identification of a distinct menopausal metabolic syndrome which originates in estrogen deficiency and which could contribute to the increased risk of coronary heart disease seen in postmenopausal women. Estrogen replacement can diminish the expression of this syndrome.
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PMID:Is there a menopausal metabolic syndrome? 938 35

In an attempt to better understand the genetic basis of the metabolic syndrome, we have undertaken a series of studies on the familial aggregation in the clustering of the coronary heart disease risk factors which characterize this syndrome. In the present study, the hypothesis of shared genetic (pleiotropy) and/or environmental factors between body fat and blood lipids is investigated by examining cross-trait (eg, father's body fat with his son's blood lipid) familial resemblance between 4 indicators of body fat (body mass index [BMI], sum of 6 skin folds [SF6]) and fat distribution (the ratio of the trunk to extremity skin folds adjusted [TER-sf] and unadjusted [TER] for SF6), and 5 blood lipid variables (total cholesterol [CH], triglycerides [TG], cholesterol associated with high-density lipoproteins [HDL], the CH/ HDL ratio and the difference between CH and HDL [CH-HDL]) measured in 1239 individuals from 309 families participating in the Quebec Family Study. A bivariate correlation model was used to obtain maximum likelihood estimates of cross-trait spouse, parent-offspring, and sibling correlations after adjustment of body fat and lipid data for the effects of age, separately in the four sex-by-generation groups. Likelihood ratio tests revealed the presence of significant (P < .05) cross-trait resemblance between body fat (BMI and SF6) and all lipid traits except CH and also between fat distribution (TER and TER-sf) and CH/HDL and CH-HDL. Only sibling cross-trait correlations were significant for all body fat-lipid pairs of measures, with bivariate familiality estimates (i.e., shared genetic and/or environmental factors) ranging from 8% to 40%. Although the hypothesis of genetic pleiotropy cannot be ruled out from the pattern of cross-trait correlations found in the present study, we conclude that environmental factors shared within sibships are probably more important than common genes in determining the covariation between body fat and blood lipids.
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PMID:Cross-trait familial resemblance for body fat and blood lipids: familial correlations in the Quebec Family Study. 940 22

Syndromes of risk factor disturbance may contribute to the development of coronary heart disease and non-insulin-dependent diabetes mellitus, but their definition and quantification remain problematic. Using factor analysis, constellations of risk factor variables that could indicate distinct syndromes of metabolic disturbance were explored in the baseline data of the first follow-up cohort of 742 men from the Heart Disease and Diabetes Risk Indicators in a Screened Cohort (HDDRISC) study. The primary analysis considered 16 intercorrelated variables measured in more than 90% of cohort participants. A missing-values estimation routine was used to ensure inclusion of all participants in the analysis. Subanalyses were undertaken, including a repeat of the primary analysis on the 522 individuals who had received measurement of HDL cholesterol, an oblique rather than orthogonal factor rotation procedure performed on primary and HDL subset analyses, a repeat of these two primary and HDL subset analyses using only those participants with complete measurements, and a repeat of these six analyses including only the seven variables conventionally associated with the metabolic syndrome. The principal factor that emerged in all analyses undertaken comprised oral glucose tolerance test insulin and glucose response, serum uric acid, and body mass index. Fasting serum triglyceride concentration was included in this factor in 11 of the 12 analyses undertaken, fasting plasma insulin in 8, fasting plasma glucose in 5, and mean arterial pressure in 3. HDL cholesterol factored in isolation from insulin in all analyses undertaken. These findings provide strong support for a core metabolic cluster, which is unlikely to include blood pressure and does not include HDL. The factor scores relating to this cluster will provide a means of assessing its quantitative importance in prospective analysis of the development of CHD and diabetes in this cohort.
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PMID:Factors of the metabolic syndrome: baseline interrelationships in the first follow-up cohort of the HDDRISC Study (HDDRISC-1). Heart Disease and Diabetes Risk Indicators in a Screened Cohort. 948 85

The reduction of coronary mortality is not as large as one would expect from the observed blood pressure lowering in trials of antihypertensive medications. This is not surprising; hypertension is a complex disease where the high blood pressure is only one of numerous coronary risk factors. Sympathetic overactivity in hypertension, independent of the blood pressure, may be conducive to premature atherosclerosis by inducing insulin resistance and dyslipidemia. Through its trophic effect on blood vessels, sympathetic overactivity potentiates vasoconstriction. This, in turn, accelerates hypertension and the metabolic syndrome. The hypertrophy of small coronary arterioles decreases the coronary reserve and enhances coronary spasms. Tachycardia, which is due to increased sympathetic tone and a decreased parasympathetic tone, favors arrhythmias and sudden death in congestive heart failure and hypertension. Increased hematocrit is frequently found in male patients with hypertension, and high hematocrit is a predictor of coronary heart disease/thrombosis. The increase of hematocrit is in part due to an alpha adrenergic postcapillary venoconstriction. Enhanced sympathetic drive, insulin resistance and dyslipidemia have been demonstrated also in congestive heart failure, but the clinical importance of these findings is not fully understood.
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PMID:Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. 954 Jan 30

Several studies have shown that insulin resistance and hyperinsulinemia are associated with many metabolic disorders predisposing to coronary heart disease (CHD). This syndrome has been termed syndrome X. However, it is not completely known whether these relationships are still present in the elderly, or whether other factors such as age, gender, and body fat distribution modulate them. Therefore, we investigated the relationship between fasting plasma insulin, total and regional adiposity, fasting plasma glucose and lipids, plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and coagulation factor VII in a sample of 100 healthy free-living octogenarians-nonagenarians (52 men and 48 women) who were disability-free according to the Katz index. By univariate analysis, fasting insulin correlated positively with all anthropometric measures except the waist to hip ratio (WHR) in women. There was a positive correlation between fasting insulin and fasting glucose (r=.40, P < .01), plasma triglycerides ([TGs] r=.21, P < .05), and PAI-1 levels (r=.33, P < .01), whereas a negative relation was found with high-density lipoprotein cholesterol (HDL-C) and apolipoprotein, A-I (apo A-I) levels (r=-.22 and =-.24, respectively, P < .05). These relationships were weaker and less significant in women. In pooled data, stepwise multiple regression analysis showed an independent relationship of both the body mass index (BMI) and fasting insulin level with TGs (R2=.14), while gender and fasting insulin were the best predictors of HDL-C variance (R2=.17). Furthermore, fasting insulin was the only variable independently related to PAI-1 (R2=.12). Our findings support the existence of a metabolic syndrome even in very old age by showing that high insulin levels are related to various metabolic and hemostatic disorders.
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PMID:Relationships between fasting plasma insulin, anthropometrics, and metabolic parameters in a very old healthy population. Associazione Medica Sabin. 959 43

In humans, production of the adipocyte-derived peptide leptin has been linked to adiposity, insulin, and insulin sensitivity. We therefore considered that alterations in plasma leptin concentrations could constitute an additional component of a metabolic syndrome of cardiovascular risk. To explore this hypothesis, we employed factor analysis, a multivariate statistical technique that allows reduction of large numbers of highly intercorrelated variables to composite, biologically meaningful factors. Seventy-four men [age, 48.4+/-1.3 years (mean+/-SEM); body mass index (BMI), 25.6+/-0.3 kg/m2] who were free of coronary heart disease and diabetes underwent anthropometric measurements (subscapular-to-triceps [S:T] and subscapular-to-biceps [S:B] skinfold thickness ratios, measurement of fasting plasma leptin, and an intravenous glucose tolerance test (IVGTT) for assessment of insulin sensitivity. Plasma leptin concentrations were correlated with BMI (r=0.57, P<0.001), S:T (r=0.34, P=0.003), S:B (r=0.37, P<0.001), systolic and diastolic blood pressures (both r=0.24, P=0.044), fasting triglycerides (r=0.31, P=0.007), serum uric acid (r=0.35, P=0.003), fasting glucose (r=0.32, P=0.003) and insulin (r=0.33, P=0.004), and IVGTT insulin (r=0.63, P<0.001). A negative correlation was observed between leptin and insulin sensitivity (r=-0.32, P=0.006). No significant correlations emerged between plasma leptin concentrations and age, high density lipoprotein cholesterol, or IVGTT glucose. In multivariate regression analyses, BMI (standardized coefficient [SC]=0.40, P=0.001), fasting insulin (SC=0.23, P=0.036), and IVGTT insulin (SC=0.51, P<0.001) emerged as independent predictors of plasma leptin concentrations (R2=0.56, P<0.001). After adjustment for BMI, only IVGTT insulin emerged as a significant predictor of plasma leptin concentrations (SC=0.56, P<0.001, R2=0.45, P<0.001). Factor analysis of plasma leptin concentrations and the variables that are considered relevant to the insulin resistance syndrome revealed a clustering of plasma leptin concentrations with a factor dominated by insulin resistance and high IVGTT insulin, separate from a high IVGTT glucose/central obesity factor and a high triglyceride/low high density lipoprotein cholesterol factor. Together, these factors accounted for 55.9% of the total variance in the dataset. In conclusion, interindividual variations in plasma leptin concentrations are strongly related to the principal components of the insulin resistance syndrome. Further studies are needed to determine whether the insulin-leptin axis plays a coordinating role in this syndrome and whether plasma leptin concentrations could provide an additional measure of cardiovascular risk.
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PMID:Hyperleptinemia as a component of a metabolic syndrome of cardiovascular risk. 963 33

Elevated plasminogen activator inhibitor-1 (PAI-1) levels have been described in some populations to associate with hyperinsulinaemia in the metabolic syndrome which predisposes to coronary heart disease (CHD). This association, if consistently present, could provide more evidence for a synergistic role for insulin resistance and altered fibrinolysis in the pathogenesis of CHD. To test the hypothesis further therefore, we explored the relationships between the fasting levels of insulin and PAI-1 and lipids in groups of non-diabetic Arab subjects classified as: A: normolipidaemic (n = 148); B: hyperlipidaemic: (n = 99), subdivided into - C: normotensive (n = 71) and D: hypertensive (n = 28); and E: patients with CHD (n = 12). In Group A, fasting insulin (FI) was 7.2+/-(SD) 3.4 mU/l, PAI-1 30.6+/-9.7 ng/ml, both levels significantly lower (P < 0.05) than in Group B as a whole (FI 9.7+/-5.2, PAI-1 36.9+/-10.6), or as normotensive Group C (FI 9.4+/-5.4, PAI-1 36.7+/-10.3) or hypertensive Group D (FI 10.9+/-4.8, PAI-1 37.2+/-11.5). These values were highest in the hyperlipidaemic hypertensive Group D. There were no significant differences relative to the hyperlipidaemic phenotype of predominant hypercholesterolaemia, hypertriglyceridaemia or mixed hyperlipidaemia. PAI-1 (34.7+/-13.8) and FI (7.0+/-2.4) levels in Group E with CHD were similar to those of Group A but lower than values seen in Groups B, C and D. Consistent positive correlations (r = 0.32-0.41, P <0.01) were demonstrable in all the groups between PAI-1 and triglycerides levels. There were also significant correlations between insulin and PAI-1 (r = 0.20, P<0.1) in all the subjects (grouped as a whole, n = 259) and in normolipidaemic Group A (r = 0.29, P < 0.01) but not in any of the hyperlipidaemic groups or in patients with CHD. This study therefore suggests that levels of insulin and PAI-1 are increased in hyperlipidaemic subjects, particularly when also hypertensive. The further observation of significant correlations between insulin and PAI-1 levels only in normolipidaemic subjects and not those who were hyperlipidaemic or with CHD is at variance with observations in Caucasians in whom strong positive correlations between insulin and PAI-1 had suggested that elevated PAI-1 levels should constitute one more component of the metabolic syndrome which strongly predisposes to CHD. Whether this is a racial variation or an artifact of the insulin/PAI-1 assay methodology is unclear and deserves further study.
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PMID:The relationships between insulin and plasminogen activator inhibitor 1 levels: assessment in groups of subjects with dyslipidaemia and hypertension. 968 96

Life style measures (weight reduction and control, reduction of total fat calories to < 30% of total calories, modification of fat intake to increased monounsaturated vegetable fat, increased intake of dietary fibers, increased physical activity, controlled stress relaxation) are the basis of longterm therapy of coronary heart disease. For transformation to daily life both patient and doctor need motivation, information, patience, and realistic aims. For realization the 10 rules of medical information should be followed. The patient must be informed that the "new lifestyle" is not punishing but means a new quality of life. With respect to the most important metabolic syndrome with hyperinsulinemia due to insulin resistance, weight reduction is the most important measure for preventing complications of atherosclerosis. The patient should use a diary for weight control and blood pressure self-measurement. Secondary prevention of CHD has been shown useful and effective; however, most patients need additionally drug therapy to avoid or retard progression of the coronary heart disease. The targets for cholesterol and blood pressure control are low; the responsibility of the patient remains high. Besides weight reduction, stopping smoking, lowering lipids, controlling hypertension, and aspirin are the most important.
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PMID:[Changes in life style as a causal therapeutic approach in coronary heart disease]. 982 71


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