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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ECAT Angina Pectoris Study is a European multicentre study investigating the pathogenetic and possibly predictive role of the haemostatic system in the progress of coronary heart disease. In this paper we report the cross-sectional analysis of haemostatic factors in 3043 patients, who underwent coronary angiography due to angina pectoris. Fibrinogen levels were higher in patients with one or more coronary stenoses of at least 50% than in patients without, by an average of 0.16 g.l-1 (P < 0.0001). Depressed fibrinolytic activity due to higher levels of PAI was also associated with the presence of coronary stenoses. There was no association with the extent of coronary arteriosclerosis, as assessed by the number of involved arteries, except that patients who had more vessels with total occlusions had higher fibrinogen levels. Depressed fibrinolytic activity was also clearly associated with diabetes, obesity, higher triglyceride levels, smoking and impaired cardiac pump function as assessed by ejection fraction. Cholesterol levels were particularly correlated with protein C and plasminogen.
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PMID:ECAT angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography. 843 97

The present study was carried out to explore the possible relation of plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and factor VII levels to other risk factors for coronary heart disease (CHD) and to serum sex hormone levels. The study group comprised 48 apparently healthy men. To avoid the confounding factor of obesity, correlations were determined in the 30 men in this group with a body mass index (BMI) < 26.4, after controlling for age. PAI-1 correlated with testosterone, estradiol/testosterone, and free testosterone/testosterone (FT/T), and fibrinogen correlated with FT/T. All three hemostatic factors correlated with glucose and with the ratio of cholesterol/high density lipoprotein cholesterol, while PAI-1 correlated with diastolic blood pressure. To test the effect of obesity, correlations were determined in the entire group of 48 men, which included 18 subjects with a BMI > 26.4. All three hemostatic factors correlated with BMI in this group after controlling for age; however, on controlling for testosterone, only PAI-1 correlated with BMI. Fibrinogen correlated with age in both groups after controlling for testosterone or BMI. These correlations support the hypothesis that PAI-1, fibrinogen, and factor VII are related to other risk factors for CHD and that an alteration in the sex hormone milieu may be the underlying factor linking them.
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PMID:Relation of hemostatic risk factors to other risk factors for coronary heart disease and to sex hormones in men. 846 82

Blood levels of the clotting factor fibrinogen and tissue plasminogen activator inhibitor-1 (PAI-1), a primary inhibitor of fibrinolysis, have been positively linked to risk of coronary heart disease. The authors have reported previously that plasma fibrinogen appears to rise after menopause and to be reduced with use of postmenopausal hormonal therapy. There is also evidence to suggest that sex hormones may influence PAI-1. To examine whether plasma fibrinogen and PAI-1 antigen levels differ among older postmenopausal women according to use of hormone therapy and by blood level of estrogen and androgens, these variables were assessed among 277 healthy women aged 65-82 years, one half of whom were receiving therapy. The study population was drawn from the Study of Osteoporotic Fractures, Pittsburgh, Pennsylvania, during 1986-1988. Overall, results showed median PAI-1 levels to be lower on average with oral and transdermal use of hormone therapy (25.0 vs. 33.5 ng/ml, p < 0.01) and mean fibrinogen levels to be lower (279 vs. 295 mg/dl, p < 0.02) with use of oral estrogen (but not transdermal) therapy compared with women not receiving therapy. Among women not receiving therapy, PAI-1 and fibrinogen levels were not related to endogenous sex hormone levels, with the exception of a modest positive relation between PAI-1 and serum estrone concentrations (rs = 0.29). In addition, a markedly higher PAI-1 level was found for women with a preponderance of upper body fat, independent of obesity. In sum, results showed that older women receiving postmenopausal hormone therapy had more favorable plasma levels of the hemostatic factors PAI-1 and fibrinogen than did those not receiving therapy, which can be explained in large part by differences between the two groups in obesity and body fat distribution.
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PMID:Association of sex hormones and adiposity with plasma levels of fibrinogen and PAI-1 in postmenopausal women. 854 17

The obese state has been recognized to accentuate the known risk factors for atherosclerotic disease as dyslipidemia, hypertension, glucose intolerance and insulin resistance. Among other risk factors, obesity is characterized by a series of lipid disturbances, such as hypercholesterolemia, high fasting (and postprandial) triglyceride levels, low HDL cholesterol, high apolipoprotein B, high small dense lipoprotein particles and alterations of serum and tissue LPL-activity. Although obesity is associated with such cluster of lipid abnormalities, these factors do not explain the complete process of atherogenesis in the obese subject. Other risk factors belonging to the polymetabolic syndrome-cluster, insulin resistance, hypertension, fibrinogen, add substantial but not full explanation to the atherothrombotic process. Over the last decade, a series of excellent studies have provided the background for a more indepth mechanism of atherosclerosis; the role of lipid peroxidation in particular has been one of the focuses of this current research. There exists a lot of evidence suggesting a major role for oxidized LDL and VLDL particles in the pathogenesis of atherosclerosis. Although obesity is characterized by dyslipidemia, less is known about the oxidation capacity of lipoproteins in obese subjects. We measured the oxidizability in vitro in 21 premenopausal women and compared them to 18 age-matched controls. The oxidizability of the non-HDL fraction is evaluated by measuring the fluorescence and thiobarbituric acid reactive substances (TBARS: MDA nM/mg non-HDL) at different time intervals of incubation. TBARS formation increased linearly with the increase of lipids both in non-obese and obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human obesity: from lipid abnormalities to lipid oxidation. 858 Oct 73

The cross-sectional correlates of three hemostatic factors--fibrinogen, factor VII, and factor VIII--were examined in the Cardiovascular Health Study, a population-based cohort study of 5,201 subjects over age 65 years. Subjects were recruited in 1989-1990 in Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. In multivariate linear regression models, cardiac risk factors significantly associated with fibrinogen were current smoking, race, lipids, and white blood count. In women, alcohol use, obesity, physical activity, and insulin level were also significant, while in men hypertension was correlated. The significant correlates of factor VII were lipids and white blood count in men and estrogen use, alcohol use, race, lipids, insulin level, white blood count, and obesity in women. The independent correlates of factor VIII were insulin, glucose, and race in both sexes; low density lipoprotein cholesterol, white blood count, and diuretic use in men; and alcohol use in women. In multivariate models, factors known to be modifiable risk factors for cardiovascular disease accounted for more of the population variance of these hemostatic factors in women than in men, especially for factor VII. The hemostatic factors may mediate some effects of risk factors on disease, and this should be considered in longitudinal studies.
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PMID:Association of fibrinogen and coagulation factors VII and VIII with cardiovascular risk factors in the elderly: the Cardiovascular Health Study. Cardiovascular Health Study Investigators. 865 Dec 28

Psychosocial job stress has been shown to be associated with the development of cardiovascular disease. However, the pathophysiological mechanisms underlying this relationship remain unclear. The aim of the present study was to elucidate whether marked job stress affects the parameters of blood coagulation and fibrinolysis, such as plasma fibrinogen concentration, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor 1 (PAI-1) activities, in 213 middleaged male workers in a computer-producing factory. Job stress was measured using a Japanese version of the Job Content Questionnaire (JCQ) developed by Karasek. The mean t-PA activity in workers with lower and higher job demands was 0.23 and 0.18 IU/ml respectively, and this difference was significant (P < 0.05). The mean plasma fibrinogen in workers with lower and higher job decision latitude was 224.8 and 236.3 mg/dl respectively, and the mean PAI-1 activity in workers with lower and higher job strain was 14.9 and 17.7 U/ml respectively, though these differences remained at a borderline level of significance (0.05 < P < 0.10). Multiple regression analyses showed that the parameters of blood coagulation and fibrinolysis were closely associated with the cardiovascular risk factors of age, obesity, blood pressure, elevated serum lipids, and smoking, but that high job demands were significantly related to decreases in t-PA activity, independently of the traditional risk factors. These results suggest that psychosocial job stress may be related, at least partly, to the development of cardiovascular disease via changes in plasma fibrinolytic activity.
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PMID:Relationship between job stress and plasma fibrinolytic activity in male Japanese workers. 883 96

Advances in genetics and molecular biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism, cancer, etc., to a great extent is genetically determined. Studies have shown that 50% of the variance in plasma cholesterol concentration is genetically determined, whereas 30%-60% of the variance in blood pressure is genetically determined. For fibrinogen, an independent risk factor for CAD, 15%-50% of the variance is genetically determined. In the U.K. population the variance for the fibrinogen level is 15% whereas in the Hawaiian population, the variance is 50%, indicating significant differences between populations. Among Australians, 75% of the variance in bone density is found to be genetically determined. Genetic variation influences the response to diet. For example, individuals with ApoE4 have higher cholesterol levels and a higher risk of CAD than those with ApoE3. Additional studies show that women of the ApoE 3/2 phenotype stand to benefit the least from a high polyunsaturate: saturate (P:S) diet because of reduction in the more 'protective' high density lipoprotein cholesterol (HDL-C), whereas men of the ApoE 4/3 phenotype showed the greatest improvement in the LDL/HDL ratio. Therefore a general recommendation to increase the polyunsaturated content of the diet in order to decrease the risk for CAD is not appropriate for women with ApoE 3/2 phenotype. Thus, specific information is needed to define the optimal diet for an individual.
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PMID:Genetic variation and nutrition. 888 22

When compared with 67 age- and sex-matched normal weight control subjects, the 71 overweight patients displayed obviously higher levels of plasma fibronectin. For a similar body mass index (BMI) the 16 overweight men younger than 45 years had a significantly (P < 0.01) higher plasma fibronectin level (455 +/- 99.3 mg/l; mean +/- SD) than the 16 age-matched overweight women (351 +/- 105 mg/l) while there was no significant difference between the 22 overweight men (446 +/- 89.2 mg/l) and the 17 overweight women (475 +/- 111 mg/l) older than 45 years. Particularly high plasma fibronectin levels were noted in the five women with upper body (android) obesity. Plasma fibronectin was positively correlated with BMI, serum triglyceride concentration, plasma fibrinogen and serum cholinesterase activity. It is considered that metabolic disturbances related to upper body obesity may lead to an enhanced hepatic secretion of VLDL and of several plasma proteins including fibronectin.
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PMID:Plasma fibronectin in overweight men and women: correlation with serum triglyceride levels and serum cholinesterase activity. 903 58

In vitro studies suggest that oxidized low density lipoprotein inhibits fibrinolysis by stimulating the production of plasminogen activator inhibitor -1 (PAI). We assessed the effects of dietary antioxidant vitamins for four weeks on three indices of copper mediated oxidation of very low and low density lipoproteins (VLDL+LDL) and plasma fibrinolytic activities in 15 male subjects with central obesity, a condition associated with increased PAI activity. Vitamin administration resulted in a decrease in production of thiobarbituric acid reactive substances from 29.3 +/- 3.9 to 13.6 +/- 3.5 nmoles/mg VLDL + LDL protein (mean +/- SE, p <0.003), an increase in the lag phase of conjugated diene formation from 94.8 +/- 5.5 to 225.0 +/- 31.9 min (p <0.001) and an increase in reactivity of lysine residues from 73.6% +/- 4.8% to 86.8% +/- 3.6% (p <0.034) demonstrating a reduction in the susceptibility of the lipoproteins to oxidation. However, antioxidant vitamins had no effect on plasma PAI activity, PAI antigen, tissue-type plasminogen activator activity and antigen, fibrinogen and fibrin degradation products. These results do not support the hypothesis that lipoprotein oxidation is a significant cause of impaired fibrinolysis in men with central obesity.
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PMID:Administration of antioxidant vitamins does not alter plasma fibrinolytic activity in subjects with central obesity. 930 62

Blood levels of C-reactive protein (CRP), a marker of inflammation, are related to cardiovascular disease risk. To determine cross-sectional correlates in the elderly, we measured CRP in 400 men and women older than 65 years and free of clinical cardiovascular disease at baseline as part of the Cardiovascular Health Study. Only 2% of the values were greater than 10 mg/L, the cut-point usually used to identify inflammation. CRP levels appeared tightly regulated, since there were strong bivariate correlations between CRP and the following: inflammation-sensitive proteins such as fibrinogen (r = .52); measures of fibrinolysis such as plasmin-antiplasmin complex (r = .23); pack-years of smoking (r = .30); and body mass index (r = .24; all P values < or = .001). The association with pack-years was independent of the length of time since cessation of smoking. CRP levels were also associated with coagulation factors VIIc, IXc, and Xc; HDL cholesterol (negative) and triglyceride; diabetes status; diuretic use; ECG abnormalities; and level of exercise. Because of effect modification, two multiple linear regression prediction models were developed for CRP, one each for never smokers and ever smokers. An a priori physiologic model was used to guide these analyses, which disallowed the use of other inflammation-sensitive variables such as fibrinogen. In never smokers, the independent predictors were body mass index (+), diabetes status (+), plasmin-antiplasmin complex (+), and the presence of ECG abnormalities (+); this model predicted 15% of the CRP population variance. In ever smokers, the predictors were body mass index (+), plasmin-antiplasmin complex (+), pack-years of smoking (+), HDL cholesterol (-), and ankle-arm blood pressure index (-); this model predicted 42% of the population variance. We conclude that levels of CRP in the healthy elderly are tightly regulated and reflect lifetime exposure to smoking as well as level of obesity, ongoing level of fibrinolysis, diabetes status, and level of subclinical atherothrombotic disease. Moreover, exposure to smoking affects the relation of CRP to these other factors.
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PMID:Lifetime smoking exposure affects the association of C-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects. 935 86


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