Abdominal obesity is associated with an impaired fibrinolytic activity and elevated plasminogen activator inhibitor-1

Landin, Kerstin; Stigendal, Lennart; Eriksson, Ejnar; Krotkiewski, M; Risberg, Bo; Tengborn, Lilian; Smith, Ulf

doi:10.1016/0026-0495(90)90164-8

Cited by 326 publications

(218 citation statements)

References 21 publications

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“…A number of studies have succeeded in lowering PAI activity and t-PA antigen, following large weight losses in subjects whose fibrinolytic activity was impaired (Landin et al, 1990;Palareti et al, 1994;Fehily et al, 1982). The PAI activity at baseline for our angina patients was 31% below the values of those 'simple obese' subjects in a previous study (Hankey et al, 1997a,b).…”

Section: Discussionmentioning

confidence: 49%

Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris

et al. 2002

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Objective: To evaluate the effects of moderate weight loss, in overweight patients with angina, on plasma coagulation, fibrinolytic indicies and pain frequency. Conclusions: A conventional dietetic intervention, resulting in 4% weight loss, offers the potential to reduce atherosclerotic and thrombotic risk, and to reduce pain frequency, in angina patients. Given the importance of this result in a public health context, these results indicate that this may be a fruitful area for future nutrition research.

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Section: Discussionmentioning

confidence: 49%

Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris

et al. 2002

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“…We were, however, unable to demonstrate a speci®c impact of fat mass, fat free mass and body fat distribution on other biochemical variables, including PAI-1 antigen concentrations. The association between central obesity and PAI-1 levels reported in some earlier reports thus could not be con®rmed (Landin et al, 1990;Mykka Ènen et al, 1994).…”

Section: Discussionmentioning

confidence: 64%

Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

Marckmann¹,

Toubro²,

Astrup³

1998

Eur J Clin Nutr

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Objective: To study whether major weight loss causes sustained improvement in blood lipids and haemostatic pro®le in obese subjects, and to compare the in¯uence of two different slimming and maintenance regimens. Design: Two-stranded randomized intervention study. Setting: University Department. Subjects: Thirty-six out of 43 obese patients recruited from out-patient waiting list completed the study. Interventions: Weight loss was achieved by very low energy formula diet (2 MJad for 8 weeks, n 18), or lowenergy conventional diet (5 MJad for 17 weeks, n 18), both combined with anorectic compound. Participants were re-randomized to consume low fat diet ad libitum (n 16), or energy-restricted diet (n 20) for weight maintenance during 24 weeks. Main outcome measures: Plasma lipids, ®brinogen, factor VII coagulant activity (FVIIc), and plasminogen activator inhibitor type 1 (PAI-1) antigen. Results: Weight loss averaged 13.6 kg (95% CI: 12.3 ± 14.9 kg). After 24 weeks' weight maintenance, plasma total cholesterol was 9% lower, high density lipoprotein cholesterol 5% higher, triglycerides 30% lower, FVIIc 12% lower, ®brinogen 6% lower, and PAI-1 antigen 34% lower than at baseline (all changes highly signi®cant). There were no signi®cant differences between slimming or maintenance regimens. Conclusions: Major weight loss is associated with sustained and marked improvements in blood lipids and hemostatic pro®le, irrespective of the tested slimming and maintenance regimens.

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“…Moreover, the mechanism responsible for impaired endothelial function in visceral fat accumulation is not fully understood. Evidence has accumulated that adipocytes synthesize some kinds of vasoactive substances such as tumor necrosis factor (TNF)-a, 36 plasminogen activator inhibitor (PAI)-1 31,37,38 and von Willebrand factor. 39 These may be involved in the mechanism of endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation

et al. 1998

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BACKGROUND: Obesity has been reported to be associated with coronary artery disease and other atherosclerotic diseases. Recently, evidence has accumulated indicating that intra-abdominal visceral fat accumulation contributes to atherogenesis; however, the mechanism underlying this remains to be determined. This study was undertaken to elucidate whether intra-abdominal visceral fat accumulation impairs vascular endothelial function in obese men. METHODS AND RESULTS: Thirty-eight obese men (body mass index (BMI) ! 26.0), aged 19±64 y (mean age 37.6 AE 1.8 y) and 23 age-matched non-obese subjects were examined. According to the ratio of the maximum thickness of preperitoneal fat to the minimum thickness of subcutaneous fat (Pmax/Smin) obtained by longitudinal ultrasound scanning in the subxiphoid region in obese men, we divided obese subjects into two categories; visceral (PmaxaSmin ! 1; n 23) and subcutaneous type (PmaxaSmin`1; n 15). To investigate endothelial function, we performed ultrasound measurement of the brachial artery diameter non-invasively both at rest and during reactive hyperaemia in the muscle distal to the brachial artery which causes endothelium-dependent vasodilatation. The brachial diameter change was also measured after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. Flow-mediated diameter (D) increase (%FMD; DDaD Â 100), in the subjects with visceral type obesity (3.09 AE 0.43%) was signi®cantly lower than those of the subjects with subcutaneous type obesity and non-obese subjects (7.90 AE 0.51%, 8.91 AE 0.44%, respectively, P`0.01). The magnitude of endothelium-independent vasodilatation by nitroglycerin was similar in all groups. On multiple regression analysis, the PmaxaSmin showed a signi®cant inverse correlation with %FMD. CONCLUSIONS: The subjects with visceral type obesity, rather than those with the subcutaneous type, are associated with impaired¯ow-mediated endothelium-dependent vasodilatation of the brachial artery.

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Abdominal obesity is associated with an impaired fibrinolytic activity and elevated plasminogen activator inhibitor-1

Cited by 326 publications

References 21 publications

Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris

Effects of moderate weight loss on anginal symptoms and indices of coagulation and fibrinolysis in overweight patients with angina pectoris

Sustained improvement in blood lipids, coagulation, and fibrinolysis after major weight loss in obese subjects

The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation

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