The effects of exercise capacity and sedentary lifestyle on haemostasis among middle-aged women with coronary heart disease.

Previous studies have established a link/relationship between haemostatic factors and increased risk of cardiovascular disease. In addition, physical conditioning is associated with lower coronary heart disease risk. The purpose of this study was to assess the association between physical exercise and haemostatic factors among middle-aged women surviving an acute coronary event.

Does body mass index, smoking, lipoprotein levels, surgically induced menopause, hormone replacement therapy, years since menopause, or age affect hemostasis in postmenopausal women?

Background: Controversy still exists as to the relative importance of menopausal status and lifestyle factors for the risk of coronary heart disease in women.

Objective: The purpose of this study was to assess the influence of body mass index (BMI), smoking,lipoprotein levels, surgically induced menopause, hormone replacement therapy (HRT), years since menopause, and age on hemostasis in apparently healthy postmenopausal women.

Methods: Lipoproteins (total cholesterol [TC], low-density lipoprotein cholesterol, high-density lipoprotein cholesterol [HDL-C], triglycerides [TG]), and hemostatic factors (fibrinogen, von Willebrand factor antigen [vWFag], coagulation factors VIIag [FVIlag] and VIIa [FVIIa], plasminogen activator inhibitor 1 [PAI-1]) were each measured once.

Influence of factor VII gene polymorphisms and environmental factors on plasma coagulation factor VII concentrations in middle-aged women with and without manifest coronary heart disease.

Plasma concentrations of coagulation factorVII (FVII) are determined by environmental and genetic factors. The influence of functional polymorphisms in the FVII gene (-670A>C, -402G>A, -401G>T and R353Q) and of established cardiovascular risk factors on plasma concentrations of FVII were investigated in a representative sample of middle-aged women with (n=238) and without (n=220) coronary heart disease (CHD). Specific and sensitive assays were used to measure FVII antigen (VIIag) and activated factorVII (VIIa).

Retained fibrinolytic response and no coagulation activation after acute physical exercise in middle-aged women with previous myocardial infarction.

Sudden physical exertion is associated with an increased risk of acute myocardial infarction (MI) and sudden cardiac death. In addition, activation of the coagulation cascade and/or reduced fibrinolytic capacity after physical exercise has been reported in patients with cardiovascular disease. We investigated the haemostatic responses to an acute submaximal physical exercise in middle-aged women with a history of MI compared with healthy, age-matched controls.

Are increased levels of von Willebrand factor in chronic coronary heart disease caused by decrease in von Willebrand factor cleaving protease activity? A study by an immunoassay with antibody against intact bond 842Tyr-843Met of the von Willebrand factor protein.

Low levels of von Willebrand factor (VWF) in von Willebrand's disease type 2A (VWD 2A) result from increased cleavage of the bond 842Tyr-843Met in the VWF protein by VWF cleaving protease. On the other hand, decreased levels of this protease result in unusually large VWF in thrombotic thrombcytopenic purpura with thrombotic complications. In the present study, we designed an enzyme-liked immunosorbent assay of VWF cleaving protease activity to be used to assess whether the high levels of VWF in coronary heart disease (CHD) relate to a deficiency of this protease.

Coagulation factor VII in middle-aged women with and without coronary heart disease.

Epidemiological studies of coagulation factor VII as a risk factor for coronary heart disease (CHD), mainly conducted in men, have shown discrepant results. We examined the associations of coagulation factor VII antigen (VIIag) and activated factor VII (VIIa) with manifest CHD in a community-based case-control study of women aged < or =65 years. Mean plasma concentrations of VIIag and VIIa in patients and controls were 443 +/- 10(8) and 418 +/- 89 ng/L (p <0.