Yarnell, J.W.G., Sweetnam, P.M., Rumley, A., and Lowe, G.D.O. (2000) Lifestyle and hemostatic risk factors for ischemic heart disease - The Caerphilly Study. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(1), pp. 271-279.
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Publisher's URL: http://atvb.ahajournals.org/cgi/content/full/20/1/271
We have recently shown that fibrin D-dimer, tissue plasminogen activator (tPA) antigen, von Willebrand factor antigen, fibrinogen, plasma viscosity, and white cell count are associated with subsequent ischemic heart disease (IHD) in men aged 49 to 65 years in the Caerphilly Study from South Wales. We now report the contribution of major lifestyle factors to plasma levels of these new risk predictors for IHD. Results were available for up to 2188 men. The contribution of factors associated with lifestyle (smoking, alcohol, body mass index, leisure and work activity, social class, and use of prescribed medicines) to variation in plasma levels of 8 hemostatic variables was examined. All results were adjusted for other lifestyle variables, age, and time of day. Most hemostatic variables increased with age and smoking habit. Increasing levels of alcohol consumption were associated with increases in tPA and plasminogen activator inhibitor (PAI-I) activity and with decreases in fibrinogen and white cell count, tPA, PAI-1, fibrinogen (nephelometric), and viscosity were positively associated with body mass index. Increasing levels of leisure activity were inversely associated with D-dimer, von Willebrand factor, nephelometric fibrinogen, and viscosity. Use of prescribed medicines (a marker for chronic illness) was associated with adverse levels of D-dimer, fibrinogen, plasma viscosity, and white cell count. tPA, PAI-1, and plasma viscosity were associated with blood pressure, cholesterol, and triglycerides but not with lipoprotein(a) or homocysteine. We conclude that several lifestyle factors are associated with hemostatic risk predictors for II-ID. Lifestyle modifications may reduce IHD risk partly by altering hemostatic function; large intervention studies are required to test this hypothesis.
|Glasgow Author(s) Enlighten ID:||Rumley, Dr Ann and Lowe, Professor Gordon|
|Authors:||Yarnell, J.W.G., Sweetnam, P.M., Rumley, A., and Lowe, G.D.O.|
|Subjects:||R Medicine > RC Internal medicine|
|College/School:||College of Medical Veterinary and Life Sciences|
|Journal Name:||Arteriosclerosis, Thrombosis, and Vascular Biology|
|Publisher:||American Heart Association|