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Lifestyle and hemostatic risk factors for ischemic heart disease : the Caerphilly Study
J W Yarnell1, P M Sweetnam, A Rumley
1Department of Epidemiology and Public Health, Queen's University, Belfast, UK. h.porter@qub.ac.uk
Insights
Lifestyle factors like smoking and alcohol consumption influence hemostatic risk predictors for ischemic heart disease (IHD). Modifying lifestyle may reduce IHD risk by improving hemostatic function, warranting further intervention studies.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Public Health
Background:
- Established risk factors for ischemic heart disease (IHD) are well-known.
- Recent studies identified novel hemostatic markers associated with IHD risk in middle-aged men.
- The influence of lifestyle on these emerging IHD risk predictors requires investigation.
Purpose of the Study:
- To examine the contribution of major lifestyle factors to plasma levels of key hemostatic variables.
- To understand how factors such as smoking, alcohol, BMI, and physical activity impact IHD risk predictors.
- To assess the relationship between lifestyle and hemostatic markers linked to subsequent IHD.
Main Methods:
- Analysis of data from up to 2188 men in the Caerphilly Study.
- Examined the association between lifestyle factors (smoking, alcohol, BMI, activity, social class, medications) and plasma levels of 8 hemostatic variables.
- Adjusted for other lifestyle variables, age, and time of day.
Main Results:
- Hemostatic variables generally increased with age and smoking.
- Alcohol consumption showed varied associations, increasing tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI-1) but decreasing fibrinogen and white cell count.
- Body mass index (BMI) was positively associated with tPA, PAI-1, fibrinogen, and viscosity; leisure activity was inversely associated with D-dimer, von Willebrand factor, fibrinogen, and viscosity.
Conclusions:
- Several lifestyle factors are significantly associated with hemostatic risk predictors for IHD.
- Lifestyle modifications may offer a pathway to reduce IHD risk by positively influencing hemostatic function.
- Further large-scale intervention studies are necessary to confirm the efficacy of lifestyle changes in mitigating IHD through hemostatic pathways.
Abstract:
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-1) 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 IHD. Lifestyle modifications may reduce IHD risk partly by altering hemostatic function; large intervention studies are required to test this hypothesis.