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Haemostatic/inflammatory markers predict 10-year risk of IHD at least as well as lipids: the Caerphilly collaborative
J W G Yarnell1, C C Patterson, P M Sweetnam
1Department of Epidemiology and Public Health, Queen's University Belfast, Belfast BT12 6BJ, UK. j.yarnell@qub.ac.uk
Insights
Plasma lipids and haemostatic/inflammatory markers predict ischaemic heart disease (IHD) risk. Haemostatic/inflammatory factors show a graded relationship to IHD, offering potential new intervention targets.
Area of Science:
- Cardiovascular epidemiology
- Biomarker research
Background:
- Ischaemic heart disease (IHD) remains a leading cause of mortality.
- Predictive models for IHD risk often focus on plasma lipids.
- The role of haemostatic and inflammatory markers in IHD prediction requires further investigation.
Purpose of the Study:
- To compare the predictive values of plasma lipids and haemostatic/inflammatory risk markers for incident ischaemic heart disease (IHD).
Main Methods:
- A prospective study of 4860 men from two UK populations screened between 1979-1983.
- 10-year follow-up recording validated coronary events, including myocardial infarction (MI).
- Comparison of multivariate models using lipid profiles versus haemostatic/inflammatory markers (fibrinogen, viscosity, white cell count).
Main Results:
- By 10 years, 525 men experienced a coronary event.
- Both lipid and haemostatic/inflammatory models demonstrated graded relationships with IHD risk.
- Decile analysis showed a 34-35% 10-year IHD risk in the highest risk decile versus 2-3% in the lowest.
Conclusions:
- Major haemostatic/inflammatory risk factors are as strongly related to incident IHD as plasma lipids.
- These haemostatic/inflammatory factors represent potential targets for therapeutic intervention in IHD prevention.
Aims:
We compare the predictive values of plasma lipids (total and HDL-cholesterol, triglycerides) and three haemostatic/inflammatory risk markers for subsequent ischaemic heart disease (IHD).
Methods And Results:
Two UK populations totalling 4860 men were screened for evidence of IHD between 1979 and 1983. Men were followed over 10 years and validated coronary events were recorded. Risk estimates were made using relative odds, receiver operating characteristic (ROC) curves and deciles of risk. Regression dilution effects were also examined. By 10 years, 525 men had a coronary event (fatal, non-fatal or silent myocardial infarction, MI). Two alternative multivariate models were compared - a lipid model (total, HDL-cholesterol, triglyceride) and a haemostatic/inflammatory model (fibrinogen, viscosity and white cell count). 'Correction' for regression dilution increased relative odds for most risk factors. In the distribution of predicted risk, using established risk factors in conjunction with either lipid or haemostatic/inflammatory factors, the deciles of risk analysis showed that the observed 10-year risk of IHD was 34-35% in men in the top tenth, compared to 2-3% in the lowest tenth of the distribution.
Conclusion:
At the 10 years' follow-up, major, haemostatic/inflammatory risk factors showed a graded relationship to incident IHD that was at least as strong as that given by plasma lipids. Haemostatic/inflammatory factors provide possible additional targets for intervention.
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