Framingham risk score and prediction of coronary heart disease death in young men
Received 22 August 2006; accepted 28 March 2007. published online 11 May 2007.
Background
We tested the ability of the Framingham Risk Score (FRS) and the online ATP III risk estimator to estimate risk and to predict 10-year and longer-term coronary heart disease (CHD) death in younger adults (age 18-39 years). Although prediction with individual risk factors has been tested in individuals <30 years, current multivariate risk prediction strategies have not been applied to prediction of clinical CHD in this age range.
Methods
We included 10551 male participants of the CHA study who were aged 18 to 39 years and free of baseline CHD and diabetes at enrollment from 1967 to 1973. Risk of CHD was estimated using both FRS and ATP III online risk estimator for each individual. Men were stratified into deciles according to the magnitude of predicted risk calculated from measured baseline risk factors (CHA-predicted risk). Observed CHD mortality rates for 10, 20, and 30 years of follow-up were compared with estimated risks. Death rates of CHD were low across 30 years of follow-up.
Results
The FRS remained <10% for all deciles of CHA-predicted risk in the 18- to 29-year-old cohort. Framingham-predicted risk reached 12% only in the 30- to 39-year-old cohort in the highest decile of CHA-predicted risk despite substantial risk factor burden.
Conclusions
Neither method classified individuals <30 years as high risk despite substantial risk factor burden. Future clinical guidelines should consider alternative strategies to estimate and communicate risk in populations <30 years.
aDepartment of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
bDepartment of Medicine, the Bluhm Cardiovascular Institute, Northwestern University Feinberg School of Medicine, Chicago, IL
Reprint requests: Donald M. Lloyd-Jones, MD, ScM, Department of Preventive Medicine and Division of Cardiology, Feinberg School of Medicine, Northwestern University, 680 N. Lake Shore Drive, Suite 1102, Chicago, IL 60611.
We acknowledge the support by the American Heart Association, Dallas, TX, and its affiliates in Chicago, IL; the National Heart, Lung, and Blood Institute, Bethesda, MD, for grants R01-HL 15174, R01-HL 21010, and R01-HL 03387; and the Chicago Health Research Foundation, Chicago, IL. A list of colleagues who contributed to earlier aspects of this work has been published (Cardiology. 1993;82:191-222). Dr Berry received support from a Ruth Kirschstein National Research Service Award/National Heart, Lung, and Blood Institute fellowship (T32HL069771) at Northwestern University Feinberg School of Medicine, Chicago, IL.
ABSTRACT