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Lifetime Risk of CHD by Polygenic Risk and Lifestyle
Quick Takes
- Both high polygenic risk and poor lifestyle confer a high lifetime risk of CHD, but lifestyle had a larger impact on the lifetime risk of CHD than genetic information.
- Managing one’s cardiovascular health according to LS7 guidelines is associated with lower lifetime risk of CHD for all individuals, suggesting that individuals with high genetic susceptibility for CHD may experience lower lifetime risk of CHD with adherence to LS7.
- Communicating the effects of LS7 and polygenic risk on CHD in terms of absolute risk may have relevance on education, policy, and environmental changes, and benefit not only high-risk individuals, but the entire population.
Study Questions:
What is the remaining lifetime risk and years free of coronary heart disease (CHD) according to polygenic risk and the American Heart Association's Life's Simple 7 (LS7) guidelines in a population-based cohort study?
Methods:
The investigators included data from participants of the ARIC (Atherosclerosis Risk in Communities) study: 8,372 White and 2,314 Black participants; 45 years of age and older; and free of CHD at baseline examination. A polygenic risk score (PRS) comprised of >6 million genetic variants was categorized into low (<20th percentile), intermediate, and high (>80th percentile). An overall LS7 score was calculated at baseline and categorized into "poor," "intermediate," and "ideal" cardiovascular health. Lifetime risk and CHD-free years were computed according to polygenic risk and LS7 categories. Lifetime risk of CHD for the joint association of PRS and LS7 score category was computed for the total population, accounting for different starting ages.
Results:
The overall remaining lifetime risk was 27%, ranging from 16.6% in individuals with an ideal LS7 score to 43.1% for individuals with a poor LS7 score. The association of PRS with lifetime risk differed according to ancestry. In White participants, remaining lifetime risk ranged from 19.8% to 39.3% according to increasing PRS categories. Individuals with a high PRS and poor LS7 had a remaining lifetime risk of 67.1% and 15.9 fewer CHD-free years than did those with intermediate polygenic risk and LS7 scores. In the high-PRS group, ideal LS7 was associated with 20.2 more CHD-free years compared with poor LS7. In Black participants, remaining lifetime risk ranged from 19.1% to 28.6% according to increasing PRS category. Similar lifetime risk estimates were observed for individuals of poor LS7 regardless of PRS category. In the high-PRS group, an ideal LS7 score was associated with only 4.5 more CHD-free years compared with a poor LS7 score.
Conclusions:
The authors concluded that ideal adherence to LS7 recommendations was associated with lower lifetime risk of CHD for all individuals, especially in those with high genetic susceptibility.
Perspective:
This study reports that both high polygenic risk and poor lifestyle confer a high lifetime risk of CHD, but lifestyle had a larger impact on the risk of CHD than genetic information. Furthermore, managing one’s cardiovascular health according to LS7 guidelines is associated with lower lifetime risk of CHD for all individuals, suggesting that individuals with high genetic susceptibility for CHD may experience a lower lifetime risk of CHD with adherence to LS7. Additional research is needed to determine how much lifestyle improvements offset the lifetime risk for CHD conferred by PRS. Finally, communicating the effects of LS7 and polygenic risk on CHD in terms of absolute risk may have relevance on education, policy, and environmental changes, and benefit not only high-risk individuals, but the entire population.
Clinical Topics: Arrhythmias and Clinical EP, Cardiovascular Care Team, Diabetes and Cardiometabolic Disease, Prevention, Genetic Arrhythmic Conditions
Keywords: African Americans, Atherosclerosis, Cardiometabolic Risk Factors, Coronary Disease, Genetic Predisposition to Disease, Genetics, Healthy Lifestyle, Heart Disease Risk Factors, Life Style, Metabolic Syndrome, Multifactorial Inheritance, Primary Prevention, Risk Factors
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