It was essential to comprehend the impact of genetic risk and lifestyle on the lifetime risk of coronary heart disease (CHD) to improve public health initiatives. With respect to polygenic risk and the American Heart Association’s Life’s Simple 7 (LS7) guidelines, the researchers’ target was to quantify the remaining lifetime risk and years of CHD in a population-based cohort study. They included data from the ARIC (Atherosclerosis Risk in Communities) study as part of their research. Of the 10,686 participants, 2,314 were Black, and 8,372 were White. The participants were over 44 years old and did not have CHD at baseline examinations. There were over 6 million genetic variants in the polygenic risk score (PRS). They classified it into three groups – low (<20th percentile), intermediate, and high (>80th percentile). They calculated the overall LS7 score at baseline and classified it into three groups – “poor,” “intermediate,” and “ideal” cardiovascular health. Afterward, they calculated the CHD-free years and lifetime risk based on the PRS and LS7 categories. Investigators found the remaining lifetime risk was 27%. It varied between 16.6% for participants with an ideal LS7 score and 43.1% for participants with a poor LS7 score. Ancestry caused variances in the link between PRS and lifetime risk. The remaining lifetime risk for White participants was between 19.8% and 39.3%, based on the increasing PRS categories. Participants with a high PRS and poor LS7 had a remaining lifetime risk of 67.1% and 15.9 fewer CHD-free years than those with intermediate polygenic risk and LS7 scores. Additionally, there were links between ideal LS7 and 20.2 more CHD-free years in the high-PRS group compared to poor LS7.

On the other hand, the remaining lifetime risk for Black participants was between 19.1% and 28.6%, based on the increasing PRS categories. The study group noted that estimates for lifetime risk were close to those with poor LS7 regardless of the PRS category. Plus, there were links between ideal LS7 and only 4.5 more CHD-free years in the high-PRS group compared to poor LS7.

Participants who ideally maintained the LS7 recommendations were linked with a lower lifetime risk of CHD, especially those with high genetic susceptibility. Black participants who followed the LS7 recommendations provided more towards the lifetime risk of CHD than current PRS. Hence, it is pertinent to improve PRSs so that genetic susceptibility can be examined in diverse populations appropriately.