Abstract
BACKGROUND: Existing evidence regarding the independent and complementary roles of distinct biological aging measures in predicting heart disease risk remains limited.</p>
OBJECTIVES: To examine the association between biological aging and the incidence of heart disease.</p>
METHODS: This study analyzed 321,324 participants from the UK Biobank. Three biological age (BA) measures were calculated: Klemera-Doubal method age (KdmAge), PhenoAge, and Homeostatic dysregulation age (HD Age). The residuals of KdmAge and PhenoAge were defined as accelerated KdmAge (KdmAgeAccel) and accelerated PhenoAge (PhenoAgeAccel), respectively. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for heart disease risk.</p>
RESULTS: During a median follow-up of 13.6 years, 36,512 new heart disease cases occurred. After multivariable-adjusted, each SD increase in accelerated BA was associated with elevated risk of heart disease (KdmAgeAccel: HR 1.20, 95% CI 1.19-1.22; PhenoAgeAccel: HR 1.20, 95% CI 1.18-1.21; HD Age: HR 1.16, 95% CI 1.15-1.17), coronary heart disease (KdmAgeAccel: HR 1.28, 95% CI 1.26-1.30; PhenoAgeAccel: HR 1.20, 95% CI 1.18-1.21; HD Age: HR 1.27, 95% CI 1.25-1.29), myocardial infarction (KdmAgeAccel: HR 1.38, 95% CI 1.34-1.41; PhenoAgeAccel: HR 1.23, 95% CI 1.20-1.26; HD Age: HR 1.38, 95% CI 1.35-1.41), and heart failure (KdmAgeAccel: HR 1.52, 95% CI 1.49-1.55; PhenoAgeAccel: HR 1.50, 95% CI 1.47-1.53; HD Age: HR 1.26, 95% CI 1.23-1.29). Incorporating accelerated BA into risk prediction models enhanced the discrimination ability of heart disease.</p>
CONCLUSION: Biological aging are independent predictors of heart disease, enhancing risk stratification and precision in cardiovascular risk assessment.</p>