Accelerated biological aging, indicated by the highest quartile of PhenoAge, significantly increased the risk of incident atrial fibrillation (HR 1.30) compared to the lowest quartile.
Cohort (n=260,198)
Yes
Does accelerated biological aging increase the risk of incident atrial fibrillation, subsequent complications, and death in adults without prior AF?
Accelerated biological aging, indicated by higher KDM-BA/PhenoAge and shorter telomere length, is significantly associated with increased risks of incident atrial fibrillation and subsequent progression to complications and death.
Effect estimate: HR 1.30 (95% CI 1.25-1.35)
p-value: p=<0.05
Background: The role of biological aging in the progression of atrial fibrillation (AF) remains unclear. Therefore, the present study aimed to investigate the influence of biological aging markers on transitions from health to AF, complications, and death. Methods: Two UK Biobank datasets were analyzed: 260,198 participants for the Klemera-Doubal method for biological age (KDM-BA) and PhenoAge analyses, and 339,603 for telomere length analyses, excluding those with AF, complications (heart failure, myocardial infarction, cerebral infarction, dementia, and arterial embolic diseases) at baseline. The present study employed a multi-state model to evaluate the associations between biological aging markers and the progression of AF. Mediation analyses were utilized to assess the role of systemic inflammation. Results: During the follow-up period, 9.51–9.67% of patients in the two datasets developed AF, among whom 17.59–17.85% progressed to complications, with 8.20–10.83% of these patients dying from AF-related complications. In comparison with Q1, Q4 of the KDM-BA and PhenoAge analyses was associated with elevated risks across transitions, particularly from baseline to AF (hazard ratios (HR): 1.09, 95% confidence interval (CI): 1.04–1.14; HR: 1.30, 95% CI: 1.25–1.35), baseline to death (HR: 1.10, 95% CI: 1.04–1.16; HR: 1.11, 95% CI: 1.06–1.16), and AF to complication (HR: 1.75, 95% CI: 1.58–1.94; HR: 1.52, 95% CI: 1.37–1.68). Moreover, Q4 of the telomere length analyses showed protective effects against AF onset (HR: 0.83, 95% CI: 0.80–0.86), progression to complications (HR: 0.78, 95% CI: 0.72–0.84), and from baseline to death (HR: 0.91, 95% CI: 0.88–0.94). Systemic inflammation was associated with up to 29.95% of these associations. Conclusions: Associations were found between biological aging markers (higher KDM-BA and PhenoAge, and shorter telomere length) and the risk of AF transitions, particularly with respect to an increased risk of AF and progression to complications. These findings underscore the importance of biological age in AF risk stratification and prevention.
Fan et al. (Fri,) conducted a cohort in Atrial fibrillation (n=260,198). Accelerated biological aging (KDM-BA, PhenoAge, telomere length) vs. Lowest quartile (Q1) of biological aging markers was evaluated on Transition from baseline to atrial fibrillation (HR 1.30, 95% CI 1.25-1.35, p=<0.05). Accelerated biological aging, indicated by the highest quartile of PhenoAge, significantly increased the risk of incident atrial fibrillation (HR 1.30) compared to the lowest quartile.