Key result
Accelerated biological aging is linked to higher risk of MACE and mortality in AF.
Why the study?
Although chronological aging predicts adverse outcomes in patients with AF, the impact of biological aging acceleration on AF progression and adverse cardiovascular outcomes remained unclear.
Does higher biological aging acceleration increase the risk of major adverse cardiovascular events and all-cause death, and improve risk prediction when added to CHA2DS2-VASc scores in hospitalized patients with atrial fibrillation?
Cohort (n=31,092)
Yes
Does higher biological aging acceleration increase the risk of major adverse cardiovascular events and all-cause death, and improve risk prediction when added to CHA2DS2-VASc scores in hospitalized patients with atrial fibrillation?
Biological aging acceleration is independently associated with adverse cardiovascular outcomes and death in atrial fibrillation patients, and adding it to standard clinical risk scores like CHA2DS2-VASc significantly improves prognostic accuracy for MACE.
Biological aging acceleration was associated with higher MACE risk in AF; extends CHA2DS2-VASc utility but leaves open prospective validation.
Background Even though aging has been demonstrated to predict adverse outcomes in atrial fibrillation (AF) patients, the impact of biological aging acceleration on the progression of AF is still unclear. Purpose To investigate the association between biological aging acceleration and the adverse cardiovascular outcomes in AF patients. Methods We retrospectively investigated AF patients hospitalized in 82 secondary or tertiary hospitals from January, 2016 to September, 2024. Biological age was calculated according to the PhenoAge algorithms. The primary outcomes were major adverse cardiovascular events (MACE, including worsening heart failure, acute ischemic stroke, acute myocardial infarction and cardiac death) and all-cause death. Cox proportional hazard models were used to assess the association between biological aging acceleration and the prognosis. Then we compared the predictive performance of the CHA2DS2-VASc score, CHA2DS2-VA score and CHA2DS2-VASc-60 score before and after incorporating biological aging acceleration by time-dependent receiver operating characteristic curves. Then the additive value of biological aging acceleration in predicting MACE in AF patients was evaluated. Results A total of 31,092 AF patients (mean age 72.19 ± 11.23 years; mean biological age 74.96 ± 17.08 years; mean biological aging acceleration 2.77 ± 11.98 years) with complete information on biological age evaluation were included. During a mean follow-up of 699 days, compared to those with the lowest tertile (mean age 70.43 ± 10.68 years; mean biological age 61.86 ± 11.42 years; mean biological aging acceleration -8.56 ± 3.69 years) of biological aging acceleration, patients with the highest tertile (mean age 73.66 ± 11.57 years; mean biological age 89.82 ± 14.64 years; mean biological aging acceleration 16.15 ± 9.92 years) and the middle tertile (mean age 72.49 ± 11.18 years; mean biological age 73.21 ± 11.61 years; mean biological aging acceleration 0.71 ± 2.56 years) showed significantly increased risk of MACE, all-cause death or worsening heart failure. When considered as continuous variable, per 1 SD increment of biological aging acceleration also resulted in poor prognosis. The restricted cubic spline analysis revealed an S-shaped correlation between biological aging acceleration and the outcomes. Compared to the traditional models alone, the combination of biological aging acceleration with the CHA2DS2-VASc score, CHA2DS2-VA score or CHA2DS2-VASc-60 score significantly improved performance in predicting MACE in AF patients. Conclusions Higher biological age acceleration is associated with poor prognosis in AF patients. Integrating biological age acceleration into the CHA2DS2-VASc score, CHA2DS2-VA score or CHA2DS2-VASc-60 score could enhance the predictive accuracy, indicating the critical role of biological age acceleration in the secondary prevention of AF management.
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Tian et al. (2026) conducted a cohort in Atrial fibrillation (n=31,092). Biological aging acceleration (PhenoAge algorithm) vs. Lowest tertile of biological aging acceleration (mean -8.56 years) was evaluated on Major adverse cardiovascular events (MACE, including worsening heart failure, acute ischemic stroke, acute myocardial infarction, and cardiac death) and all-cause death.
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