Abstract
BACKGROUND: Biological processes of aging significantly contribute to cardiovascular disease (CVD) development. Phenotypic age acceleration (PhenoAgeAccel) is recognized as convenient proxy for biological aging. However, its relationship with sudden cardiac arrest (SCA) remains unclear.</p>
OBJECTIVE: The purpose of this study was to evaluate associations between the PhenoAgeAccel and the risk of incident SCA.</p>
METHODS: This retrospective cohort analysis included 360,663 participants in the UK Biobank with available PhenoAgeAccel data and no history of SCA. Cox proportional hazards models assessed the association between PhenoAgeAccel and SCA risk. Moreover, accelerated failure time models were used to investigate the timing of SCA onset. The impact of dynamic increases in PhenoAgeAccel levels on SCA risk was evaluated using restricted cubic splines.</p>
RESULTS: Over a median follow-up period of 13.68 years, 2194 cases of SCA were recorded. Multivariate Cox regression analysis revealed an 83% increase in SCA risk per 10-year increase in PhenoAgeAccel (adjusted hazard ratio = 1.83, 95% confidence interval 1.69-1.98). Accelerated failure time models indicated earlier median times to SCA occurrence with increasing quartiles of PhenoAgeAccel than with the lowest quartile (P for trend < .05). SCA risk increased linearly with gradual increases in PhenoAgeAccel levels (P for linearity = .629). Sex-stratified analyses showed stronger associations in women.</p>
CONCLUSION: Accelerated biological aging could increase the risk of SCA, especially for women, and could reduce the life expectancy of people without CVD. The identification of populations with accelerated biological aging has important implications for reducing the risk of SCA and the risk of decreased life expectancy.</p>