Maturitas · 2026
Association between phenotypic age acceleration and all-cause and cardiovascular mortality risk among individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: a cohort study.
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Mai Weiliang, Zhong Guohong, He Zibang, Liu Ting, Mao Lijie, Yang Jielan
Аннотация
BACKGROUND: Phenotypic age acceleration (PhenoAge acceleration) is closely associated with adverse events, but its association with mortality risk in individuals with cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3 remains unclear.
METHODS: A total of 8404 participants with CKM syndrome stages 0-3 from the National Health and Nutrition Examination Survey were included. PhenoAge acceleration was calculated as the residual difference between PhenoAge (assessed by inflammatory markers, immune function, metabolic indicators, and liver function) and chronological age. Cox proportional hazards regression models were applied to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) of mortality.
RESULTS: Over a median follow-up of 5.83 years, 713 all-cause deaths occurred, including 203 deaths related to cardiovascular disease (CVD). After adjusting for multiple potential confounders, participants in the Q2, Q3, and Q4 of PhenoAge acceleration exhibited progressively higher risks of all-cause mortality compared with those in the Q1 group, with HRs (95% CI) of 0.90 (0.70-1.15), 1.60 (1.29-2.00), and 2.81 (2.22-3.56), respectively. A similar trend was observed for CVD mortality. Notably, each 1-year increase in PhenoAge acceleration was significantly associated with elevated risks of both all-cause and CVD mortality (P < 0.001). Compared with the non-accelerated aging group, the accelerated aging group had an HR (95% CI) of 2.15 (1.81-2.56) for all-cause mortality and 1.96 (1.30-2.97) for CVD mortality. Restricted cubic spline analysis revealed a linear, positive association between PhenoAge acceleration and mortality risk.
CONCLUSION: PhenoAge acceleration is significantly associated with increased risks of all-cause and CVD mortality among individuals with CKM syndrome stages 0-3.
METHODS: A total of 8404 participants with CKM syndrome stages 0-3 from the National Health and Nutrition Examination Survey were included. PhenoAge acceleration was calculated as the residual difference between PhenoAge (assessed by inflammatory markers, immune function, metabolic indicators, and liver function) and chronological age. Cox proportional hazards regression models were applied to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) of mortality.
RESULTS: Over a median follow-up of 5.83 years, 713 all-cause deaths occurred, including 203 deaths related to cardiovascular disease (CVD). After adjusting for multiple potential confounders, participants in the Q2, Q3, and Q4 of PhenoAge acceleration exhibited progressively higher risks of all-cause mortality compared with those in the Q1 group, with HRs (95% CI) of 0.90 (0.70-1.15), 1.60 (1.29-2.00), and 2.81 (2.22-3.56), respectively. A similar trend was observed for CVD mortality. Notably, each 1-year increase in PhenoAge acceleration was significantly associated with elevated risks of both all-cause and CVD mortality (P < 0.001). Compared with the non-accelerated aging group, the accelerated aging group had an HR (95% CI) of 2.15 (1.81-2.56) for all-cause mortality and 1.96 (1.30-2.97) for CVD mortality. Restricted cubic spline analysis revealed a linear, positive association between PhenoAge acceleration and mortality risk.
CONCLUSION: PhenoAge acceleration is significantly associated with increased risks of all-cause and CVD mortality among individuals with CKM syndrome stages 0-3.