Ling Yao, Haixia Li
This commentary refers to ‘Frailty and long-term outcomes in younger patients with acute myocardial infarction’, by Hasan Mohiaddin et al., https://doi.org/10.1093/eurheartj/ehaf876 and the discussion piece ‘Frailty and the biology of accelerated ageing’, by H. Mohiaddin and M. Rashid, https://doi.org/10.1093/eurheartj/ehag193. We commend Mohiaddin and colleagues for their pivotal study, which compellingly demonstrates that frailty is a critical prognostic factor in younger adults with acute myocardial infarction (AMI).1 By quantifying a staggering near four-fold higher mortality risk in severely frail young patients compared with their older counterparts, the authors successfully dismantle the outdated notion that frailty is synonymous with old age. This work is a clarion call to integrate frailty assessment across all ages in cardiology. However, the very terminology of ‘young frailty’, while useful for epidemiological distinction, may inadvertently become a clinical dead end. As the authors astutely observe, the phenotype in younger patients is dominated by cardiometabolic deficits.1 Labelling a 50-year-old with diabetes and heart failure as ‘frail’ adds a layer of abstraction but scant clinical utility beyond recognizing their high-risk multimorbidity. In other young populations, this same label stems from vastly different roots: accelerated biological ageing after childhood cancer,2 the chronic inflammatory milieu of HIV,3 or the complex burdens in adult spinal deformity.4 This heterogeneity reveals that frailty is not a discrete disease of the young but a final common pathway of depleted physiological reserve, arrived at through diverse and individual aetiological routes.