The biological reality of frailty in the young

Le résumé fourni par la source

This commentary refers to ‘Frailty and long term outcomes in younger patients with acute myocardial infarction’, by H. Mohiaddin et al., https://doi.org/10.1093/eurheartj/ehaf876 and the discussion piece ‘Beyond relative risk: a deeper look at frailty in younger AMI patients’, by M. Wang, https://doi.org/10.1093/eurheartj/ehag157. We thank Dr Wang for their correspondence regarding our study.1 We appreciate the opportunity to clarify the methodological rationale underpinning our analysis and maintain that the conceptual and statistical frameworks applied are robust and appropriate for delineating the specific clinical impact of frailty in young patients with acute myocardial infarction. First, regarding the conceptual validity of frailty in younger populations, the author suggests that our findings may conflate multimorbidity with physiological frailty, advocating for performance-based measures like the Fried criteria.2 While performance measures have value, they are often unfeasible for very large population-level analyses and are scarcely recorded in administrative datasets. Our study utilizes the cumulative deficit model, a widely established and validated framework, which defines frailty as the accumulation of health deficits resulting in heightened vulnerability.3 Here, the core premise is that the quantity of deficits, rather than their specific nature, erodes physiological reserve. Consequently, the distinct ‘cardiometabolic phenotype’ identified in our young frail cohort is not a confounding factor but a central finding: it represents a state of accelerated biological aging. To dismiss this as ‘just multimorbidity’ ignores the fundamental biological insight that a young patient with deficit accumulation matching a frail octogenarian has moved to a trajectory of profound vulnerability.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.