PhenoAge acceleration and outcomes after acute myocardial infarction in older adults
In a retrospective cohort of 192 older adults with acute myocardial infarction, PhenoAge acceleration was independently associated with in-hospital mortality, and all three aging metrics were associated with intermediate-term composite endpoints. [1]
Automatic summary · not editorially reviewed
The key findings
The retrospective cohort included 192 consecutive adults with acute myocardial infarction, median age 71 years, admitted in 2022 and followed until 30 August 2025. [1]
PhenoAge acceleration was independently associated with in-hospital mortality, whereas chronological age was not. [1]
Over a median follow-up of 1285 days, all three aging metrics were independently associated with both composite endpoints and heart failure hospitalization. [1]
The source at a glance
- Study type / format
- Retrospective cohort study (abstract)
- Population / context
- Adults with acute myocardial infarction, median age 71 years (range 62–78), admitted to a national tertiary center in 2022.
- Summary based on
- Study abstract
- Original publication
- June 1, 2026
PhenoAge metrics in 192 older AMI patients
This retrospective cohort included 192 consecutive adults with acute myocardial infarction (AMI) at a national tertiary center in 2022; median age was 71 years (range 62–78). PhenoAge metrics were calculated from routine laboratory values at admission. Patients were followed until 30 August 2025. Outcomes were in-hospital mortality and two composite endpoints: (1) all-cause mortality, non-fatal myocardial infarction or revascularization, and (2) those plus hospitalization for heart failure. Models were adjusted for baseline cardiovascular comorbidities.
Supporting source [1]
In-hospital mortality and intermediate-term associations
PhenoAge acceleration was independently associated with in-hospital mortality (odds ratio 1.051, 95% confidence interval 1.018–1.084, P = 0.002), while chronological age was not; PhenoAge itself was also independently associated (odds ratio 1.042, 95% confidence interval 1.013–1.072, P = 0.004). Over a median follow-up of 1285 days, all three aging metrics were independently associated with both composite endpoints and with heart failure hospitalization in multivariable analyses. Discrimination for intermediate-term outcomes was similar across metrics (area under the curve 0.63–0.71). PhenoAge added incremental value over chronological age (net reclassification improvement 0.38–0.43; integrated discrimination improvement 0.059–0.069; P ≤ 0.005). These are associations, not proof of causation.
Supporting source [1]
Abstract-only scope and proposed risk stratification
The authors conclude that PhenoAge acceleration independently predicted in-hospital mortality after AMI and may reflect acute physiological vulnerability not captured by chronological age. They suggest biological aging assessment may help identify biologically vulnerable patients at presentation and support personalized risk stratification in geriatric cardiology, and they call for further prospective evaluation in older adults with acute coronary syndromes. Only the abstract was reviewed; the full text was not reviewed, so details of the cohort, laboratory derivation and model adjustment could not be checked.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a single-center retrospective cohort of 192 patients, so the findings are associations and cannot establish causation or generalizability.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Grech M, Grech G, Schembri J, Fenech A, Fava S. · europepmc.org · June 1, 2026