Heart failure & cardiomyopathiesCohort study
Longitudinal proteomic organ-specific aging in heart failure
- Prospective cohort study
- two cohorts
- repeated plasma proteomic profiling
- exploratory
Authors' conclusion
In this exploratory study, multi-organ aging accelerated before adverse events, and the kidney, lung, and immune OAGs predicted outcome independently of conventional severity markers, supporting a dynamic, organ-level view of HF risk that warrants confirmation in larger cohorts.
Study context
- Population
- Individuals at risk for heart failure (HF), with pre-HF or with HFtwo cohorts
- Participants
- 557 vs 382
- Exposure
- Organ age gaps and HF progression and outcome
- HELPFuln = 557
- Bio-SHiFTn = 382
- Outcome
- Primary endpoint (Bio-SHiFT) related to OAGs, Cox models adjusted up to NT-proBNP and troponin T
Main finding
As reported in the abstract
OAGs and the primary endpoint (Bio-SHiFT)
- Higher organ age gaps (OAGs) predicted the primary endpoint
- Kidney, lung and immune OAGs remained prognostic after full adjustment incl. NT-proBNP and troponin T
Observational data: associations, not effects.
Further findings
Baseline OAGs by HF severity
- Baseline OAGs differed across HF severity in both cohorts
Longitudinal OAG trajectories, HELPFul individuals with LVDD (n = 50) · 4.6 years
- Increasing artery and immune OAGs
Longitudinal OAG trajectories, Bio-SHiFT patients with adverse events · 2.1 years
- Immune OAG β (z-score per year), 95% CI 0.26 to 0.47
- 0.36
- Heart OAG β, 95% CI 0.17 to 0.40
- 0.29
- Event-free patients had stable trajectories
- sharply accelerating multi-organ aging
Original publication
Longitudinal proteomic organ-specific aging in heart failure. Eur J Heart Fail. Published 25 September 2026. doi:10.1093/ejhf/xuag298
Summarised from the published abstract; every number is checked against it