Cardio-oncology & otherCohort study
Ex Vivo Perfusion Unmasks a Proteomic Signature of Primary Graft Dysfunction in Donor Hearts
- Prospective proteomic study
- propensity-matched
Authors' conclusion
PGD is defined less by baseline differences than by divergent proteomic trajectories during EVHP. Early enrichment of senescence-associated pathways is followed by coordinated activation of apoptotic and catabolic programs.
Study context
- Population
- Human donation after circulatory death (DCD) hearts supported on ex vivo heart perfusion (EVHP)
- Participants
- 37 participants · 10 matched pairs
- Exposure
- Primary graft dysfunction (PGD) vs non-PGD DCD hearts on EVHP
- PGDn = 10
- non-PGDn = 10reference
- Outcome
- Circulating perfusate proteome (differential protein abundance and pathway enrichment) associated with PGD
- Follow-up
- EVHP initiation (0-2 hours) and termination (3-6 hours)
Main finding
As reported in the abstract
Perfusate proteome, PGD vs non-PGD
| Group | Proteins associated with perfusion time |
|---|---|
| PGD | 33 proteins; median |ρ| = 0.78; q < 0.05 |
| non-PGD | 3 proteins; median |ρ| = 0.83; q < 0.05 |
- Senescence-associated pathways enriched in PGD at EVHP initiation
- NES: 1.93; q < 0.01
- Increased proteins in PGD
- 1,242 increased proteins (742 unique; q < 0.05)
- Decreased proteins in PGD
- 745 decreased proteins (619 unique; q < 0.05)
- Apoptotic pathway enrichment in PGD
- NES: 1.75; q < 0.05
- Catabolic program enrichment in PGD
- NES: 1.42; q < 0.05
- Inflammatory pathway activation in PGD
- NES: 1.68; q < 0.05
Observational data: associations, not effects.
Original publication
Ex Vivo Perfusion Unmasks a Proteomic Signature of Primary Graft Dysfunction in Donor Hearts. JACC Heart Fail. Published 28 August 2026. doi:10.1016/j.jchf.2026.103298
Summarised from the published abstract; every number is checked against it