Recipient contributions to primary graft dysfunction in heart transplantation
- 1Temerty Faculty of Medicine, University of Toronto
- 2Division of Cardiac Surgery, University of Toronto
- 3Peter Munk Cardiac Center, University Health Network
Abstract
Primary graft dysfunction (PGD) remains the leading cause of early mortality post heart transplantation (HT). Across several international and national registries, the incidence of PGD has continued to increase. The mechanistic contributions of donor and procedural insults, namely brain or circulatory death, ischemic exposure, and ischemia-reperfusion injury, have been consistently emphasized across various reports. As the surgical techniques and procurement strategies within the current era of HT continue to improve, the net of recipients broadens and includes more high-risk, frail, and comorbid patients. This review therefore aims to explore the recipient contributions of PGD across four domains: hemodynamics and use of mechanical circulatory support, preoperative medical therapy, end-organ dysfunction, and recipient-driven operative characteristics. For each domain, we describe its incidence, the predictor's underlying mechanism, and its contribution to the recipient's biology. Durable LVAD support, pre-transplant ECMO, amiodarone exposure, renal dysfunction, and prior sternotomy emerge as consistently reported independent predictors of PGD, whereas findings for temporary VAD and IABP remain inconsistent. These exposures provide distinct pathways to generate a hostile recipient environment characterized by a primed innate immune system, systemic inflammation, hemodynamic burden, vasomotor dysfunction, multi-organ dysfunction, and operative burden. However, no interventional study has yet to examine the effect of modifying recipient risk factors on PGD development; thereby, existing evidence are derived from observational studies implying association rather than causation. Bridging the gap between recipient risk factors and biologic contributions to PGD may unveil areas for recipient optimization, ultimately improving HT outcomes.
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BibTeX
@article{elhamad2026recipient,
title = {{Recipient contributions to primary graft dysfunction in heart transplantation}},
author = {Ahmed El-Hamad and Nitish K. Dhingra and Vivek Rao},
journal = {Frontiers in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.3389/fcvm.2026.1984203},
url = {https://www.frontiersin.org/articles/10.3389/fcvm.2026.1984203/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Recipient contributions to primary graft dysfunction in heart transplantation
AU - Ahmed El-Hamad
AU - Nitish K. Dhingra
AU - Vivek Rao
PY - 2026
DA - 2026/10/27
JO - Frontiers in Cardiovascular Medicine
DO - 10.3389/fcvm.2026.1984203
UR - https://www.frontiersin.org/articles/10.3389/fcvm.2026.1984203/full
AB - Primary graft dysfunction (PGD) remains the leading cause of early mortality post heart transplantation (HT). Across several international and national registries, the incidence of PGD has continued to increase. The mechanistic contributions of donor and procedural insults, namely brain or circulatory death, ischemic exposure, and ischemia-reperfusion injury, have been consistently emphasized across various reports. As the surgical techniques and procurement strategies within the current era of HT continue to improve, the net of recipients broadens and includes more high-risk, frail, and comorbid patients. This review therefore aims to explore the recipient contributions of PGD across four domains: hemodynamics and use of mechanical circulatory support, preoperative medical therapy, end-organ dysfunction, and recipient-driven operative characteristics. For each domain, we describe its incidence, the predictor's underlying mechanism, and its contribution to the recipient's biology. Durable LVAD support, pre-transplant ECMO, amiodarone exposure, renal dysfunction, and prior sternotomy emerge as consistently reported independent predictors of PGD, whereas findings for temporary VAD and IABP remain inconsistent. These exposures provide distinct pathways to generate a hostile recipient environment characterized by a primed innate immune system, systemic inflammation, hemodynamic burden, vasomotor dysfunction, multi-organ dysfunction, and operative burden. However, no interventional study has yet to examine the effect of modifying recipient risk factors on PGD development; thereby, existing evidence are derived from observational studies implying association rather than causation. Bridging the gap between recipient risk factors and biologic contributions to PGD may unveil areas for recipient optimization, ultimately improving HT outcomes.
SN - 2297-055X
ER -