Donor Acidosis and Post-Transplant Survival Across Heart Allocation Eras: A National Registry Analysis.

Authors

Sajid Kadir, Sandeep Sasidharan, Victor Perez, Ataul Qureshi, Swethika Sundaravel, Erol Belli

Published in

Clinical transplantation. Volume 40. Issue 9. Pages e70691.

Abstract

Donor blood pH, recorded for nearly all heart donors, may reflect shock, but its value as an isolated predictor of outcomes is unestablished. The 2018 allocation change altered donor use and acuity, so its prognostic weight may be era-dependent.
We studied adult, first-time, isolated heart transplant recipients in the OPTN/UNOS registry (2015-2025), with donor blood pH classified as acidosis (<7.35), normal (7.35-7.45), or alkalosis (>7.45). The primary outcome was all-cause mortality. A covariate-adjusted Cox model tested the donor acid-base-by-allocation-era interaction. Secondary analyses examined short-term mortality, contemporary mechanical circulatory support, allograft failure, dialysis, and stroke.
The primary model included 31,349 recipients and 5,962 deaths. Donor acidosis was associated with mortality before 2018 (hazard ratio 1.18, 95% CI 1.07-1.29) but not after (0.97, 0.86-1.09); the ratio of post- to pre-2018 hazard ratios was 0.82 (0.71-0.96; interaction p = 0.010). The composite of allograft failure or death showed the same pattern (p = 0.009). Continuous donor pH showed no significant association in either era. Among recipients transplanted on or after October 1, 2023, donor acidosis was associated with a higher adjusted risk of extracorporeal membrane oxygenation (risk ratio 1.52, 1.22-1.90) but not 90-day mortality.
Among donor hearts selected for transplantation, donor acidosis was associated with mortality before but not after the 2018 allocation change, although it remained associated with greater mechanical circulatory support. These findings do not establish that all acidotic hearts are suitable or that donor pH can be disregarded; it remains one component of comprehensive donor assessment.

PMID:
42767659
Bibliographic data and abstract were imported from PubMed on 22 Sep 2026.

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