Development and Validation of a CMR Protocol for Assessing Myocardial Viability in Cardiac Explants: a Porcine Heart Model

Background: Heart transplantation remains the gold standard therapy for patients with end-stage heart failure who have exhausted therapeutic options¹. One of the most critical and yet insufficiently addressed determinants of early graft dysfunction is the viability of the donor myocardium at the time of implantation² especially in the context of Maastricht III grafts (controlled donors after circulatory death).

Methods: This study assessed myocardial viability in ex vivo porcine hearts using CMR. 25 hearts were procured under three distinct conditions: optimal retrieval with minimal ischemic injury (n=4), prolonged warm ischemia (n=9), and controlled donation after circulatory death according to Maastricht III criteria (n=12). After cardioplegic arrest and hypothermic storage, hearts were transported to the CMR platform and stabilized in a polystyrene container and oriented for reproducible acquisition (Figure 1). Imaging was performed on a 1.5T system starting ~90 minutes post-excision and repeated hourly for four hours. In randomly selected cases, acquisitions were continued for 12-24 h, including all minimal ischemia, one extended ischemia, and three Maastricht III hearts. Measurements were standardized with ROI propagation across time points for longitudinal monitoring of tissue integrity.

Results: Polynomial regression of native T1 revealed distinct trajectories across groups (Figure 2). Hearts subjected to extended warm ischemia consistently exhibited the lowest T1, with their polynomial trendline remaining markedly below the other groups. This may be related to the reduction in cellular content caused by necrosis, as the low T1 of pure collagen suggests that early cell death leads to fluid release into the ECM, followed by a further decrease in T1 due to ongoing cellular death. In contrast, the Maastricht III group followed a trajectory closer to that of the minimal ischemia group, with intermediate T1 and a similar upward trend over time. Minimal ischemia hearts displayed the highest overall T1, remaining elevated across the 12-24 h acquisitions. This ordering (Extended ischemia < Maastricht III < Minimal ischemia) provided a clear separation between groups. Importantly, lower native T1 were associated with extended ischemic injury at baseline and may indicate compromised graft viability, while preserved or higher T1 values were consistent with greater structural integrity. The progressive increase in T1 observed across groups may also partly reflect a cumulative rise due to radiofrequency exposure associated with repeated acquisitions, as well as underlying tissue non-viability.

Conclusion: Native T1 mapping allows discrimination between explanted hearts exposed to different ischemic conditions. The ordered separation of groups suggests its potential as a non-invasive biomarker of graft viability, although technical factors such as temperature must be monitored and considered in interpretation.

Evolution of myocardial native T1 over time across groups (Minimal ischemia-green, Extended ischemia-red, Maastricht III-orange). Scatter plots represent individual acquisitions, with second-order polynomial regression lines demonstrating distinct trajectories for each group.