Surveillance of Chronic Graft Failure Utilizing Cardiac Magnetic Resonance Imaging in Pediatric Heart Transplantation

Abstract

<h3>Purpose</h3> The cause of chronic graft failure (CGF) in heart transplantation (HT) is multifactorial including cardiac allograft vasculopathy (CAV) and rejection. Previous studies have shown that endomyocardial biopsy (EMB) can detect fibrosis and microvessel disease (MVD) in patients with CGF. We sought to evaluate associations between, 1. CAV, 2. Historical moderate to severe (M/S) rejection, and 3. Histopathologic changes of CGF on EMB with cardiac magnetic resonance imaging (CMR) parameters to assess its use as a non-invasive surveillance modality for CGF in pediatric heart transplant patients (PHT). <h3>Methods</h3> Retrospective evaluation of PHT who underwent CMR between 9/2015 and 10/2021 was performed. Those with EMB within 6 months of CMR were included; PHT with M/S rejection on EMB were excluded. CAV was assessed per ISHLT guidelines. Historical M/S rejection, included PHT with a history of ACR >2R or AMR>2. CMR included assessment of cardiac function, myocardial edema (T2 mapping), fibrosis (pre-contrast T1 mapping and extracellular volume fraction), and myocardial perfusion reserve index (MPRi) calculated from stress perfusion imaging. On EMB, fibrosis was qualitatively scored on a scale of 0-5 and MVD was quantified as number of capillaries with stenotic wall thickening per fields of view. Wilcoxon rank sum test or Spearman rank correlation investigated relationships between presence of CAV, historical M/S rejection, EMB and CMR findings. Unadjusted p-values are reported. <h3>Results</h3> Forty-one PHT with median age at CMR of 15.7 years (11.6,19.3) and time from HT of 6.4 years (4.1,11.0) were studied. CAV was present in 9/41(22.0%), although only 2/9 had greater than CAV 1. Historical M/S rejection was present in 14/41 (34.2%). Presence of CAV was associated with lower LVEF (60% vs 56%; p=0.03), higher peak T2 (53 vs 56 ms; p=0.04). Historical M/S rejection was associated with higher global T2 (47 vs 49 ms; p=0.01) and peak T2 (53 vs 57 ms; p=0.02). Higher fibrosis score on EMB was associated with lower MPRi on CMR (rho= -0.35; p=0.04). <h3>Conclusion</h3> Abnormalities in CMR parameters are noted in those with CAV, historical M/S rejection, and greater fibrosis on EMB in a relatively healthy PHT cohort. Longitudinal follow up studies in larger cohorts may aid in further refining the role of CMR in CGF surveillance.