A Pilot Study: Serial Characterization of Pediatric Heart Transplant Myocardium by Cardiac Magnetic Resonance Imaging (CMR) at 3T (RF_TH_241)

In pediatric heart transplant recipients (PHTR), unique progressive myocardial changes may occur post-transplantation. PHTR receive long-term immunosuppressants, may experience acute rejection (AR), and are at risk for coronary vasculopathy. AR remains one of the leading causes of morbidity and mortality for the transplant population. Currently, a gap in knowledge exists regarding serial changes in myocardial characteristics as PHTR age. While AR is traditionally assessed by cardiac catheterization with endomyocardial biopsy, this is invasive, costly, and subject to sampling error. Novel cardiac magnetic resonance imaging (CMR) techniques utilize parametric (T1, T2) mapping to non-invasively assess myocardium for signs of AR. We aimed to assess serial, pediatric myocardial changes by CMR at 3T. We hypothesized that CMR parametric mapping changes over time, dramatically with AR.

Methods: We performed a single-center study on PHTR at the Herma Heart Institute (Children’s Wisconsin) from September 2016 to June 2024. Inclusion criteria: PHTR ≤18y at transplantation and ≥2 consecutive CMR (Siemens 3T Skyra®) between 8-25y. REDCap® database included cardiac history and CMR volumetric, parametric, and strain data (Circle CVI analysis). Paired Student’s t-tests compared changes between first and last CMR. Independent Student’s t-tests assessed CMR for those with and without AR (SPSS28, SAS 9.4).

Results: The 20 PHTR were predominantly male (60%) and White (90%), with mean transplant age 4.2±4.8y. Eight PHTR had 2 CMR; 4 had 3 CMR, and 8 had 4 CMR at 3T. Mean transplant duration at recent CMR was 11.7±3.9y. 65% of PHTR had at least two AR episodes; 30% required treatment (acute cellular rejection ≥2R or antibody mediated rejection ≥2). Left ventricular end-diastolic volume and cardiac output increased over time (p=0.022 and p=0.01). Strain was no different over time. Native T1 significantly increased with AR (p=0.035). (Tables 1 and 2, Figure 1).

Conclusion: This pilot, single-center, longitudinal PHTR study is novel, providing baseline 3T data against which changes in CMR parametric and strain data can be viewed. We demonstrated that serial mapping of PHTR by CMR revealed increased native T1 with AR. These results complement previous studies conducted on 1.5T systems; Sethi et al. performed a small study where T2 increased with AR, and Usman et al. showed this in adults, with resolution after treatment. Understanding these myocardial characteristics, definable by CMR, will allow clinicians to better appreciate the specific changes that occur with AR. In the future, large, multi-center longitudinal 3T studies are needed for more sufficient serial 3T data.

Figure. Changes in CMR parametric imaging in individual PHTR: For the first scan, PHTR with rejection have a significantly increased myocardial native T1 than PHTR without rejection (p=0.035). No significant differences in myocardial T2 and ECV between both groups.