Association of donor and recipient demographics with CMR tissue mapping parameters in healthy pediatric heart transplant patients (RF_TH_244)

Presenting Author(s)

• AL

  Andrew A. Lawson, MD

  Fellow
  Ann & Robert H. Lurie Children's Hospital of Chicago

Primary Author(s)

• AL

  Andrew A. Lawson, MD

  Fellow
  Ann & Robert H. Lurie Children's Hospital of Chicago

Co-Author(s)

• DM

  Defne Magnetta, MD

  Attending Physician
  Ann & Robert H. Lurie Children's Hospital of Chicago
• MC

  Matthew Cornicelli, MD

  Assistant Professor of Pediatrics
  Ann & Robert H. Lurie Children's Hospital of Chicago
• AP

  Andrada R. Popescu, MD

  Attending Physician
  Ann & Robert H. Lurie Children's Hospital of Chicago
• KW

  Kae Watanabe, MD

  Attending Physician
  Baylor College of Medicine
• 

  Simon Lee, MD

  Associate Professor of Pediatrics
  Ann & Robert H. Lurie Children's Hospital of Chicago
• 

  Michael Markl, PhD

  Professor
  Northwestern University Feinberg School of Medicine
• 

  Nazia Husain, MD, MPH

  Attending Physician
  Ann & Robert H. Lurie Children's Hospital of Chicago

Background: Multiparametric CMR has an evolving role in graft surveillance after pediatric heart transplantation. Normal myocardial T1, ECV, and T2 values differ based on patient age in healthy pediatric patients without heart transplants. However, there is little normative data for children < 8 years. In heart transplant recipients, graft pathology also influences mapping values. Our goal was to identify normal myocardial mapping values in pediatric heart transplant recipients (PHTR) without history of significant graft pathology and to identify associations with patient- and donor-characteristics.

Methods: We performed a retrospective chart review of consecutive, first-time CMR studies in PHTR from 2017-2023. PHTR were < 18y at the time of transplant.  Exclusion criteria included any prior rejection episode (any AMR, ACR >1R, or treated, biopsy negative rejection) before or up to 1 year after CMR, cardiac allograft vasculopathy (CAV), elevated donor-derived cell-free DNA > 0.15% before or up to 3 months after CMR, CMR-derived RV EF < 50%, LV EF < 55%, or presence of LGE. A single reviewer performed parametric mapping analysis (QMap, Medis), with segmental values averaged to yield global values. We evaluated differences in global parametric mapping values based on baseline patient clinical characteristics.

Results: Of 137 PHTR meeting inclusion criteria, 28 met all exclusion criteria were included for further analysis. Median age at CMR was 10.6y (IQR 5.9-14.9), with median time since transplant 4.6y (3.9-8.0). For the entire cohort, median mapping values were: native T1 1033 ms (1013-1076), ECV 31% (27.8-35.0), T2 49.0 ms (46.5-51.6). Segmental medians and interquartile ranges are provided in Figure 1.  Univariate regression analysis identified significant negative associations between both patient age and donor age with T1, ECV, and T2 (p-value range: < 0.001 - 0.01); pre-transplant diagnosis of congenital heart disease was associated with higher ECV compared to patients with pre-transplant diagnosis of cardiomyopathy (p = 0.03); no significant associations between mapping parameters and heart rate, time since transplant, or ischemic time were found (Table 1). By multivariate regression analysis, patient age remained negatively correlated with T1 (β = -5.2, R² = 0.45, p=0.005), ECV (β = -0.4%, R² = 0.65, p< 0.001), and T2 (β = -0.5, R² = 0.47, p=0.003), independent of donor age, which was no longer a significant predictor variable in the models. Multiparametric mapping values for healthy PHTR < 10 and >10 years-old are presented in Table 2.

Conclusion: We present myocardial parametric mapping values for healthy PHTR without history of significant graft pathology across a wide age range. Younger patient age is associated with higher T1, T2, and ECV, independent of donor age.

Figure 1: Segmental myocardial T1, ECV, and T2 medians and interquartile ranges among pediatric heart transplant recipients without history of significant identified graft pathology.