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Final Program


Program-At-A-Glance

Rapid Fire Session

Session: Rapid Fire Session 5: Peds/CHD - Strain, Amyloidosis (Monitor 12)

Pediatric heart transplant patients with cardiac allograft vasculopathy have abnormal regional strain patterns as measured by novel 4D cardiac magnetic resonance strain analysis

Saturday, February 7, 2026
10:43 AM - 10:50 AM  
Location: Galapagos / Aruba / Ilhabela (2nd Lower Level)

    Presenting Author(s)

  • Marco A. Prado, BSc

    PhD Candidatee
    Purdue University
    West Lafayette, Indiana, United States

    • Primary Author(s)

  • CH

    Christopher Henderson, MD

    Resident Physician
    Vanderbilt University Medical Center, United States

    • Co-Author(s)

  • CE

    Conner Earl, BSc

    MD/PhD Candidate
    Purdue University, Indiana, United States

  • KG

    Kristen George-Durrett, BSc, RT

    Research MRI Technologist
    Vanderbilt University Medical Center
    Nashville, Tennessee, United States

  • Simon Lee, MD

    Medical Director, Kawasaki Disease and Coronary Anomalies Program
    Ann & Robert H. Lurie Children's Hospital of Chicago
    Chicago, Illinois, United States

  • DN

    Deipanjan Nandi, MD, MSc

    Assistant Professor of Pediatrics
    Nationwide Children's Hospital, United States

  • KC

    Kak-Chen Chan, MD

    Medical Director, Complex Pediatric Cardiac Specialty Services
    Joe DiMaggio Children's Hospital, United States

  • SS

    Svetlana Shugh, MD

    Pediatric Cardiologist
    Joe DiMaggio Children's Hospital, United States

  • SK

    Sandra Kikano, MD

    Pediatric Cardiologist
    Duke University Medical Center, United States

  • Margaret M. Samyn, MD, MBA

    Professor of Pediatrics/ Assistant Dean for Scholarly Activities
    Medical College of Wisconsin
    Milwaukee, Wisconsin, United States

  • BD

    Bruce Damon, PhD

    Director of Clinical Imaging Research
    University of Illinois / Carle Foundation Hospital, United States

  • Lazaro Hernandez, MD, MPH

    Pediatric Cardiology Imaging Specialist
    Joe DiMaggio Children's Hospital
    Hollywood, Florida, United States

  • CG

    Craig Goergen, PhD

    Professor
    Purdue University, Indiana, United States

  • JS

    Jonathan H. Soslow, MD

    Assistant Professor, Division of Pediatric Cardiology
    Vanderbilt University Medical Center
    Nashville, Tennessee, United States

Background: Cardiac allograft vasculopathy (CAV) is a leading cause of morbidity and mortality after pediatric heart transplant (PHT). Cardiac catheterization with coronary angiography is the gold standard for diagnosing CAV, but it is invasive and costly. Cardiac magnetic resonance (CMR) has potential to non-invasively detect regional strain abnormalities in CAV, but standard software requires selection of one slice for base, mid and apex, resulting in a significant loss of data. We hypothesized that a novel, 4D CMR strain analysis would detect segmental abnormalities in CAV patients as compared with healthy transplant patients, particularly in apical segments.

Methods: PHT patients undergoing cardiac catheterization and concomitant CMR were prospectively enrolled from 3 sites. For each patient, we used a custom MATLAB analysis toolbox to compile short-axis CMR image stacks into four-dimensional sequences. Using feature tracking, we generated a deformable 3D mesh throughout the cardiac cycle which allowed us to calculate regional surface area and transmural peak strain, time to peak strain, systolic strain rate and diastolic strain rate.



Myocardial segments were assigned to the left anterior descending (LAD), left circumflex (LCA) and right coronary (RCA) artery distributions according to standard myocardial segmentation nomenclature1. CAV was diagnosed by angiography and graded from CAV 1 to CAV 3 based on the 2013 International Society for Heart Lung Transplant classification criteria. Variables between groups were compared with a Wilcoxon rank-sum test.

Results: Forty-six patients were included (median age 17 years [IQR 15-18 years]), eight with CAV (17%). The median LV ejection fraction (LVEF) in the CAV group was 57% [IQR 55-62%] and 60% [IQR 57%-65%] in healthy PHT (p = 0.096). One (12%) CAV patient had LAD stenosis, three (38%) had RCA stenosis, and one (12%) had LCA stenosis. Three (38%) had multivessel disease. Six (75%) were graded as CAV 1 and two (25%) as CAV 2.

When evaluating transmural and surface area peak strain, systolic strain rate and diastolic strain rates, multiple segments were worse in CAV compared with control (Figures 1 and 2). The apex and apical segments tended to be more severely affected than mid and basal segments in the CAV group (Table 1). Eight segments had abnormal strain within the distribution of the affected coronary artery, but only two reached statistical significance.

Conclusion: CAV patients have worse segmental transmural and surface area strain compared to healthy PHT patients with similar LVEF, particularly in the apical segments and apex. These data suggest that abnormal strain in segments supplied by distal coronary artery branches may indicate subclinical ventricular dysfunction in mild CAV. Results are limited by small sample size, inclusion of predominantly mild CAV cases, and anatomic variations in coronary distribution. Further investigation is needed to understand segmental strain patterns in CAV.

Table 1- Abnormal Transmural and Surface Area Strain Metrics in Apical Segments



















































































































Transmural StrainHealthy PHT (n=38)CAVLAD (n=3)(p-value)CAVRCA (n=6)(p-value)CAVLCA (n=2)(p-value)
Apical Septal    
Time to Peak Strain (ms)48.3 [40.0 to 53.3]70.0 [60.0 to 83.3] *(0.020)58.3 [48.3 to 83.3] *(0.045)70.8 [46.7 to 95.0](0.351)
Systolic Strain Rate (%/s)2.05 [0.69 to 3.92]0.54 [-1.25 to 1.40] †(0.072)1.2 [-0.50 to 1.88](0.132)0.78 [-0.50 to 2.06](0.291)
Late Diastolic Strain Rate (%/s)-0.54 [-2.08 to -0.03]-0.99 [-3.87 to -0.80](0.271)-1.65 [-3.14 to -0.74](0.259)0.51 [0.47 to 0.55] *(0.047)
Apex    
Time to Peak Strain (ms)50.0 [16.7 to 55.0]10.0 [1.67 to 71.7](0.598)27.5 [1.67 to 46.7] †(0.060)23.3 [1.67 to 45.0](0.181)
Systolic Strain Rate (%/s)0.66 [-0.28 to 4.21]-1.98 [-2.08 to 0.41] †(0.051)-0.29 [-1.98 to 1.08] †(0.094)-0.25 [-1.05 to 0.56](0.291)
Late Diastolic Strain Rate (%/s)-0.34 [-3.05 to 0.41]1.26 [-1.42 to 1.69](0.109)0.66 [0.19 to 1.26] *(0.020)-0.04 [-0.86 to 0.77](0.495)
Surface Area StrainHealthy PHT (n=38)CAVLAD (n=3)(p-value)CAVRCA (n=6)(p-value)CAVLCA (n=2)(p-value)
Apical Inferior    
Time to Peak Strain (ms)51.7 [45.0 to 56.7]60.0 [58.3 to 76.7] *(0.016)48.3 [45.0 to 60.0](0.877)39.2 [33.3 to 45.0] †(0.099)
Early Diastolic Strain Rate (%/s)3.12 [2.21 to 3.93]3.45 [2.36 to 3.5](1.000)3.00 [1.70 to 3.51](0.393)1.53 [1.36 to 1.70] †(0.082)
Late Diastolic Strain Rate (%/s)1.72 [0.95 to 3.09]3.49 [3.38 to 5.40] *(0.021)3.44 [2.49 to 3.94](0.116)1.19 [-0.23 to 2.60](0.495)
Apical Lateral    
Time to Peak Strain (ms)51.7 [43.3 to 56.7]60.0 [51.7 to 78.3] †(0.070)47.5 [45.0 to 60.0](0.959)43.3 [38.3 to 48.3](0.170)

Data presented as median [IQR] (interquartile range) with p-values from the Wilcoxon rank-sum test comparing CAV subgroups to Healthy PHT.PHT = Pediatric Heart Transplant, CAV = Cardiac Allograft Vasculopathy, LAD = Left Anterior Descending Artery, RCA = Right Coronary Artery, LCA = Left Circumflex Artery* = Statistical significance (p-value < 0.05)† = Approaching statistical significance (p-value < 0.10)Myocardial segments with abnormal strain reaching statistical significance (p < 0.05) or approaching significance (p < 0.10) are highlighted.
Myocardial segments with abnormal strain reaching statistical significance (p < 0.05) or approaching significance (p < 0.10) are highlighted.