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Reduced Biventricular Volumes and Myocardial Dysfunction Long-term After Pediatric Heart Transplantation Assessed by CMR

Latus, Heiner MD1,2; Hachmann, Pauline MD1; Voges, Inga MD1,3; Mueller, Simon PhD4; Gummel, Kerstin MD1; Reich, Bettina MD1; Sarikouch, Samir MD5,6; Peters, Brigitte6; Mazhari, Nona MD1; Behnke-Hall, Kachina MD1; Jux, Christian MD1; Apitz, Christian MD1,7; Thul, Josef MD1; Akintuerk, Hakan MD1; Bauer, Juergen MD1; Schranz, Dietmar MD1

doi: 10.1097/TP.0000000000002738
Original Clinical Science—General
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Background. Long-term cardiac remodeling after heart transplantation (HT) in children has been insufficiently characterized. The aim of our study was to evaluate ventricular size in HT patients using cardiovascular magnetic resonance (CMR) imaging, to find underlying factors related to potentially abnormal cardiac dimensions and to study its impact on functional class and ventricular function.

Methods. Seventy-five pediatric HT recipients (age 14.0 ± 4.2 y) were assessed by using CMR 11.2 ± 5.4 years after HT. Right ventricular (RV) and left ventricular (LV) volumes and mass were derived from short-axis cine images and myocardial strain/strain rate was assessed using myocardial feature tracking technique. Results were compared with a healthy reference population (n = 79, age 13.7 ± 3.7 y).

Results. LV end-diastolic ventricular volumes were smaller (64 ± 12 versus 84 ± 12 mL/m2; P < 0.001) while mass-to-volume ratio (0.86 ± 0.18 versus 0.65 ± 0.11; P < 0.001) and heart rate (92 ± 14 versus 78 ± 13 beats/min; P < 0.001) were higher in HT patients. LV-ejection fraction (EF) was preserved (66% ± 8% versus 64% ± 6%; P = 0.18) but RV-EF (58 ± 7 versus 62% ± 4%, P = 0.004), LV systolic longitudinal strain (−12 ± 6 versus −15% ± 5%; P = 0.05), diastolic strain rate (1.2 ± 0.6 versus 1.5 ± 0.6 1/s; P = 0.03), and intra and interventricular synchrony were lower in the HT group. Smaller LV dimensions were primarily related to longer follow-up time since HT (β = −0.38; P < 0.001) and were associated with worse functional class and impaired ventricular systolic and diastolic performance.

Conclusions. Cardiac remodeling after pediatric HT is characterized by reduced biventricular size and increased mass-to-volume ratio. These adverse changes evolve gradually and are associated with impaired functional class and ventricular dysfunction suggesting chronic maladaptive processes affecting allograft health.

1 Pediatric Heart Centre, University Children’s Hospital, Giessen, Germany.

2 Department of Pediatric Cardiology and Congenital Heart Disease, German Heart Centre, Munich, Germany.

3 Department of Pediatric Cardiology, Royal Brompton and Harefield NHS Foundation Trust, London, United Kingdom.

4 MUON-STAT Statistical Consulting, Stuttgart, Germany.

5 Department of Heart, Thoracic, Transplantation and Vascular Surgery, Hannover Medical School, Germany.

6 German Competence Network for Congenital Heart Defects, Berlin, Germany.

7 Department of Pediatric Cardiology, University Children’s Hospital Ulm, Ulm, Germany.

Received 21 January 2019. Revision received 26 February 2019.

Accepted 20 March 2019.

The study was supported by the Doris-Haag Stiftung, Frankfurt am Main, Germany and the Willy Robert Pitzer Stiftung, Bad Nauheim, Germany. This work was further supported by the Competence Network for Congenital Heart Defects funded by the Federal Ministry of Education and Research (BMBF, FKZ 01G10210 für 1. Förderphase; FKZ 01GI0601 für Studien der 2. und 3. Förderphase).

The authors declare no conflicts of interest.

H.L., I.V., S.S., C.J., C.A., and D.S. have contributed to the conception and design of the study. H.L., P.H., S.M., K.G., B.R., S.S., B.P., N.M., and K.B.H. have contributed to the acquisition of data, analysis, and interpretation of the data. H.L., I.V., S.S., C.A., J.T., H.A., J.B., and D.S. have contributed to the drafting of the article and have revised it critically for important intellectual content.

Supplemental digital content (SDC) is available for this article. Direct URL citations appear in the printed text, and links to the digital files are provided in the HTML text of this article on the journal’s Web site (www.transplantjournal.com).

Correspondence: Heiner Latus, MD, Department of Pediatric Cardiology and Congenital Heart Disease, German Heart Centre Munich, Technical University Munich, Lazarettstr. 36, 80636 Munich, Germany. (heiner.latus@googlemail.com).

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