Open Access

ARTICLE

Coronary artery intimal thickening and ventricular dynamics in pediatric heart transplant recipients

by

1 Department of Pediatrics, University of British Columbia & British Columbia Children’s Hospital Research Institute, Vancouver, Canada
2 School of Human Kinetics, Trinity Western University, Langley, Canada
3 British Columbia Children’s Hospital, Children’s Heart Centre, Vancouver, Canada

* Corresponding Author: Dr. Kevin Harris, Rm. 1F27, British Columbia Children’s Hospital, 4480 Oak Street, Vancouver, Canada. Email:

Congenital Heart Disease 2018, 13(5), 663-670. https://doi.org/10.1111/chd.12629

Abstract

Objective: Pediatric heart transplant recipients are at risk of posttransplant coronary artery disease known as cardiac allograft vasculopathy (CAV), and also may develop diastolic dysfunction. As CAV begins with a process of progressive intimal thickening, these occult diffuse changes may be detected using optical coherence tomography (OCT). We hypothesized that the development of CAV, as identified via OCT, may be a mechanism of declining ventricular function. Accordingly, the purpose of this study was to assess coronary artery intimal thickening and LV strain in children who have undergone heart transplantation.
Methods: In 17 children, we analyzed OCT images for coronary intima and media thickness, and cross‐sectional area (CSA). We also performed speckle tracking imag‐ ing (STI) of the LV to determine longitudinal strain and strain rate, in addition to standard echocardiographic measures.
Results: Longitudinal diastolic strain rate was associated with maximum intima thick‐ ness (r = −.497, P = .042), intima CSA, (r = −.489, P = .047), maximum media thickness (r = −.503, P = .039), and media CSA (r = −.614, P = .009). The intima maximum thick‐ ness, intima/media, and intima/lumen ratios were associated with stroke volume index (Std. β = −0.487, P = .023 and Std. β = −0.488, P = .022, respectively).
Conclusions: These findings suggest coronary artery intimal thickening may be mechanistically linked to changes in ventricular function following cardiac transplantation.

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