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Comprehensive left ventricular myocardial deformation assessment in children with Kawasaki disease
1 Section of Pediatric Cardiology, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas
2 Division of Pediatric Cardiology, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota
3 Smidt Heart Institute, Cedars‐Sinai Medical Center, Los Angeles, California
* Corresponding Author: Aura A. Sanchez, Section of Pediatric Cardiology, Texas Children’s Hospital, Baylor College of Medicine, 6651 Main Street, Suite E1920, Houston, TX 77030. Email:
Congenital Heart Disease 2019, 14(6), 1024-1031. https://doi.org/10.1111/chd.12787
Abstract
Objective: Children with Kawasaki disease (KD) with persistent coronary artery aneurysms (CAAs) can develop chronic vasculopathy and subsequent myocardial ischemia. Early detection of this process is challenging. Myocardial deformation anal‐ ysis can detect early alterations in myocardial performance. We aim to determine whether there are differences in myocardial deformation between KD patients with and without CAAs.Design: This is a cross‐sectional study of 123 echocardiograms performed on 103 children with KD. Myocardial deformation was measured with two‐dimensional speckle tracking (2DSTE). The echocardiograms were divided into groups according to the KD phase in which they were performed: acute, subacute, and convalescent/ chronic. The convalescent/chronic phase group was then divided based on the pres‐ ence or absence of CAAs. Left ventricular (LV) global longitudinal strain (GLS), global longitudinal strain rate (GLSSR), global circumferential strain (GCS), global circum‐ ferential systolic strain rate (GCSSR), peak torsion, and torsion rate were measured.
Results: The numbers of echocardiograms analyzed in each of the KD phase groups were: 31 acute, 25 subacute, and 67 convalescent/chronic. Myocardial deformation was within normal limits in all groups. However, GLSSR, GCSSR, peak torsion, and torsion rate were lower in the convalescent/chronic phase group than in the acute phase group (mean, −1.37 ± 0.24 vs −1.55 ± 0.21 1/s; −1.63 ± 0.27 vs −1.84 ± 0.35 1/s; 2.49 ± 1.13 vs 3.41 ± 2.60 °/cm, and 21.97 ± 8.36 vs 26.69 ± 10.86 °/cm/s; P < .05 for all). The convalescent/chronic phase subgroup with CAAs had lower GLSSR and GCSSR than the subgroup without CAAs (mean, −1.23 ± 0.22 vs −1.42 ± 0.22 1/s; −1.46 ± 0.25 vs −1.68 ± 0.26 1/s, P < .05 for both).
Conclusions: Children in the convalescent/chronic phase of KD have a subtle de‐ crease in strain rate when compared to the acute phase, although within the normal range. This decrease is more pronounced in children with CAAs than those without CAAs. Longitudinal studies are needed to discern whether low‐normal strain rate predicts decreased myocardial function in the long term.
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