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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 analysis 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 presence or absence of CAAs. Left ventricular (LV) global longitudinal strain (GLS), global longitudinal strain rate (GLSSR), global circumferential strain (GCS), global circumferential 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 decrease 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., (© 2019 Wiley Periodicals, Inc.)

Background: Right ventricular (RV) dilation, RV dysfunction, RV outflow tract obstruction, and branch pulmonary artery stenosis are risk factors associated with the need for future surgical or catheter-based intervention commonly assessed by cardiac magnetic resonance in patients with tetralogy of Fallot who have undergone initial repair. The ability of echocardiography to predict the presence of these risk factors is limited., Objective: We aimed to determine the association between echocardiographic parameters of right ventricular diastolic dysfunction and risk factors for intervention as identified on cardiac magnetic resonance imaging (CMR)., Design: We reviewed all echocardiograms and CMRs performed at our institution within 1 year of each other in patients with repaired tetralogy of Fallot. We evaluated patients for the following: RV systolic dysfunction (RV ejection fraction <45%), RV dilation (right ventricular end-diastolic volume ≥ 160 mL/m(2)), and RV obstruction (RV outflow tract gradient ≥ 3 m/s by echocardiogram or branch pulmonary artery stenosis assessed by CMR). We evaluated for associations between the above CMR findings and echocardiographic parameters of diastolic function., Results: CMR and echocardiographic images performed between March 2007 and March 2012 were available in 99 patients. RV obstruction was associated with lower E/A ratio (P = .02), E/A reversal (P = .02), and prograde end diastolic pulmonary flow (P < .01). Low tricuspid annular a' and low septal s' were associated with lower RV ejection fraction (P < .01, P < .01). Elevated E/e' was associated with higher RV end diastolic volume (P = .04). In predicting the presence of any of the evaluated risk factors for future intervention, TV E/e' ≥ 4.7 had positive predictive value (PPV) of 86% and negative predictive value (NPV) of 50%, TV E/A reversal had PPV of 89% and NPV of 34, and prograde end diastolic pulmonary flow on echocardiogram had PPV of 91% and NPV of 38%., Conclusions: Echocardiographic parameters of diastolic dysfunction have a reasonable PPV but poor NPV for predicting clinically significant risk factors identified by CMR., (© 2015 Wiley Periodicals, Inc.)

Background: Doppler tissue imaging (DTI) velocities have been reported to be relatively independent of changes in ventricular loading conditions in adult studies. The clinical impact of altered left ventricular (LV) preload and afterload on DTI velocities in children with congenital heart disease has not been adequately evaluated. The purpose of this study was to evaluate the impact of chronic LV preload and afterload on DTI velocities in children with isolated ventricular septal defect and aortic valve stenosis compared with age-matched normal and abnormal (dilated cardiomyopathy) control groups., Methods: From an apical 4-chamber view, DTI velocities were obtained at the cardiac base at the lateral mitral annulus, lateral tricuspid annulus, and interventricular septum in early diastole, late diastole, and ventricular systole., Results: The majority of DTI velocities did not change significantly in patients with increased LV preload. Patients with increased LV afterload had significantly decreased systolic and early diastolic DTI velocities at both the lateral mitral annulus and ventricular septum compared with control subjects. Children with dilated cardiomyopathy had significantly decreased DTI velocities at all myocardial annular locations., Conclusions: We conclude that increases in chronic LV preload do not significantly affect the majority of DTI velocities in children with ventricular septal defects. In addition, significantly increased chronic LV afterload in children with aortic valve stenosis is associated with decreased DTI velocities in the absence of other identifiable abnormalities of LV function. Decreased DTI velocity may be secondary to increased afterload or may alternatively be an early marker of subclinical LV longitudinal dysfunction.