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  • Title: Characterization of Left Ventricular Dysfunction by Myocardial Strain in Critical Pulmonary Stenosis and Pulmonary Atresia After Neonatal Pulmonary Valve Balloon Dilation.
    Author: Ronai C, Ghelani SJ, Marshall AC, Harrild DM, Gauvreau K, Colan SD, Brown DW.
    Journal: Am J Cardiol; 2019 Feb 01; 123(3):454-459. PubMed ID: 30503800.
    Abstract:
    Transient left ventricular (LV) dysfunction occurs in some infants born with critical pulmonary stenosis (PS) or membranous pulmonary atresia with intact ventricular septum (PAIVS) after pulmonary valve (PV) balloon dilation (BD). The cause for this is not well understood. We sought to characterize this LV dysfunction by investigating regional differences in this cohort using myocardial strain imaging. Patients who underwent neonatal (<2 weeks age) PV BD for critical PS or PAIVS from Jan, 2007 to March, 2014 with echocardiographic images suitable for strain analysis were identified; infants with ≥moderate post-BD LV dysfunction (ejection fraction <40%, n = 8) were matched 1:1 with controls who underwent PV BD but did not develop LV dysfunction. Longitudinal and circumferential global and segmental strain were analyzed before and after PV BD. For the 8 LV dysfunction cases, LV global longitudinal strain worsened after PV BD (-16% pre- vs -8% post-PV BD, p = 0.008) with similar impairment in global LV circumferential strain (-17% vs -8%, p = 0.008); there was no significant change in RV global or segmental longitudinal strain pre- vs post-PVBD. No significant pre/post-BD differences in global or circumferential strain were found in control pts. Segmental analysis of longitudinal and circumferential LV strain before and after balloon dilation in cases demonstrated decreased strain in all segments, but more pronounced and statistically significant in septal segments as compared with the free wall. In conclusion, transient LV dysfunction post-PV BD for critical PS/PAIVS is characterized by impaired global longitudinal and circumferential LV strain, with the most significant reductions in strain at the interventricular septum; longitudinal RV strain remains unchanged. These findings suggest that the mechanism of LV dysfunction post-PV BD is adverse ventricular-ventricular interactions specifically involving the interventricular septum.
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