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  • Title: Increased systolic vorticity in the left ventricular outflow tract is associated with abnormal aortic flow formations in Tetralogy of Fallot.
    Author: Schäfer M, Barker AJ, Morgan GJ, Jaggers J, Stone ML, Browne LP, Ivy DD, Mitchell MB.
    Journal: Int J Cardiovasc Imaging; 2020 Apr; 36(4):691-700. PubMed ID: 31907684.
    Abstract:
    Aortopathy is a recognized comorbidity of Tetralogy of Fallot (TOF). Aortic flow in children with repaired TOF is abnormal despite normal aortic valve anatomy and early surgical repair that results in aortic size normalization. The purpose of this study was to investigate the flow hemodynamics inside the left ventricle (LV) of children with repaired TOF using 4D-Flow MRI derived vorticity. Vorticity is the spatial derivative of flow velocity and is sensitive to anatomic and geometric variations. Vorticity was calculated inside the LV of children with repaired TOF having normal aortic size (n = 14) and normal controls (n = 10) during systolic ejection phase. All subjects underwent comprehensive biventricular analysis including the MRI based feature-tracking based LV strain analysis and mechanical dyssynchrony. Right ventricular (RV) volumetric indices along with LV mechanical indices were correlated with LV vorticity. All TOF patients had supraphysiologic helical flow in the ascending aorta. The generated peak systolic vorticity integrated over the LV volume was elevated in TOF group compared to control (median: 1344 vs. 858 s-1, P < 0.001). TOF patients had increased LV mechanical dyssynchrony (47 ± 11 vs. 32 ± 7 ms, P < 0.001) and reduced LV global circumferential strain (19 ± 2 vs. 21 ± 2%, P = 0.020). In the TOF group, LV systolic vorticity was independent of RV size and LV mechanical indices. Pathologic aortic flow in children with repaired TOF is associated with abnormal ejection flow patterns inside the LV. Increased systolic vorticity was not associated with LV mechanical dyssynchrony and RV dilation, suggesting that systolic flow inside the LV is independent of impaired LV contractile mechanics and inter-ventricular interactions.
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