Echocardiographic Prediction of Left Ventricular Dysfunction After Transcatheter Patent Ductus Arteriosus Closure in Children
Objectives: To evaluate the change of left ventricular (LV) systolic function after transcatheter patent ductus arteriosus (PDA) closure in children, and to identify whether echocardiography parameters could be the predictors of LV dysfunction post-PDA closure if present.
Methods: This study enrolled 191 pediatric PDA patients, and all of them underwent successful transcatheter PDA closure between January 2016 and December 2018. The patent ductus arteriosus diameter (PDAd), aortic root diameter (AOd), left atrial diameter (LAd), right ventricular outflow tract dimension (RVOT), LV end-diastolic dimension (LVEDD), and LV end-systolic dimension (LVESD) were all measured by echocardiography at pre-closure, post-closure (within 24 h after the procedure), and follow-up (3 months after the procedure). The ratio of PDAd to AOd (PDAd/AOd), the ratio of LAd to AOd (LAd/AOd), the left ventricular ejection fraction (LVEF), and the fractional shortening (FS) were calculated.
Results: The LAd, LVESD, LVEDD, FS, and LVEF decreased significantly in the 24 h after closure, compared to pre-closure levels. However, all echocardiography parameters recovered to pre-closure levels at 3 months after PDA closure in all patients. Moreover, the pre-closure LAd, LVEF, PDAd/AOd, and LAd/AOd were higher in the patients with post-closure LV systolic dysfunction than in those without post-closure LV systolic dysfunction. Furthermore, the pre-closure LVEF, PDAd/AOd, and LAd/AOd were correlated with the post-closure LVEF, and pre-closure LVEF ≤ 66.5%, PDAd/AOd ≥ 0.28, and LAd/AOd ≥ 1.54 predict the post-closure LV systolic dysfunction.
Conclusion: Transcatheter closure of PDA causes a significant deterioration in LV systolic function early after PDA closure, which recovered completely within 3 months of post-closure in children. Pre-closure LVEF, PDAd/AOd, and LAd/AOd can be the predictors of post-closure left ventricular systolic dysfunction.
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REFERENCES
- https://doi.org//10.1016/j.acvd.2014.01.008
- https://doi.org//10.1161/01.CIR.52.1.157
- https://doi.org//10.1161/01.CIR.38.1S5.V-45
- https://doi.org//10.1053/j.semperi.2011.09.025
- https://doi.org//10.1093/eurheartj/ehq249
- https://doi.org//10.1016/j.ahj.2007.04.045
- https://doi.org//10.1136/hrt.2010.208967.495
- https://doi.org//10.1177/021849230501300106
- https://doi.org//10.1016/j.jacc.2005.09.067
- https://doi.org//10.3389/fped.2017.00280
- https://doi.org//10.1016/0888-6296(89)90105-1
- https://doi.org//10.1007/BF01249624
- https://doi.org//10.1016/j.echo.2017.06.004
- https://doi.org//10.2215/CJN.01660216
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