146 - Slower Placental Growth in Fetuses with Congenital Heart Disease
Friday, April 28, 2023
5:15 PM – 7:15 PM ET
Poster Number: 146 Publication Number: 146.135
Sonali Ajwani, Washington University in St. Louis School of Medicine, St. Louis, MO, United States; Kaylin Taylor, Washington University in St. Louis School of Medicine, St. Louis, MO, United States; James D. Quirk, Washington University School of Medicine, St. Louis, MO, United States; Erica L. Jamro, Washington University in St. Louis School of Medicine, Clifton Park, NY, United States; Anthony Odibo, Washington University in St. Louis School of Medicine, Saint Louis, MO, United States; Yong Wang, Washington University in St. Louis School of Medicine, Town and Country, MO, United States; Joshua Shimony, Washington University School of Medicine, St. Louis, MO, United States; Cynthia Ortinau, Washington University in St. Louis School of Medicine, St. Louis, MO, United States
Research Assistant Washington University in St. Louis School of Medicine
Background: Fetuses with complex congenital heart disease (CHD) display altered brain development that likely results from disturbances in genetic, physiologic, and maternal environmental pathways, all of which may also alter placental development. Placental abnormalities are common in pregnancies affected by fetal CHD, but the trajectory of placental growth and its contributions to regional fetal brain development are not well studied. Objective: 1) Compare third trimester placental growth between fetuses with CHD and controls, and 2) Determine the associations between placental growth and regional fetal brain growth. Design/Methods: Pregnant women with a fetal diagnosis of complex CHD and pregnant women with a healthy fetus were recruited from 2018-2022. Participants underwent magnetic resonance imaging (MRI) at 28-30 and 34-36 weeks gestation. Whole placental volume was measured at each MRI and cerebral white matter (WM), cortical gray matter (CGM), and subcortical gray matter (SCGM) volumes were measured at the second MRI. Multivariable mixed-effects linear regression models were fit using backwards stepwise selection. Results: There were 47 fetuses with CHD (hypoplastic left heart syndrome: n=9, 19%; dextro-transposition of the great arteries: n=7, 15%; tetralogy of Fallot: n=6, 13%; other: n=25, 53%) and 26 controls included in the study. The CHD and control groups were comparable on all maternal factors except for abnormal amniocentesis (p=0.003). In the mixed-effects models, placental volumes were 93.7 cm3 lower in the CHD group compared to controls (standard error [SE]: 36.7, p=0.01), adjusted for gestational age at MRI, maternal body mass index, tobacco exposure, fertility treatment, and fetal growth restriction (Figure 1). Other clinical factors did not relate to placental volumes. The CHD group had smaller brain volumes across all regions (WM volume: β=-17.8, SE=3.8, p< 0.0001; CGM: β=-10.1, SE=2.6, p< 0.001; SCGM: β=-0.54, SE=0.18, p< 0.01), but placental volume was not associated with brain volumes (WM: β=0.012, SE=0.009, p=0.19; CGM: β=0.005, SE=0.006, p=0.36; SCGM: β=0.0008, SE=0.0004, p=0.06).
Conclusion(s): Pregnancies with fetal CHD have significant reductions in placental volume over the third trimester, which do not appear to differentially affect regional fetal brain growth. Investigations incorporating measures of placental function alongside genetic/epigenetic factors may lend further insight for understanding the potential role of the placenta for fetal brain development in CHD.
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