Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease

Introduction: Fetuses with CHD have smaller total brain volume (TBV) and are at risk for acquired brain white matter injury (WMI), both of which are linked to neurodevelopmental impairments. Social determinants of health (SDOH) and other fetal environmental factors have been linked to fetal brain health in other populations. Our aim was to test our hypothesis that these exposures influence fetal brain growth and postnatal WMI risk in severe CHD. Methods: Our prospective longitudinal cohort study enrolled fetuses with severe CHD to undergo fetal brain MRI and postnatal pre-operative brain MRI. Participants completed home environment surveys on individual SDOH and exposures. Community SDOH metrics were determined using Child Opportunity Index (COI) based on home address. An ‘at risk’ fetus composite was created if there was exposure to: personal/household smoking, welfare/food stamps, or poverty. TBV was calculated at both time points. Presence/degree of WMI was determined on postnatal MRI. Repeated measures analysis and logistic regression were performed to determine association between individual and community SDOH metrics with rate of TBV growth and risk of WMI. Results: 55 participants enrolled (54 fetal scans: mean GA 33.9 wks, 95%CI: 33.7,34.1; 47 neonatal scans: mean GA 39.3 wks 95%CI: 38.9,39.6). Fetal sex, smoking exposure, and several individual SDOH were associated with TBV growth. Adjusting for fetal sex and GA at scan, rate of TBV growth was slower with smoking exposure (coeff: -5.2, 95%CI: -10.3, -0.2, p= 0.04) and trended towards significance for those with welfare/food stamps or poverty. ‘At risk’ fetuses had slower rate of TBV growth than those without risk (coeff: -2.5, 95%CI: -5.0, -0.07, p= 0.04) (Figure 1). There were lower odds of pre-operative WMI with high COI compared to low after adjusting for GA at scan (OR= 0.16, 95%CI: 0.03, 0.9, p= 0.04). Conclusion: Smoking exposure and individual-level SDOH influence brain growth, while community COI is associated with risk of postnatal pre-op WMI in CHD. Our findings identify targets for intervention to optimize brain growth and outcomes in the CHD population, including smoking cessation programs, and nutritional and needs assessment during pregnancy.

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Publication Details

Journal
Circulation
Published
2024-11-12
DOI
https://doi.org/10.1161/circ.150.suppl_1.4122507
Primary Topic
Congenital Heart Disease Studies
Type
article
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article

Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease

Lesje DeRose, Flora Nuñez Gallegos, Megan Martin, Shabnam Peyvandi et al.
Circulation
Congenital Heart Disease Studies
article

Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease

Lesje DeRose, Flora Nuñez Gallegos, Megan Martin, Shabnam Peyvandi, Martina A. Steurer, Elizabeth George, Patrick S. McQuillen, Karla Luna Silva, Xu Duan
article en

Abstract

Introduction: Fetuses with CHD have smaller total brain volume (TBV) and are at risk for acquired brain white matter injury (WMI), both of which are linked to neurodevelopmental impairments. Social determinants of health (SDOH) and other fetal environmental factors have been linked to fetal brain health in other populations. Our aim was to test our hypothesis that these exposures influence fetal brain growth and postnatal WMI risk in severe CHD. Methods: Our prospective longitudinal cohort study enrolled fetuses with severe CHD to undergo fetal brain MRI and postnatal pre-operative brain MRI. Participants completed home environment surveys on individual SDOH and exposures. Community SDOH metrics were determined using Child Opportunity Index (COI) based on home address. An ‘at risk’ fetus composite was created if there was exposure to: personal/household smoking, welfare/food stamps, or poverty. TBV was calculated at both time points. Presence/degree of WMI was determined on postnatal MRI. Repeated measures analysis and logistic regression were performed to determine association between individual and community SDOH metrics with rate of TBV growth and risk of WMI. Results: 55 participants enrolled (54 fetal scans: mean GA 33.9 wks, 95%CI: 33.7,34.1; 47 neonatal scans: mean GA 39.3 wks 95%CI: 38.9,39.6). Fetal sex, smoking exposure, and several individual SDOH were associated with TBV growth. Adjusting for fetal sex and GA at scan, rate of TBV growth was slower with smoking exposure (coeff: -5.2, 95%CI: -10.3, -0.2, p= 0.04) and trended towards significance for those with welfare/food stamps or poverty. ‘At risk’ fetuses had slower rate of TBV growth than those without risk (coeff: -2.5, 95%CI: -5.0, -0.07, p= 0.04) (Figure 1). There were lower odds of pre-operative WMI with high COI compared to low after adjusting for GA at scan (OR= 0.16, 95%CI: 0.03, 0.9, p= 0.04). Conclusion: Smoking exposure and individual-level SDOH influence brain growth, while community COI is associated with risk of postnatal pre-op WMI in CHD. Our findings identify targets for intervention to optimize brain growth and outcomes in the CHD population, including smoking cessation programs, and nutritional and needs assessment during pregnancy.

CirculationVol. 150(Suppl_1)
No poverty
Openalex Percentile: Top 69%
Congenital Heart Disease Studies
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