Adverse Maternal Fetal Environment Partially Mediates Disparate Outcomes in Non-White Neonates with Major Congenital Heart Disease

Stephanie Santana; Shabnam Peyvandi; John M Costello; Rebecca J Baer; James W Collins Jr; Tonia Branche; Laura L Jelliffe-Pawlowski; Martina A Steurer

doi:10.1016/j.jpeds.2022.06.036

Adverse Maternal Fetal Environment Partially Mediates Disparate Outcomes in Non-White Neonates with Major Congenital Heart Disease

J Pediatr. 2022 Dec:251:82-88.e1. doi: 10.1016/j.jpeds.2022.06.036. Epub 2022 Jul 5.

Authors

Stephanie Santana¹, Shabnam Peyvandi², John M Costello³, Rebecca J Baer⁴, James W Collins Jr⁵, Tonia Branche⁵, Laura L Jelliffe-Pawlowski⁶, Martina A Steurer²

Affiliations

¹ Department of Pediatrics, Division of Cardiology, Shawn Jenkins Children's Hospital, Medical University of South Carolina, Charleston, SC. Electronic address: santanas@musc.edu.
² Department of Pediatrics, Division of Critical Care, University of California San Francisco, San Francisco, CA; Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA.
³ Department of Pediatrics, Division of Cardiology, Shawn Jenkins Children's Hospital, Medical University of South Carolina, Charleston, SC.
⁴ Department of Pediatrics, University of California San Diego, La Jolla, CA.
⁵ Department of Pediatrics, Division of Neonatology, Ann & Robert H. Lurie Children's Hospital of Chicago at Northwestern University Feinberg School of Medicine, Chicago, IL.
⁶ Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA.

Abstract

Objective: To determine whether differential exposure to an adverse maternal fetal environment partially explains disparate outcomes in infants with major congenital heart disease (CHD).

Study design: Retrospective cohort study utilizing a population-based administrative California database (2011-2017). Primary exposure: Race/ethnicity. Primary mediator: Adverse maternal fetal environment (evidence of maternal metabolic syndrome and/or maternal placental syndrome).

Outcomes: Composite of 1-year mortality or severe morbidity and days alive out of hospital in the first year of life (DAOOH). Mediation analyses determined the percent contributions of mediators on pathways between race/ethnicity and outcomes after adjusting for CHD severity.

Results: Included were 2747 non-Hispanic White infants (reference group), 5244 Hispanic, and 625 non-Hispanic Black infants. Hispanic and non-Hispanic Black infants had a higher risk for composite outcome (crude OR: 1.18; crude OR: 1.25, respectively) and fewer DAOOH (-6 & -12 days, respectively). Compared with the reference group, Hispanic infants had higher maternal metabolic syndrome exposure (43% vs 28%, OR: 1.89), and non-Hispanic Black infants had higher maternal metabolic syndrome (44% vs 28%; OR: 1.97) and maternal placental syndrome exposure (18% vs 12%; OR, 1.66). Both maternal metabolic syndrome exposure (OR: 1.21) and maternal placental syndrome exposure (OR: 1.56) were related to composite outcome and fewer DAOOH (-25 & -16 days, respectively). Adverse maternal fetal environment explained 25% of the disparate relationship between non-Hispanic Black race and composite outcome and 18% of the disparate relationship between Hispanic ethnicity and composite outcome. Adverse maternal fetal environment explained 16% (non-Hispanic Black race) and 21% (Hispanic ethnicity) of the association with DAOOH.

Conclusions: Increased exposure to adverse maternal fetal environment contributes to racial and ethnic disparities in major CHD outcomes.

Keywords: cardiac defects; cardiovascular pregnancy complication; fetal diseases; health inequities; hospital mortality; infant morbidity; retrospective studies; risk factors.

MeSH terms

Female
Heart Defects, Congenital*
Hispanic or Latino
Humans
Infant
Infant, Newborn
Metabolic Syndrome*
Placenta
Pregnancy
Retrospective Studies

Grants and funding

T37 MD014248/MD/NIMHD NIH HHS/United States