Abstract

INTRODUCTION: Emerging research supports a common dysfunctional angiogenic mechanism that manifests in mothers as preeclampsia (PE) and in fetuses as congenital heart defects (CHD). METHODS: CHD fetuses came from patients assessed by UMMC's Fetal Heart Program. Controls were identified retrospectively from our ultrasound database, and those with known chromosomal or non-CHD anomalies were excluded. PE was diagnosed by the American College of Obstetricians and Gynecologists’ 2013 guidelines and categorized as early (delivery < 34 weeks) or late. Contributors to early and late PE were assessed and compared with controls using binary logistics regression and Chi-square analysis. RESULTS: Of 2856 meeting inclusion criteria, 215 (7.5%) had CHD. PE occurred in 182 (6.4%) cases, early PE in 28 (1%) and late PE in 153 (5.4%). CHD cases had no increased risk for early PE (OR:2.07 CI:0.71-6.01) or late PE (OR:0.85 CI:0.44-1.64) compared to controls. In the CHD group, developing late PE was significantly increased by diabetes (OR:7 (1.9-26) p=0.0005), or chronic hypertension (CHT) (OR:15 (3.7-63) p< 0.0001). In the CHD group, CHT was the major determinant of late PE (Logistic regression R2=0.23 p < 0.0001). In patients with CHT, CHD significantly determined late PE (OR:3.43 CI:1.3-9.1 p=0.001.) In those without CHD, late PE was not increased by diabetes (OR:1.4 CI: 0.93-2.11 p=0.11) or CHT (OR: 1.4 CI: 0.79-2.32 p=0.26). No maternal characteristics significantly correlated with early PE in either cohort. CONCLUSION: Fetal CHD did not solely predict an increased risk of PE. However, in women with CHT, fetal CHD increases risk of PE. Enhanced surveillance and treatment appear warranted in these women.

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