An underlying mechanism for congenital heart defects includes abnormal vascular development, a phenomenon also linked with preeclampsia. This study by Boyd et al. (Circulation, 2017) sought to determine if having a fetus or newborn with a heart defect was similarly associated with a higher risk of hypertensive disorders during pregnancy.
Retrospective Cohort Study
Data from 1,972,857 singleton pregnancies without chromosomal abnormalities ≥20 weeks gestation born in Denmark between 1978-2011, complicated by offspring with congenital heart defects and preeclampsia were analyzed. Congenital heart defects in offspring was most strongly associated with early preterm preeclampsia (odds ratio 7.00, 95% CI 6.11-8.03). Congenital heart defects were also associated with late term preterm preeclampsia (odds ratio 2.82, 95% CI 2.38-3.34) and less so with term preeclampsia (odds ratio 1.16, 95% CI 1.06-1.27)
However, congenital heart defects were not associated with gestational hypertension (odds ratio 1.07, 95% CI 0.92-1.25). These results held regardless of type of congenital heart disease. The investigators also looked at congenital heart defects in offspring in a previous pregnancy as a predictor of preeclampsia in subsequent pregnancies and found similar associations: there was a risk for early preterm preeclampsia (odds ratio 2.37, 95% CI 1.68-3.34) and late preterm preeclampsia (odds ratio 2.04, 95% CI 1.52-2.75), minimal association with term preeclampsia, and no association with gestational hypertension. When assessing preeclampsia in a previous pregnancy as a risk for congenital heart disease in subsequent pregnancies, preterm preeclampsia but not term preeclampsia or gestational hypertension was strongly associated with congenital heart defects in the offspring of later pregnancies (odds ratio 7.91, 95% CI 6.06-10.3). Late preterm preeclampsia was also associated with subsequent offspring with congenital heart disease (odds ratio 2.83, 95% CI 2.11-3.79) but term preeclampsia and gestational hypertension were not. Because these associations appear to be present across multiple pregnancies, the authors suggest that the underlying pathophysiology is maternal and not fetal in origin.
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