The placenta as the window to congenital heart disease

There is an increasing recognition that structural abnormalities and functional changes in the placenta can have deleterious effects on the development of the fetal heart. This article reviews the role of the placenta and the potential impact of placental insufficiency on fetuses with congenital heart disease.

The fetal heart and the placenta are directly linked because they develop concurrently with shared regulatory and signaling pathways. Placental disease is more common in pregnancies carrying a fetus with congenital heart disease and the fetal response to placental insufficiency may lead to the postnatal persistence of cardiac remodeling. The mechanisms underlying this placental-fetal axis of interaction potentially include genetic factors, oxidative stress, chronic hypoxia, and/or angiogenic imbalance.

The maternal-placental-fetal circulation is critical to advancing our understanding of congenital heart disease. We must first expand our ability to detect, image, and quantify placental insufficiency and dysfunction in utero. Elucidating the modifiable factors involved in these pathways is an exciting opportunity for future research, which may enable us to improve outcomes in patients with congenital heart disease.