The placenta is the central player of the maternal–fetal interface, able to communicate with both the fetus and the mother and to regulate signals from one to the other. Consequently, disturbing its development, growth, or function can have major impacts on both the maternal response to pregnancy and the development of the fetus. Currently, very little is known about the effects of maternal cardiac conditions on the placenta, but what we do know highlights the need to investigate this topic further and to consider the contribution of the placenta during pregnancies with mothers who have cardiac disease. This chapter discusses placental–maternal communication, placenta and fetal outcomes, substance abuse and the placenta, and congenital vascular dysfunction.

Placental–Maternal Communication

Although maternal adaptation to pregnancy is generally thought of as a response to pregnancy hormones that alter the maternal heart, blood volume, and kidneys, the bigger picture includes the critical communication between the placenta and the maternal environment.

In early pregnancy, the interplay between the maternal immune cells resident in the decidua (e.g., uterine natural killer cells) and the invading placental trophoblast is finely balanced, and if disrupted, it can result in early pregnancy loss or aberrant invasion of the trophoblast. The consequences of disrupted trophoblast invasion can manifest as preeclampsia or an overinvasive placenta (percreta, accreta, or increta). Recent research has identified multiple communication pathways between the placenta and the mother that occur throughout pregnancy. These include both secreted factors and placental “debris.” Secreted factors consist of many placenta-specific molecules but also include factors typically expressed by adipose tissue or immune cells, such as leptin, adiponectin, and cytokines. “Placental debris” is used to describe the trophoblast-derived material that is composed of extracellular vesicles of various sizes, including exosomes and apoptotic bodies. These are intentionally shed by the placenta and are found circulating in maternal blood. In the future, they may be used as biomarkers for the diagnosis of pregnancy pathologies. Currently, cell-free nucleic acids are commonly assessed during the first trimester in high-risk patients undergoing noninvasive prenatal testing.

One proposed mechanism of placental–maternal communication goes so far as to propose “placentalization” of the maternal endothelium by targeted exosomes and extracellular vesicles, expanding the placental output of secreted factors to the entire maternal circulation. Recently, targeted communication in this manner has been proposed to occur between the placenta and the maternal kidneys, with a potential application for this system to impact the maternal heart, which, when successful, enables proper maternal adaptation to pregnancy.

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