Abstract
The placenta is the largest fetal organ, and toward the end of pregnancy the umbilical circulation receives at least 40% of the biventricular cardiac output. It is not surprising, therefore, that there are likely to be close haemodynamic links between the development of the placenta and the fetal heart. Development of the placenta is precocious, and in advance of that of the fetus. The placenta undergoes considerable remodeling at the end of the first trimester of pregnancy, and its vasculature is capable of adapting to environmental conditions and to variations in the blood supply received from the mother. There are two components to the placental membranes to consider, the secondary yolk sac and the chorioallantoic placenta. The yolk sac is the first of the extraembryonic membranes to be vascularized, and condensations in the mesenchyme at ~17 days post-conception (p.c.) give rise to endothelial and erythroid precursors. A network of blood vessels is established ~24 days p.c., with the vitelline vein draining through the region of the developing liver into the sinus venosus. Gestational sacs of early pregnancy failures often display aberrant development of the yolk sac, which is likely to be secondary to abnormal fetal development. Vasculogenesis occurs in the villous mesenchyme of the chorioallantoic placenta at a similarly early stage. Nucleated erythrocytes occupy the lumens of the placental capillaries and end-diastolic flow is absent in the umbilical arterial circulation throughout most of the first trimester, indicating a high resistance to blood flow. Resistance begins to fall in the umbilico-placental circulation around 12–14 weeks. During normal early pregnancy the placental capillary network is plastic, and considerable remodeling occurs in response to the local oxygen concentration, and in particular to oxidative stress. In pregnancies complicated by preeclampsia and/or fetal growth restriction, utero-placental malperfusion induces smooth muscle cells surrounding the placental arteries to dedifferentiate and adopt a proliferative phenotype. This change is associated with increased umbilical resistance measured by Doppler ultrasound, and is likely to exert a major effect on the developing heart through the afterload. Thus, both the umbilical and maternal placental circulations may impact on development of the heart.
Highlights
The placenta and the fetal heart are two of the first organs to differentiate, and it is assumed that their development is interlinked
A recent study in a nonhuman primate has indicated that growth restriction mimics accelerated aging of the heart (Kuo et al, 2017), but a detailed consideration of these effects is beyond the scope of the current review
Cardiac and placental abnormalities may coexist through polymorphisms in genetic developmental pathways common to both organs, in particular those regulated by Wnt/ßcatenin signaling, or through a lack of key micronutrients, such as folate (Linask, 2013)
Summary
The placenta and the fetal heart are two of the first organs to differentiate, and it is assumed that their development is interlinked. Regression is associated with the progressive onset of the maternal arterial circulation to the placenta, first in the periphery and in the rest of the placenta This process is mediated by the migration of extravillous trophoblastic cells (EVT) into the placental bed and modulated by locally high levels of oxidative stress within the villi (Jauniaux et al, 2003a). Consistent with this theory, the junctional complexes between endothelial cells forming the capillaries within the regressing villi loose their integrity, and the villi become avascular, hypocellular ghosts (Burton et al, 2010) Events at this stage of development play a key role in determining the final size and shape of the placenta (Burton et al, 2010; Salafia et al, 2012), and so may impact development of the fetal heart. The local increase in capillary cross-sectional area leads to a slowing in flow velocity, facilitating exchange
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