Abstract
The development of the fetal heart is exquisitely controlled by a multitude of factors, ranging from humoral to mechanical forces. The gatekeeper regulating many of these factors is the placenta, an external fetal organ. As such, resistance within the placental vascular bed has a direct influence on the fetal circulation and therefore, the developing heart. In addition, the placenta serves as the interface between the mother and fetus, controlling substrate exchange and release of hormones into both circulations. The intricate relationship between the placenta and fetal heart is appreciated in instances of clinical placental pathology. Abnormal umbilical cord insertion is associated with congenital heart defects. Likewise, twin-to-twin transfusion syndrome, where monochorionic twins have unequal sharing of their placenta due to inter-twin vascular anastomoses, can result in cardiac remodeling and dysfunction in both fetuses. Moreover, epidemiological studies have suggested a link between placental phenotypic traits and increased risk of cardiovascular disease in adult life. To date, the mechanistic basis of the relationships between the placenta, fetal heart development and later risk of cardiac dysfunction have not been fully elucidated. However, studies using environmental exposures and gene manipulations in experimental animals are providing insights into the pathways involved. Likewise, surgical instrumentation of the maternal and fetal circulations in large animal species has enabled the manipulation of specific humoral and mechanical factors to investigate their roles in fetal cardiac development. This review will focus on such studies and what is known to date about the link between the placenta and heart development.
Highlights
Since David Barker first documented the relationship between infant birth weight and adult onset disease (Barker and Osmond, 1986; Barker et al, 1989), there has been a revolutionary shift in thinking about how the early environment can impact life-long health and susceptibility to disease
The placental circulation is considered one of low vascular resistance (Trudinger et al, 1985; Thompson and Trudinger, 1990), but in instances of poor placental development associated with fetal growth restriction, deficient remodeling of uterine spiral arteries can lead to malperfusion of the placenta and an increase in placental vascular resistance, which impair the placenta’s endocrine and nutrient transport functions (For review, Chaddha et al, 2004; Burton and Jauniaux, 2018)
As ∼45% of the combined ventricular output from the fetal heart is directed toward the placenta, an increase in placental vascular resistance may increase cardiac afterload, increasing the mechanical force that the heart beats against
Summary
Since David Barker first documented the relationship between infant birth weight and adult onset disease (Barker and Osmond, 1986; Barker et al, 1989), there has been a revolutionary shift in thinking about how the early environment can impact life-long health and susceptibility to disease.
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