Fetal Growth Restriction (FGR): Review

 In recent years, there has been a growing amount of interest in the possibility that inadequate maternal hemodynamic adaptations to the pregnancy and adverse pregnancy outcomes (APOs) are connected. It has been suggested that "placental syndromes," such as preeclampsia (PE) and fetal growth restriction (FGR), may be linked to later maternal cardiovascular diseases (CVD). The two subtypes of FGR have distinct clinical and pathogenetic characteristics. It is thought that poor trophoblastic invasion of the maternal spiral arteries during placentation is a major factor in the development of early-onset PE and FGR. A pre-existing or subsequent cardiovascular impairment may play a significant role in the pathogenesis of early-onset FGR because placental functioning is dependent on the cardiovascular system of the mother. A primary abnormal placentation in the first trimester does not appear to be the factor that determines late FGR. A primary cardiovascular maladaptation in the mother may be the cause of the pathological pathway of late-onset FGR: The CV system displays a profile that is flat and remains comparable to that of non-pregnant women. A hypovolemic state could result in placental hypoperfusion, altered villous tree maturation, and altered fetal growth during the second trimester, when the placenta is already developed and has a higher functional demand. As a result, the focus of this review is on the possible connection between placentation and maternal cardiac function during pregnancy and the onset and progression of FGR. A superior comprehension of maternal hemodynamics in pregnancies confounded by FGR could get different advantages in clinical work, further developing screening and therapeutic tools.