More Perspectives on Preeclampsia and Fetal Growth Restriction

The “classical” theory of preeclampsia is that decreased intervillous perfusion from defectively remodeled spiral arteries causes intervillous hypoxia, which damages both chorionic villi and the fetus and thereby causes preeclampsia, fetal growth restriction, or both conditions. Another theory has been advanced that defective spiral artery remodeling does cause preeclampsia, but not because of reduced intervillous blood flow but rather because of violent blood flow. The theory is that high-velocity jets of maternal blood emerging from unremodeled spiral arteries damage or destroy chorionic villi. Recent MRI studies support this “violent blood flow” model by finding that, in vivo, the placentas of women with preeclampsia have higher blood flow velocities and greater heterogeneity of placental oxygenation than the placentas of healthy controls. The combination of the “classical” and the “violent flow” model would predict exactly these findings—high velocity flow and a wider variation of placental oxygenation than in normal placentas. The model of “V/Q mismatching” in the lung can be fruitfully adapted to the placenta, in which the “V” or ventilation in the lung becomes the maternal perfusion of the intervillous spaces, and the “Q” or pulmonary perfusion in the lung becomes the fetal perfusion of the chorionic villi within the intervillous spaces. In an abnormal placenta already at risk for causing preeclampsia or fetal growth restriction, obstruction of uterine venous return would further decrease fetal and chorionic villus oxygenation and thereby accelerate the onset of clinically apparent injury to both chorionic villi and the fetus. Therefore, prevention of obstruction of uterine venous return during gestation might allow longer intrauterine fetal development, with delivery at a later date than if obstruction of uterine venous return is allowed to occur.