Association of Maternal Endothelial Dysfunction With Preeclampsia

Abstract

Preeclampsia remains a major cause of maternal and fetal morbidity and mortality,¹ complicating up to 10% of first pregnancies and accounting for 40% of iatrogenic premature deliveries.² The fetal and maternal mechanisms underlying preeclampsia are not well understood. Endothelial dysfunction is considered to underlie many of the manifestations of preeclampsia, including hypertension, proteinuria, and edema.³ It is widely believed that inadequate trophoblast invasion of the uterine spiral arteries leads to placental ischemia and release of placental factors that damage the maternal vascular endothelium.^3-5 A role for placental factors is further supported by findings of increased lipid peroxidation and oxidation stress in the placentas of women with preeclampsia.^6,7 Abnormal placentation may not be the sole basis for preeclampsia though, since maternal factors such as hypertension, diabetes, and obesity are associated with an increased risk of preeclampsia.⁸ However, most studies of preeclampsia have been conducted during pregnancy, and it has not been possible to separate maternal from placental mechanisms underlying the development of preeclampsia.