*5.2. Fetal Size in Preeclampsia*

Fetal growth restriction is considered a typical feature of preeclampsia resulting from the primary placental dysfunction that causes the disorder. It is fetal growth restriction and associated hypoxemia that predispose to increased risk of fetal, neonatal, and long-term adverse outcomes [38–40]. Epidemiological studies demonstrate that the majority of preterm preeclampsia cases result in fetal growth restriction. However, over 80% of preeclampsia occurs at a term where the rate of large-for-gestational-age births are as common as small-for-gestational-age births (both 15%), and most neonates are of normal size, even after the exclusion of diabetic pregnancies [41,42]. The finding of normal or excessive fetal growth in the majority of term preeclampsia cases is not consistent with impaired trophoblast invasion with placental dysfunction being the primary etiological process in preeclampsia.

#### **6. Evidence for Cardiovascular Origins of Preeclampsia**

Earlier, we outlined the strong associations between uterine artery blood flow and trophoblast cell biology. The data also suggested that trophoblast invasion was not directly responsible for early pregnancy changes in uterine, ophthalmic, and radial artery hemodynamics, leaving us to entertain the alternative possibility that maternal cardiovascular function might be involved. If maternal cardiovascular function plays such an etiological role, this should also be evident from the epidemiology of preeclampsia.
