Preeclampsia is defined as new onset hypertension and albuminuria in previously normotensive pregnant women after 20 weeks of pregnancy. There is no cure; management is reliant on a structured antenatal surveillance programme and antihypertensives. Recent advances in immune histochemistry study of placenta have elucidated an increased Vascular Endothelial Growth Factor (VEGF) expression in various placental bed disorders like recurrent pregnancy loss, preeclampsia, fetal growth restriction, preterm and abruption placenta. Increased release of VEGF family proteins has been attributed to atherosis and placental hypoxia. However, some studies have found normal VEGF concentrations in placenta in these disorders of feto-maternal interphase. This chapter aims to analyse the VEGF expression in placental biopsy from preeclampsia and normotensive pregnancies.
VEGF density is more in the placentas from preeclampsia pregnancies as compared to placenta from a normal pregnancy. The mean weight of placenta is smaller in preeclampsia group. Additionally, the fetal capillaries are also small in diameter and lumen was collapsed. The pulsatility index of uterine artery supplying the placenta is also higher in preeclampsia pregnancies. The high velocity blood flow can mechanically damage the tender fetal villi floating in the intervillous space. This damage collapses the fetal capillaries as evidenced by the smaller diameter of fetal capillaries in the placental biopsy.
Placental hypoxia in cases of preeclampsia is a potent stimulus for VEGF expression. Nevertheless, the increased VEGF expression should be seen in the light of collapsed fetal vessels in a small placenta.