Description

The development of placentation during pregnancy involves two simultaneous processes: the invasion of maternal spiral arteries by cytotrophoblasts and the branching of the fetal vascular tree. These mechanisms, regulated by factors such as VEGF, PlGF, sFlt-1, and PAPP-A, ensure an adequate supply of oxygen and nutrients to the fetus. When these processes are impaired, placental dysfunction develops, characterized by high vascular resistance, hypoperfusion, and oxidative stress, which can predispose to complications such as preeclampsia, fetal growth restriction, gestational diabetes, placental abruption, and preterm birth.

During labor, uterine contractions can reduce uteroplacental perfusion by up to 60%. A healthy fetus with a normally functioning placenta can tolerate these transient reductions through compensatory mechanisms, whereas a fetus with abnormal placentation may exhibit signs of compromise, such as abnormal heart rate patterns or the presence of meconium, and, in cases of severe hypoxia, may face more serious risks.

The clinical challenge is to identify, before labor, fetuses that, despite appropriate growth, have a placenta unable to withstand the stress of delivery. Some studies have investigated Doppler velocimetry, particularly the Cerebro-Placental Ratio, but its predictive ability at term is modest. The role of placental markers (PlGF, sFlt-1, sFlt-1/PlGF) in predicting intrapartum fetal compromise also remains uncertain, with conflicting results reported in the literature. Since these markers are altered in pregnancies with placental dysfunction, their combination with antenatal risk factors may allow better identification of fetuses at risk, guiding clinicians in labor management and the choice of delivery mode.

This study will enroll participants using a retrospective and prospective approach. The primary aim is to evaluate the association between placental markers and intrapartum fetal compromise based on cardiotocographic tracings. Secondary aims include assessing their relationship with fetal acidosis, low Apgar scores, and admission to the neonatal intensive care unit.