Origins of abnormal placentation: why maternal veins must not be forgotten

Abstract

For decades now, it is well established how important uterine microvascular adaptations during placentation are for the course of pregnancy. Inadequate dilatation of spiral arteries is associated with gestational complications as preeclampsia and/or intrauterine growth restriction. More recently however, it has become clear that trophoblast cells invade and adapt decidual veins and lymphatic vessels already one month before spiral arteries become patent and intervillous space perfusion starts. Normal intervillous space hemodynamics is characterized by high volume flow at low velocity and pressure in the inter-septal compartments surrounding the chorionic villi, hereby facilitating efficient maternal-fetal exchange. In case of shallow decidual vein dilatation, intervillous arterial supply exceeds venous drainage. This will cause congestion in the inter-septal compartments with subsequent reduced perfusion and increased pressure. An efficient mechanism to counteract venous congestion and safeguard the viability of the conceptus is by reducing arterial inflow via shallow dilatation of the spiral arteries. This review makes the case for intervillous space congestion as an unexplored trigger for inadequate spiral artery dilatation during the placentation process, eventually leading to abnormal systemic circulatory dysfunctions. Abnormal maternal venous function can result from an abnormal maternal immune response to paternal antigens with imbalanced release of vasoactive mediators, or can already exist before conception. In order to get the full picture of abnormal placentation, maternal veins must not be forgotten.