The Placenta as a Resistive Organ in the Maternal–Fetal Circulation: A Conceptual Model Linking HELLP Syndrome and Fetal Growth Restriction

HELLP syndrome and fetal growth restriction (FGR) have traditionally been regarded as distinct disorders arising primarily from the maternal and fetal sides, respectively. However, these conditions may also represent different phenotypic manifestations of dysfunction within a single maternal–placental–fetal circulatory system. The placenta lies at the interface between the maternal and fetal circulations. In this study, the maternal and fetal circulations are conceptualized as two fluid circuits that are mechanically coupled through the placenta. Within this framework, the placenta functions not only as an exchange organ but also as a resistive element that links the two circulatory systems. An increase in placental resistance may elevate maternal blood pressure while simultaneously reducing fetal perfusion and impairing fetal growth. In addition, placental stress may influence maternal vascular function through the release of vasoactive factors such as soluble fms-like tyrosine kinase-1 (sFlt-1). From this perspective, HELLP syndrome and fetal growth restriction can be interpreted as related phenotypes positioned along a shared hemodynamic continuum, even when their upstream causes differ. We therefore propose a conceptual biophysical framework in which the maternal and fetal circulations are viewed as two coupled circuits linked by placental resistance. This framework offers a mechanistic reinterpretation of the conventional classification into maternal, placental, and fetal factors.