Modeling acardiac twin pregnancies

Abstract

Acardiac twin pregnancies are a rare but severe complication of monochorionic twinning, where the acardiac twin lacks cardiac function but nevertheless grows during pregnancy because it is perfused by the pump twin through a set of placental arterioarterial and venovenous anastomoses. Because the acardiac twin's body is only perfused by the pump twin's arterial blood, acardiac twins have reduced blood oxygen saturation (SO(2)) levels. Furthermore, the pump twin has reduced blood oxygen saturation because the anastomoses merge the blood of the two twins. We suggested that angiogenesis from hypoxia mediated neovascularization increases the capillary density in the acardiac twin and causes a continuously decreasing vascular resistance of the acardiac body. The pump twin therefore has a continuously increasing cardiac output and decreasing oxygen saturation, which may cause a vicious circle of increasing levels of pump twin complications, often leading to intrauterine fetal death. Our aim in this article was twofold. First, to summarize our previous modeling work of acardiac twin pregnancies, and add an estimate of the capillary density in mammals at different levels of SO(2) from a literature search on angiogenesis related to SO(2), Hypoxia Inducible Factor, and Vascular Endothelial Growth Factor. Second, to speculate that combination of these efforts and our most recent model of monochorionic twin pregnancies and twin-twin transfusion syndrome may result in an improved computational model for acardiac twin pregnancies, aimed at identifying early clinical prognostic markers for pump twin complications.