Hypothesized pathogenesis of acardius acephalus, acormus, amorphus, anceps, acardiac edema, single umbilical artery, and pump twin risk prediction.

Background: Acardiac twinning complicates monochorionic twin pregnancies in ≈2.6%, in which arterioarterial (AA) and venovenous placental anastomoses cause a reverse circulation between prepump and preacardiac embryos and cessation of cardiac function in the preacardiac. Literature suggested four acardiac body morphologies in which select (groups of) organs fail to develop, deteriorate, or become abnormal: acephalus (≈64%, [almost] no head, part of body, legs), amorphus (≈22%, amorphous tissue lump), anceps (≈10%, cranial bones, well-developed), and acormus (≈4%, head only).

Why does second trimester demise of a monochorionic twin not result in acardiac twinning?

Background: We previously explained why acardiac twinning occurs in the first trimester. We raised the question why a sudden demised monochorionic twin beyond the first trimester does not lead to acardiac twinning. We argued that exsanguinated blood from the live twin would strongly increase the demised twins' vascular resistance, preventing its perfusion and acardiac onset.

Acardiac twin pregnancies part VI: Why does acardiac twinning occur only in the first trimester?

Background: Clinical observation suggests that acardiac twinning occurs only in the first trimester. In part, this contradicts our previous analysis (part IV) of Benirschke's concept that unequal embryonic splitting causes unequal embryo/fetal blood volumes and pressures. Our aim is to explain why acardiac onset is restricted to the first trimester.

Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?

Background: Acardiac twinning is a complication of monochorionic twin pregnancies. From literature reports, 30 of 41 relatively large acardiac twins with renal tissue produced polyhydramnios within their amniotic compartment. We aim to investigate the underlying mechanisms that cause excess amniotic fluid using an established model of fetal fluid dynamics.

Pressure and Flow Relations in the Systemic Arterial Tree Throughout Development From Newborn to Adult.

Distributed models of the arterial tree allow studying the effect of physiological and pathophysiological changes in the vasculature on hemodynamics. For the adult, several models exist; however, a model encompassing the full age range from newborn to adult was until now lacking. Our goal is to describe a complete distributed hemodynamic model for normal development from newborn to adult.