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

Abstract

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. Methods: We applied the vascular resistance scheme of two fetuses connected by arterio-arterial (AA) and veno-venous (VV) anastomoses, the small VV resistance approximated as zero. The smaller twin has volume fraction α < 1 of the assumed normal larger twin, and has only access to fraction X < 1 of its placenta; the larger twin's larger mean arterial pressure accesses the remaining fraction. Before 13 weeks, embryos have a much smaller vascular resistance than placentas. After 13 weeks, when maternal blood provides oxygen, smaller twins can increase their vascular volume by hypoxemia-mediated neovascularization. Estimated AA radii at 40 weeks, r AA (40), are 0.5-1.3 mm.Results: Embryos with α < 0.33 unlikely survive 13 weeks and acardiac twinning occurs under appropriate conditions (AA-VV, small placenta). Acardiac body perfusion occurs because of a much smaller vascular resistance than the placenta. When α > 0.33 and r AA (40)=1.3 mm, modeled survival is >32 weeks. Conclusion: Before 13 weeks, embryos with α < 0.33 cannot survive and may result in the onset of acardia. Beyond 13 weeks, fetuses with α ≥ 0.33 survive because r AA (40) is too small for acardiac onset. Following fetal demise, exsanguination from the live twin increases its blood volume and, we assumed also, its vascular resistance. Perfusion then occurs through the lower resistance placenta.

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

“…The demised twin remains perfused by deoxygenated arterial blood from the live twin, however, the predicted perfusion flow is so small that the demised body hardly if at all grows and hence cannot become an acardiac twin. Much more likely is that it will macerate as shown in figure 6 of previous work (van Gemert et al, 2021).…”

“…In previous work (van Gemert et al, 2021), we argued that a healthy embryo that survives the first trimester has at least a weight of 33% compared to normal, thus…”

“…In previous work (van Gemert et al, 2021), we provided a pathophysiological mechanism that could explain why acardiac twinning occurs in the first trimester. We gave evidence that first trimester placental resistances are significantly larger than their corresponding embryo resistances, and that acardiac twinning then occurs under appropriate conditions, as explained in the previous paragraph.…”

“…Acardiac onset requires that the future pump twin has a mean arterial pressure that exceeds that of the future acardiac twin. Sufficiently unequal arterial pressures result in the larger twin perfusing part of the smaller twin's placenta (van Gemert, Ross, van den Wijngaard, & Nikkels, 2021 ; van Gemert, van den Wijngaard, Paarlberg, Gardiner, & Nikkels, 2017 ), which hampers the smaller twin's development. When this mechanism is sufficiently strong, cardiac arrest occurs in the smaller twin, which forces the larger twin to start a circulation of less oxygenated arterial blood through the AA–VV anastomoses and the demised smaller twin, thus promoting a growing acardiac twin.…”

“…Nevertheless, demise of the smaller twin will markedly increase its venous blood volume because the larger twin will exsanguinate into the venous compartment that has a much larger compliance than the arterial part. We then tacitly assumed (van Gemert et al, 2021 ) that the demised twin's vascular resistance would concomitantly increase to a significantly larger value than the placental resistance. A much larger resistance of the body than the placenta prevents perfusion of the body, thus preventing its growth, and hence precludes onset of an acardiac twin pregnancy.…”