Acardiac twin pregnancies part IV: Acardiac onset from unequal embryonic splitting simulated by a fetoplacental resistance model. Issue 3 (15th February 2017)

• Record Type: Journal Article
• Authors: Gemert, Martin J.C. van; Wijngaard, Jeroen P.H.M. van den; Paarlberg, K. Marieke; Gardiner, Helena M.; Nikkels, Peter G.J.
• Is Part Of: Birth defects research. Volume 109:Issue 3(2017)
• Page Start: 211
• Page End: 223
• Publication Date: 2017-02-15
• Subjects: acardiac twinning etiology -- fetoplacental resistance scheme -- AA anastomotic radius -- chronic placental hypoperfusion -- pseudo‐acardiac twinning -- computational model simulations; Teratology -- Periodicals; Abnormalities, Human -- Periodicals; Congenital Abnormalities; Embryo, Mammalian -- abnormalities; Teratology; Abnormalities, Human; Teratology; Periodicals; Periodicals; 616.043
• DOI: 10.1002/bdra.23581
• Languages: English
• ISSNs: 2472-1727

Abstract

Abstract : Background: Benirschke postulated that acardiac twinning occurs when markedly unequal embryonic splitting combines with arterioarterial (AA) and venovenous placental anastomoses. We tested this hypothesis by model simulations and by comparison of outcomes with 18 "pseudo‐" (twin fetus with beating heart but otherwise with clear signs of an acardiac) and 3 "normal" acardiac cases. Methods: The smaller/larger cell volume ratio at embryonic splitting becomes the smaller/larger embryonic/fetal blood volume ratio ( a ). From a, we derived nonpulsating blood pressures using normal values (larger twin) and normal values at an appropriate earlier gestational age (smaller twin). These unequal pressure sources were used in a linear resistance fetoplacental network to calculate umbilical venous diameter ratios. Acardiac onset occurs when the smaller twin has 50% left of its normal, singleton placenta. Comparison with clinical cases approximated a by crown‐rump‐length‐ratio to the 3rd power. Input parameters are a and the AA‐radius at 40 weeks. Results: Acardiacs can be small or large, can occur early or late, earlier at smaller a and larger AA, with larger umbilical venous diameter ratios at smaller a and smaller AA. Comparison with the 21 clinical cases was good, except for 2. Conclusion: Our analysis supports Benirschke's hypothesis. The smaller twin has to share its placental perfusion with the larger twin, which is a novel finding. The AA size is essential for the future of both fetuses but complicates easy understanding of (pseudo‐)acardiac clinical presentations. Late acardiac onset occurs infrequently. Using nonpulsating circulations may have caused our extensive predictions of late onset. An improved model requires including hypoxemia in the smaller twin from chronic placental hypoperfusion. Birth Defects Research 109:211–223, 2017. © 2016 Wiley Periodicals, Inc.