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Acardiac twin pregnancies part VI: Why does acardiac twinning occur only in the first trimester?
van Gemert, Martin J C; Ross, Michael G; van den Wijngaard, Jeroen P H M; Nikkels, Peter G J.
Afiliación
  • van Gemert MJC; Department of Biomedical Engineering & Physics, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
  • Ross MG; Department of Obstetrics and Gynecology, Harbor UCLA Medical Center, Torrance, California, USA.
  • van den Wijngaard JPHM; Department of Clinical Chemistry, Hematology and Immunology, Diakonessenhuis, Utrecht, The Netherlands.
  • Nikkels PGJ; Department of Pathology, Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands.
Birth Defects Res ; 113(9): 687-695, 2021 05 15.
Article en En | MEDLINE | ID: mdl-33580607
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, rAA (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 rAA (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 rAA (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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transfusión Feto-Fetal / Embarazo Gemelar Límite: Female / Humans / Pregnancy Idioma: En Revista: Birth Defects Res Año: 2021 Tipo del documento: Article País de afiliación: Países Bajos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transfusión Feto-Fetal / Embarazo Gemelar Límite: Female / Humans / Pregnancy Idioma: En Revista: Birth Defects Res Año: 2021 Tipo del documento: Article País de afiliación: Países Bajos Pais de publicación: Estados Unidos