title: Acardiac twin pregnancies part IV: Acardiac onset from unequal embryonic splitting simulated by a fetoplacental resistance model.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Biomedical Engineering & Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Martin J C van
authors.initials: MJ
authors.lastname: Gemert
authors.affiliation: Department of Biomedical Engineering & Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.|Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: Jeroen P H M van den
authors.initials: JP
authors.lastname: Wijngaard
authors.affiliation: Department of Obstetrics and Gynecology, Gelre Hospitals, location Apeldoorn, The Netherlands.
authors.forename: K Marieke
authors.initials: KM
authors.lastname: Paarlberg
authors.affiliation: The Fetal Center, McGovern Medical School at UTHealth, University of Texas, Houston, TX, USA.
authors.forename: Helena M
authors.initials: HM
authors.lastname: Gardiner
authors.affiliation: Department of Pathology, Wilhelmina Children's Hospital, University Medical Center, Utrecht, The Netherlands.
authors.forename: Peter G J
authors.initials: PG
authors.lastname: Nikkels
mesh_terms: D003198:Computer Simulation; D004200:Diseases in Twins / Q000503:physiopathology; D005260:Female; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D005333:Fetus / Q000098:blood supply / Q000503:physiopathology*; D006330:Heart Defects, Congenital / Q000503:physiopathology; D006801:Humans; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D059285:Pregnancy, Twin; D014428:Twins, Conjoined / Q000503:physiopathology; D014430:Twins, Monozygotic; D014471:Umbilical Veins / Q000503:physiopathology
keywords: AA anastomotic radius; acardiac twinning etiology; chronic placental hypoperfusion; computational model simulations; fetoplacental resistance scheme; pseudo-acardiac twinning