title: Acardiac twin pregnancies part III: Model simulations.
abstract: BACKGROUND
  Acardiac monochorionic twins lack cardiac function but grow by passive perfusion of the pump twin's deoxygenated arterial blood through placental arterioarterial (AA) and venovenous (VV) anastomoses and by hypoxia-mediated neovascularization. Pump twins therefore must continuously increase their cardiac output which may cause heart failure. Our aims were: to adapt our twin-twin transfusion syndrome model for acardiac twin pregnancies, to simulate pump and acardiac twin development, and to examine the model for early prognostic markers of pump twin survival.
  
  
  METHODS
  We used an infinite acardiac placental resistance, based on placental dye injection studies and simulations, suggesting the AA-Acardiac-VV series resistance determines the pump twin's excess cardiac output. Pump and acardiac development were expressed by the pump's excess cardiac output versus its normal value, represented by pump/acardiac umbilical venous diameter (UVD) ratios.
  
  
  RESULTS
  UVD ratios distinguish between AA-VV anastomoses that do and do not cause hydropic pump twins. Pump twins can handle relative larger acardiac perfusion at later than earlier gestation. Both VV and acardiac resistances are significantly smaller than the AA resistance, based on respectively clinical data and acardiac blood volumetric growth.
  
  
  CONCLUSIONS
  Our simulations support clinical results which show that UVD ratios aid in the prediction of pump twin risk. The AA anastomosis controls the future of both the pump and the acardiac. Correlation between acardiac size and pump twin risk is secondary to the AA size but remains clinically usable. These factors may aid in the development of methods for pump twin prognosis and the promotion of selective clinical interventions.Birth Defects Research (Part A), 2016.© 2016 Wiley Periodicals, Inc. Birth Defects Research (Part A) 106:1008-1015, 2016. © 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
authors.initials: MJ
authors.lastname: van Gemert
authors.affiliation: Department of Obstetrics and Gynecology, Harbor UCLA Medical Center, Torrance, California.
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
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
authors.affiliation: Department of Biomedical Engineering & Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Jeroen P H M van den
authors.initials: JP
authors.lastname: Wijngaard
mesh_terms: D002302:Cardiac Output; D003198:Computer Simulation; D004200:Diseases in Twins / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005333:Fetus; D006330:Heart Defects, Congenital / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D009389:Neovascularization, Pathologic / Q000473:pathology / Q000503:physiopathology*; D010920:Placenta / Q000002:abnormalities / Q000098:blood supply*; D021041:Placental Circulation; D011247:Pregnancy; D059285:Pregnancy, Twin; D014430:Twins, Monozygotic; D014471:Umbilical Veins / Q000473:pathology / Q000503:physiopathology
keywords: acardiac hypoxia; acardiac monochorionic twin pregnancy; computational model; fetoplacental resistance scheme; twin reversed arterial perfusion sequence