title: Prenatal cardiovascular manifestations in the twin-to-twin transfusion syndrome recipients and the impact of therapeutic amnioreduction.
abstract: OBJECTIVE
  We evaluated the cardiovascular pathologic condition in the recipient twin in twin-to-twin transfusion syndrome and the influence of amnioreduction.
  
  
  METHODS
  Fetal echocardiograms and medical records of 54 pregnancies that were complicated by twin-to-twin transfusion syndrome were reviewed. Recipient twin right and left ventricular wall thickness, diameters, systolic and diastolic function, valve regurgitation, and structural cardiac defects were assessed at examination and after amnioreduction.
  
  
  RESULTS
  At examination (n = 28 pregnancies), cardiomegaly because of right ventricular and/or left ventricular hypertrophy was observed in 58% of recipient twins, and biventricular hypertrophy was observed in 33% of recipient twins, without ventricular dilation. Biventricular diastolic dysfunction was present in two thirds of recipient twins, and right ventricular systolic dysfunction and significant atrioventricular valve regurgitation was observed in one third of recipient twins. Serial assessment (n = 21 pregnancies) revealed progressive biventricular hypertrophy and right ventricular systolic and biventricular diastolic dysfunction in most recipient twins. Steeper progression of hypertrophy, diastolic dysfunction, and structural or functional right ventricular outflow disease (20% incidence) were associated with an increased perinatal mortality rate.
  
  
  CONCLUSIONS
  In twin-to-twin transfusion syndrome, the recipient twin has progressive biventricular hypertrophy with predominant right ventricular systolic and biventricular diastolic dysfunction. Despite amnioreduction, the cardiovascular disease persists and even progresses in many recipient twins.
authors.affiliation: Department of Pediatrics, Division of Cardiology, Fetal Cardiac Program, The Hospital for Sick Children, Ontario, Canada.
authors.forename: Catherine
authors.initials: C
authors.lastname: Barrea
authors.forename: Fawaz
authors.initials: F
authors.lastname: Alkazaleh
authors.forename: Greg
authors.initials: G
authors.lastname: Ryan
authors.forename: Brian W
authors.initials: BW
authors.lastname: McCrindle
authors.forename: Anita
authors.initials: A
authors.lastname: Roberts
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Bigras
authors.forename: Jon
authors.initials: J
authors.lastname: Barrett
authors.forename: Gareth P
authors.initials: GP
authors.lastname: Seaward
authors.forename: Jeffrey F
authors.initials: JF
authors.lastname: Smallhorn
authors.forename: Lisa K
authors.initials: LK
authors.lastname: Hornberger
mesh_terms: D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology; D004452:Echocardiography; D005260:Female; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D006801:Humans; D006984:Hypertrophy; D011247:Pregnancy; D018487:Ventricular Dysfunction, Left / Q000209:etiology*; D018497:Ventricular Dysfunction, Right / Q000209:etiology*