title: MRI reveals hemodynamic changes with acute maternal hyperoxygenation in human fetuses with and without congenital heart disease.
abstract: OBJECTIVE
  We investigated the physiologic impact of acute maternal hyperoxygenation (MH) in human fetuses with and without congenital heart disease (CHD) using fetal cardiac magnetic resonance (CMR) in order to explore the potential therapeutic benefits of chronic MH.
  
  
  METHODS
  We examined 17 normal and 20 late gestation human fetuses with CHD on a 1.5 T CMR system. Flows were measured in major fetal vessels using phase contrast MRI. The T2 of umbilical venous blood was measured using T2 mapping. The measurements were repeated during acute MH. The results were compared using a Student's t-test, with p-value ≤0.05 considered statistically significant.
  
  
  RESULTS
  At baseline, the umbilical venous T2 (oxygen saturation) was lower in CHD fetuses than in normals, with significant increase with MH (p = 0.01). Both groups showed significant increase in pulmonary blood flow during MH, which was more dramatic in CHD (p = 0.005). There was a reduction in ductus arteriosus flow in CHD during MH (p = 0.04). There was no significant difference in blood flow in any of the other major vessels.
  
  
  CONCLUSIONS
  This study suggests that fetal MR identifies the expected hemodynamic changes associated with acute MH. MRI could be useful as a method for monitoring the impact of chronic MH in fetuses with CHD.
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Prashob
authors.initials: P
authors.lastname: Porayette
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Sujana
authors.initials: S
authors.lastname: Madathil
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Liqun
authors.initials: L
authors.lastname: Sun
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Edgar
authors.initials: E
authors.lastname: Jaeggi
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Lars
authors.initials: L
authors.lastname: Grosse-Wortmann
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Shi-Joon
authors.initials: SJ
authors.lastname: Yoo
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Edward
authors.initials: E
authors.lastname: Hickey
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Steven P
authors.initials: SP
authors.lastname: Miller
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Christopher K
authors.initials: CK
authors.lastname: Macgowan
authors.affiliation: The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: Mike
authors.initials: M
authors.lastname: Seed
mesh_terms: D000208:Acute Disease; D000328:Adult; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006330:Heart Defects, Congenital / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D018496:Hyperoxia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D011247:Pregnancy; D011248:Pregnancy Complications / Q000000981:diagnostic imaging* / Q000503:physiopathology