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MRI reveals hemodynamic changes with acute maternal hyperoxygenation in human fetuses with and without congenital heart disease

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 a...

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Bibliographic Details
Published in:Prenatal diagnosis 2016-03, Vol.36 (3), p.274-281
Main Authors: Porayette, Prashob, Madathil, Sujana, Sun, Liqun, Jaeggi, Edgar, Grosse-Wortmann, Lars, Yoo, Shi-Joon, Hickey, Edward, Miller, Steven P., Macgowan, Christopher K., Seed, Mike
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Language:English
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Summary: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. Conclusion 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. © 2015 John Wiley & Sons, Ltd.
ISSN:0197-3851
1097-0223
DOI:10.1002/pd.4762