Abstract
Background Maternal hyperoxygenation (MH) has been used for intrauterine growth restriction and proposed as a way to improve ventricular growth in the setting of congenital heart disease (CHD)[1,2]. Fetal lamb experiments reveal increases in the SaO2 of umbilical venous (UV) blood and a reduction in pulmonary vascular resistance during MH [3]. Doppler suggests that MH increases the human fetal pulmonary blood flow (PBF) [4]. The combination of fetal phase contrast (PC) MRI and MR oximetry using T2 mapping offers the potential for a comprehensive hemodynamic assessment of late gestation fetal circulation [5]. We investigated the physiologic impact of MH in human fetuses with and without CHD using MRI to explore the potential therapeutic benefits of chronic MH.
Highlights
Maternal hyperoxygenation (MH) has been used for intrauterine growth restriction and proposed as a way to improve ventricular growth in the setting of congenital heart disease (CHD)[1,2]
At baseline, the umbilical venous (UV) T2 was lower in CHD fetuses than in normals
UV T2 did not change significantly with MH in normals, we observed a significant increase in UV T2 in CHD fetuses with MH (p=0.01, Fig. 1, Table 1)
Summary
Maternal hyperoxygenation (MH) has been used for intrauterine growth restriction and proposed as a way to improve ventricular growth in the setting of congenital heart disease (CHD)[1,2]. Fetal lamb experiments reveal increases in the SaO2 of umbilical venous (UV) blood and a reduction in pulmonary vascular resistance during MH [3]. Doppler suggests that MH increases the human fetal pulmonary blood flow (PBF) [4]. The combination of fetal phase contrast (PC) MRI and MR oximetry using T2 mapping offers the potential for a comprehensive hemodynamic assessment of late gestation fetal circulation [5].
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