Abstract 19532: Maternal Hyperoxia Increases Cerebral Oxygenation in Fetuses With Complex Congenital Heart Disease: A Functional MRI Study
Introduction: Fetal brain growth is altered in congenital heart disease (CHD). The role of disturbed placental and fetal blood flow/oxygenation remains poorly understood. We compared the effect of maternal hyperoxia on cerebral and placental oxygenation in CHD vs control fetuses using blood oxygenation level dependent (BOLD) functional MRI (fMRI).
Methods: We studied 85 pregnant women (51 healthy /34 CHD fetuses) at 22-39 weeks gestational age (GA), using MRI and Doppler. After 2min baseline recording at normoxia (NO), we made BOLD fMRI measurements in 4 phases, (1) early hyperoxia (HO; 100% O2) for 2min (2) late HO (2min), (3) early return NO (1.75min), (4) late return NO (1.75min). We measured % BOLD signal changes in fetal brain and placenta and correlated these with umbilical artery (UA) pulsatility index (PI) obtained at baseline.
Results: Mean GA of CHD vs control fetuses was 32 4/7 and 32 2/7 (p=0.77). 41.2% had 1-ventricle (1V; all HLHS) vs 2-ventricle (2V) physiology. In controls, brain BOLD signal increased in phase 1 HO and remained elevated through phase 4. In CHD fetuses, the BOLD signal increased in phase 1 and continued to rise through phase 4. Differences in brain BOLD elevation in CHD vs controls (3.1% vs 0.9%, p=0.04) was significant in phase 4 (Fig. 1). Brain BOLD differed between 1V (3.4%, p=0.04) and 2V (0.9%, p=0.15) in phases 3 & 4. Placental BOLD signal increased during HO in control (4.4%, p<0.001) and CHD fetuses (6.4%, p<0.001). UA PI in CHD fetuses was higher than controls (1.11 vs 1.03, p=0.03). UA PI correlated with placental BOLD during HO in healthy and CHD fetuses (p<0.05).
Conclusions: In this first report of placental and fetal brain responses to maternal HO, we show a significantly increased brain BOLD response in CHD fetuses, specifically 1V. These data suggest that maternal HO improves brain oxygenation in CHD fetuses in the short-term. Studies evaluating the prolonged effects of HO are needed to determine the role of HO management in select CHD fetuses.
Author Disclosures: W. You: None. M. Donofrio: None. D. Wessel: None. Z. Zun: None. J. De Asis-Cruz: None. G. Vezina: None. D. Bulas: None. R. Jonas: None. A. du Plessis: None. C. Limperopoulos: None.
- © 2015 by American Heart Association, Inc.