Impaired Placental Vascular Reactivity in Congenital Heart Disease Quantified Using Blood Oxygen Level-Dependent MRI.

PURPOSE: Placental pathology is directly associated with adverse fetal outcomes congenital heart disease (CHD). However, in vivo placental dysfunction has been poorly characterized. We aimed to compare placental vascular reactivity (PLVR), the fetally-mediated placental response to transient changes in maternal carbon dioxide (CO2) quantified using BOLD MRI, in pregnancies with and without fetal CHD.

METHODS

In a prospective study, placental BOLD MRI was acquired concurrently with maternal end-tidal CO2 (EtCO2) for 7-8 min as pregnant women followed audio-visual breathing cues. Following motion correction and manual delineation of placental anatomy, PLVR was computed using a coherence-weighted general linear model between MRI signal and EtCO2 stimulus. Global PLVR was calculated as the mean of voxel-wise PLVR across the placenta. Associations among PLVR, CHD status, and maternal health risks were analyzed using multiple, linear regression after correction for gestational age.

RESULTS

The study included 103 pregnant women; 31 with fetal CHD (34 ± 2.9 gestational weeks) and 72 with healthy fetuses (30.7 ± 4.9 gestational weeks). Gestational age at MRI was greater in the CHD group due to typical timing of CHD diagnosis. PLVR was lower in CHD (0.024 ± 0.02 ∆BOLD/mmhg CO2) compared to non-CHD group (0.03 ± 0.04 ∆BOLD/mmhg CO2). Maternal diabetes has differential effects on PLVR in CHD versus non-CHD groups.

CONCLUSION

We present a novel, in vivo characterization of placental dysfunction in CHD. PLVR is reduced in placentas of CHD compared to non-CHD pregnancies, providing evidence of impaired vascular integrity and corroborating previous histopathologic findings. Ongoing research is investigating the association between PLVR and fetal/infant outcomes in CHD.