Abstract 15584: Magnetic Resonance Imaging Reveals Decreased Oxygen Delivery and Consumption in Human Fetuses with Congenital Heart Disease

Introduction: Animal models suggest chronic hypoxia in utero results in down regulation of brain metabolism, impairing brain growth and development. A new approach to assessing fetal hemodynamics with phase contrast (PC) MRI and T2 mapping offers the means to assess the impact of congenital heart disease (CHD) on cerebral oxygen delivery (DO2) and consumption (VO2). Hypothesis: Fetuses with CHD might have reduced cerebral DO2 and VO2 with associated reductions in brain size. Methods: 28 normal fetuses and 23 fetuses with CHD with either single ventricle (SV) or biventricular physiology (BV) underwent MRI close to term. Assuming a hemoglobin concentration of 15g/dL, we calculated oxygen delivery (DO2) = umbilical vein flow (Q UV ) х UV oxygen content, where oxygen content = oxygen saturation of hemoglobin [HbO2] х 1.36 х [Hb]. We calculated fetal oxygen consumption (VO2) as Q UV х AV[[Unable to Display Character: ∆]]O2, where AV[[Unable to Display Character: ∆]]O2 is the arterio-venous difference in oxygen content between the UV and umbilical artery. Cerebral DO2 and VO2 were similarly measured using aortic and superior vena cava oxygen content and flow. Fetal brain volume was measured by segmenting a 3D steady state free precession acquisition of the fetal brain. Normal and CHD fetal VO2 and DO2 and cerebral VO2 and DO2 were compared using a Student’s t -test. The correlation between brain size and hemodynamic parameters was examined using Pearson’s Correlation. Results: The combined ventricular output (CVO; p =0.0003), Q UV ( p =0.0007) were reduced in fetuses with SV (n=6) compared with normals and fetuses with BV hearts (n=17) ( p =0.02), while UV T2 was lower in CHD fetuses ( p =0.0001). This resulted in mean reductions of >25% in fetal VO2 and DO2 in SV and BV CHD fetuses compared to normals ( p p =0.01). In fetuses with brain sizes below the mean, brain size correlated with cerebral VO2 ( r =0.58, p =0.01). Conclusions: This study provides evidence of a potential hemodynamic cause for the delayed brain growth and development that has been previously described in newborns with CHD. This is of interest because delayed brain development is associated with greater susceptibility to white matter injury around neonatal cardiac surgery.