Reduced fetal cerebral oxygen consumption is associated with smaller brain size in fetuses with congenital heart disease

Liqun Sun, Christopher K Macgowan, John G Sled, Shi-Joon Yoo, Cedric Manlhiot, Prashob Porayette, Lars Grosse-Wortmann, Edgar Jaeggi, Brian W McCrindle, John Kingdom, Edward Hickey, Steven Miller, Mike Seed, Liqun Sun, Christopher K Macgowan, John G Sled, Shi-Joon Yoo, Cedric Manlhiot, Prashob Porayette, Lars Grosse-Wortmann, Edgar Jaeggi, Brian W McCrindle, John Kingdom, Edward Hickey, Steven Miller, Mike Seed

Abstract

Background: Fetal hypoxia has been implicated in the abnormal brain development seen in newborns with congenital heart disease (CHD). New magnetic resonance imaging technology now offers the potential to investigate the relationship between fetal hemodynamics and brain dysmaturation.

Methods and results: We measured fetal brain size, oxygen saturation, and blood flow in the major vessels of the fetal circulation in 30 late-gestation fetuses with CHD and 30 normal controls using phase-contrast magnetic resonance imaging and T2 mapping. Fetal hemodynamic parameters were calculated from a combination of magnetic resonance imaging flow and oximetry data and fetal hemoglobin concentrations estimated from population averages. In fetuses with CHD, reductions in umbilical vein oxygen content (P<0.001) and failure of the normal streaming of oxygenated blood from the placenta to the ascending aorta were associated with a mean reduction in ascending aortic saturation of 10% (P<0.001), whereas cerebral blood flow and cerebral oxygen extraction were no different from those in controls. This accounted for the mean 15% reduction in cerebral oxygen delivery (P=0.08) and 32% reduction cerebral Vo2 in CHD fetuses (P<0.001), which were associated with a 13% reduction in fetal brain volume (P<0.001). Fetal brain size correlated with ascending aortic oxygen saturation and cerebral Vo2 (r=0.37, P=0.004).

Conclusions: This study supports a direct link between reduced cerebral oxygenation and impaired brain growth in fetuses with CHD and raises the possibility that in utero brain development could be improved with maternal oxygen therapy.

Keywords: brain; heart diseases; hemodynamics; magnetic resonance imaging; pediatrics.

© 2015 American Heart Association, Inc.

Figures

Figure 1
Figure 1
Fetal brain volumetry in a normal term fetus by MRI using segmentation of a three dimensional steady state free precession acquisition.
Figure 2
Figure 2
T2 mapping of fetal vessels in a normal term fetus. Umbilical vein (UV), umbilical arteries (UA), ascending aorta (AAo), main pulmonary artery (MPA), superior vena cava (SVC).
Figure 3
Figure 3
Interobserver variation in fetal phase contrast flow and vessel T2 measurements.
Figure 4
Figure 4
Comparison of measured variables in fetuses with congenital heart disease (CHD) versus normal controls. Umbilical vein (UV), ascending aorta (AAo) superior vena caval (SVC), combined ventricular output (CVO), umbilical vein (UV) single ventricle (SV), biventricular (BV).
Figure 5
Figure 5
Comparison of calculated fetal cerebral hemodynamic parameters and brain volume in fetuses with congenital heart disease (CHD) versus normal controls. Cerebral oxygen delivery (DO2), oxygen extraction fraction (OEF) oxygen consumption (VO2)
Figure 6
Figure 6
Comparison of calculated fetal hemodynamic parameters in fetuses with congenital heart disease (CHD) versus normal controls. Oxygen delivery (DO2) oxygen extraction fraction (OEF), oxygen consumption (VO2), estimated fetal weight (EFW).
Figure 7
Figure 7
Correlations between estimated brain weight (EBW) Z-score and cerebral oxygen consumption (VO2) and ascending aortic oxygen saturation (AAo SaO2).
Figure 8
Figure 8
Fetal hemodynamics in representative examples of transposition (TGA), hypoplastic left heart syndrome (HLHS), and Tetralogy of Fallot (TOF) by MRI.

Source: PubMed

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