In Utero Brain Development in Fetuses With Congenital Heart Disease: Another Piece of the Jigsaw Provided by Blood Oxygen Level-Dependent Magnetic Resonance Imaging.

I n his seminal textbook on the physiology of congenital heart disease (CHD), Dr Rudolph suggests that disruption of the normal streaming of well-oxygenated blood from the placenta to the cerebral circulation via the ductus venosus and foramen ovale resulting from the abnormal connections and obstructions of blood flow that characterize congenital heart malformations should result in hypoxemia of the blood supplied to the developing brain in utero. 1 More recently, Dr Rudolph has pointed out that this blood may also be depleted of glucose, resulting in a reduction in the delivery of these 2 primary substrates for normal brain growth and development. 2 Donofrio et al 3 and others have since produced Doppler evidence of the known adenosine-mediated fetal cerebral vasodilatory response to acute hypoxemia in fetuses with CHD, whereas magnetic resonance oximetry has been used to confirm desaturation of the blood supplied to the fetal brain in the setting of transposition, single-ventricle hearts, and tetralogy of Fallot. In their article published in this issue of Circulation: Cardiovascular Imaging, Lauridsen et al 6 provide further evidence that the blood in the brains of fetuses with CHD contains less oxygen than normal controls. This time, the evidence is comprised by the diminished blood oxygen level-dependent magnetic resonance imaging signal obtained from the brains of fetuses with a range of congenital cardiac anomalies. The blood oxygen level-dependent signal, or T2*, of brain tissue is determined by several factors, including the oxygen saturation of the blood in the small arteries and veins, hemoglobin concentration, the density of blood vessels in the brain, and the magnetic properties of the surrounding cerebral parenchyma. It follows that the diminished brain blood oxygen level-dependent signal in fetuses with CHD compared with normal controls demonstrated in this study is primarily because of desaturation of the blood passing through their cerebral vasculature.