In Utero Brain Development in Fetuses With Congenital Heart Disease
Another Piece of the Jigsaw Provided by Blood Oxygen Level–Dependent Magnetic Resonance Imaging
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In 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 al3 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.4,5 In their article published in this issue of Circulation: Cardiovascular Imaging, Lauridsen et al6 provide further …