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Published on: March 14, 2013
Cerebral Oxygenation Measurements by Magnetic Resonance Imaging in Fetuses With and Without Heart Defects
Mette H Lauridsen1, Niels Uldbjerg2, Tine B Henriksen2
1From Pediatrics and Adolescent Medicine, Neonatal and Intensive Care Unit (M.H.L., T.B.H.), Department of Obstetrics and Gynecology (N.U., O.B.P.), Department of Pediatrics, Perinatal Epidemiology Research Unit (T.B.H., N.B.M.), Department of Radiology (B.S.-G.), and Department of Cardio-Thoracic and Vascular Surgery (V.E.H.), Aarhus University Hospital, Denmark; Institute for Clinical Medicine (M.H.L., N.U., S.R., V.E.H.) and the MR Research Centre (S.R.), Aarhus University, Denmark; and Department of Clinical Engineering, Central Denmark Region, Aarhus (D.A.P.). lauridsen.mette@auh.rm.dk.
Insights
Fetal brain oxygenation, measured by T2* magnetic resonance imaging, is lower in fetuses with major heart defects. This finding suggests reduced oxygen supply may impact brain development in these infants.
Area of Science:
- Medical Imaging
- Fetal Medicine
- Neuroscience
Background:
- Major congenital heart defects pose risks to fetal brain development, including impaired growth and maturation.
- Reduced cerebral tissue oxygenation is suspected in fetuses with congenital heart defects.
- T2* magnetic resonance imaging (MRI) can estimate cerebral tissue oxygenation, as low T2* indicates high deoxyhemoglobin concentrations.
Purpose of the Study:
- To compare fetal cerebral tissue oxygenation using T2* MRI in fetuses with and without major heart defects.
- To investigate the relationship between congenital heart defects and fetal brain oxygenation levels.
Main Methods:
- A comparative study involving 15 fetuses with major heart defects and 28 controls.
- Fetal cerebral T2* values were measured using 1.5 T MRI at two gestational age points (mean 32 and 37 weeks).
- Specific congenital heart defects included transposition of the great arteries, coarctation of the aorta, and others.
Main Results:
- Fetal cerebral T2* values were significantly lower in fetuses with heart defects compared to controls at both early (143 ms vs. 157 ms) and late (111 ms vs. 125 ms) gestational assessments.
- The difference in T2* values was statistically significant (P<0.001).
- T2* measurements were feasible in fetal brains.
Conclusions:
- Fetal cerebral T2* is a measurable indicator of cerebral tissue oxygenation.
- Fetuses with major heart defects exhibit lower cerebral tissue oxygenation compared to unaffected fetuses.
- Tissue hypoxia is a potential pathogenic factor affecting brain development in fetuses with congenital heart defects.
Background:
Children with major congenital heart defects are risking impaired cerebral growth, delayed cerebral maturation, and neurodevelopmental disorders. We aimed to compare the cerebral tissue oxygenation of fetuses with major heart defects to that of fetuses without heart defects as estimated by the magnetic resonance imaging modality T2*. T2* is low in areas with high concentrations of deoxyhemoglobin.
Methods And Results:
At gestational age mean 32 weeks (early) and mean 37 weeks (late), we compared the fetal cerebral T2* in 28 fetuses without heart defects to that of 15 fetuses with major heart defects: transposition of the great arteries (n=7), coarctation of the aorta/hypoplastic aortic arch (n=5), tetralogy of Fallot (n=1), hypoplastic right heart (n=1), and common arterial trunk (n=1). The women were scanned with a 1.5 T Philips scanner using a breath-hold multiecho gradient echo sequence. Among fetuses without heart defects, the mean T2* value was 157 ms (95% confidence interval [CI], 152-163) early and 125 ms (95% CI, 120-130) late. These figures were significantly lower (mean 14 ms; 95% CI, 6-22; P<0.001) among fetuses with heart defects 143 ms (95% CI, 136-150) early and 111 ms (95% CI, 104-118) late.
Conclusions:
Our findings indicate that fetal cerebral T2* is measurable and that fetal cerebral tissue oxygenation measured by T2* is lower in fetuses with heart defects compared with fetuses without heart defects. This corroborates the hypothesis that tissue hypoxia may be a potential pathogenic factor that possibly affects brain development in fetuses with heart defects.
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