Cerebral Oxygenation Measurements by Magnetic Resonance Imaging in Fetuses With and Without Heart Defects

TY - JOUR

T1 - Cerebral Oxygenation Measurements by Magnetic Resonance Imaging in Fetuses With and Without Heart Defects

AU - Lauridsen, Mette H.

AU - Uldbjerg, Niels

AU - Henriksen, Tine B.

AU - Petersen, Olav B.

AU - Stausbøl-Grøn, Brian

AU - Matthiesen, Niels B.

AU - Peters, David A.

AU - Ringgaard, Steffen

AU - Hjortdal, Vibeke E.

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

KW - deoxyhemoglobin

KW - fetus

KW - gestational age

KW - heart diseases

KW - hypoxia

KW - magnetic resonance imaging

KW - prognosis

U2 - 10.1161/circimaging.117.006459

DO - 10.1161/circimaging.117.006459

M3 - Journal article

C2 - 29141840

AN - SCOPUS:85037700283

SN - 1941-9651

VL - 10

JO - Circulation: Cardiovascular Imaging

JF - Circulation: Cardiovascular Imaging

IS - 11

M1 - e006459

ER -