Brain volume and metabolism in fetuses with congenital heart disease: evaluation with quantitative magnetic resonance imaging and spectroscopy.
Brain volume and metabolism in fetuses with congenital heart disease: evaluation with quantitative magnetic resonance imaging and spectroscopy.
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DOI:
10.1161/circulationaha.109.865568
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发表时间:
2010-01-05
期刊:
影响因子:
37.8
通讯作者:
du Plessis AJ
中科院分区:
文献类型:
--
作者:
Limperopoulos C;Tworetzky W;McElhinney DB;Newburger JW;Brown DW;Robertson RL Jr;Guizard N;McGrath E;Geva J;Annese D;Dunbar-Masterson C;Trainor B;Laussen PC;du Plessis AJ
Adverse neurodevelopmental outcome is an important source of morbidity in children with congenital heart disease (CHD). A significant proportion of newborns with complex CHD have abnormalities of brain size, structure, and/or function, suggesting that antenatal factors may contribute to childhood neurodevelopmental morbidity. Brain volume and metabolism were compared prospectively between 55 fetuses with CHD and 50 normal fetuses using 3-D volumetric magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (1H-MRS). Fetal intracranial cavity (ICV), cerebrospinal fluid, and total brain volumes (TBV) were measured by manual segmentation. 1H-MRS was used to measure the cerebral N-acetyl aspartate:choline ratio (NAA:Cho) and identify cerebral lactate. Complete fetal echocardiograms were performed. Gestational age (GA) at MRI ranged from 25 1/7 to 37 1/7 weeks (median 30 weeks). During the third trimester, there were progressive and significant declines in GA-adjusted TBV and ICV in CHD fetuses relative to controls. NAA:Cho increased progressively over the third trimester in normal fetuses, but the rate of rise was significantly slower (p<0.001) in CHD fetuses. On multivariable analysis adjusting for GA and weight percentile, cardiac diagnosis and percentage of combined ventricular output through the aortic valve were independently associated with TBV. Independent predictors of lower NAA:Cho included diagnosis, absence of antegrade aortic arch flow, and evidence of cerebral lactate (p<0.001). Third-trimester fetuses with some forms of CHD have smaller GA- and weight-adjusted TBV than normal fetuses, and evidence of impaired neuroaxonal development and metabolism. Hemodynamic factors may play an important role in this abnormal development.