Delayed Cortical Development in Fetuses with Complex Congenital Heart Disease
Delayed Cortical Development in Fetuses with Complex Congenital Heart Disease
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DOI：
10.1093/cercor/bhs281
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发表时间：
2013-12-01
期刊：
影响因子：
3.7
通讯作者：
Limperopoulos, C.
中科院分区：
文献类型：
--
作者：
Clouchoux, C.;du Plessis, A. J.;Limperopoulos, C.
神经功能损害是复杂先天性心脏病（CHD）的主要并发症。越来越多的证据表明，神经功能障碍可能存在于一个显着的比例，这一高风险的人口在新生儿早期手术干预之前。我们最近提供了第一个证据，证明复杂CHD胎儿的脑生长障碍起源于子宫内。在这里，我们扩展了这些观察的特点，全球和区域的大脑发育的胎儿与发育不良的左心综合征（HLHS），最严重的形式之一的CHD。使用先进的磁共振成像技术，我们比较了18个胎儿与HLHS和30个对照胎儿从孕25.437.0周的体内脑生长。我们的研究结果表明，HLHS胎儿的皮质灰质和白色物质体积（P 0.001）以及皮质下灰质（P 0.05）在妊娠晚期逐渐下降。在HLHS胎仔中，皮质脑回形成的显著延迟也很明显（P 0.001）。在HLHS胎儿中，早在25周时就在额叶、顶叶、距状核、颞叶和侧支区域检测到局部皮质折叠延迟，并且出现在体积脑生长障碍之前，这可能是妊娠晚期脑生长障碍风险升高的早期标志。
Neurologic impairment is a major complication of complex congenital heart disease (CHD). A growing body of evidence suggests that neurologic dysfunction may be present in a significant proportion of this high-risk population in the early newborn period prior to surgical interventions. We recently provided the first evidence that brain growth impairment in fetuses with complex CHD has its origins in utero. Here, we extend these observations by characterizing global and regional brain development in fetuses with hypoplastic left heart syndrome (HLHS), one of the most severe forms of CHD. Using advanced magnetic resonance imaging techniques, we compared in vivo brain growth in 18 fetuses with HLHS and 30 control fetuses from 25.437.0 weeks of gestation. Our findings demonstrate a progressive third trimester fall-off in cortical gray and white matter volumes (P 0.001), and subcortical gray matter (P 0.05) in fetuses with HLHS. Significant delays in cortical gyrification were also evident in HLHS fetuses (P 0.001). In the HLHS fetus, local cortical folding delays were detected as early as 25 weeks in the frontal, parietal, calcarine, temporal, and collateral regions and appear to precede volumetric brain growth disturbances, which may be an early marker of elevated risk for third trimester brain growth failure.