Cromb Daniel, Steinweg Johannes, Aviles Verdera Jordina, van Poppel Milou P M, Bonthrone Alexandra F, Lloyd David F A, Pushparajah Kuberan, Simpson John, Razavi Reza, Rutherford Mary, Counsell Serena J, Hutter Jana
Centre for the Developing Brain, School of Biomedical and Engineering Sciences, King's College London, London, UK.
Department of Cardiovascular Imaging, School of Biomedical Engineering & Imaging Science, King's College London, London, UK.
J Magn Reson Imaging. 2025 Mar;61(3):1246-1255. doi: 10.1002/jmri.29498. Epub 2024 Jul 12.
Congenital heart disease (CHD) has been linked to impaired placental and fetal brain development. Assessing the placenta and fetal brain in parallel may help further our understanding of the relationship between development of these organs.
Retrospective case-control.
Fifty-one human fetuses with CHD (32 male; median [IQR] gestational age [GA] = 32.0 [30.9-32.9] weeks) and 30 from uncomplicated pregnancies with normal birth outcomes (18 male; median [IQR] GA = 34.5 [31.9-36.7] weeks).
FIELD STRENGTH/SEQUENCE: 1.5 T single-shot multi-echo-gradient-echo echo-planar imaging.
Masking was performed using an automated nnUnet model. Mean brain and placental T2* and quantitative measures of placental texture, volume, and morphology were calculated.
Spearman's correlation coefficient for determining the association between brain and placental T2*, and between brain and placental characteristics with GA. P-values for comparing brain T2*, placenta T2*, and placental characteristics between groups derived from ANOVA. Significance level P < 0.05.
There was a significant positive association between placental and fetal brain T2* (⍴ = 0.46). Placental and fetal brain T2* showed a significant negative correlation with GA (placental T2* ⍴ = -0.65; fetal brain T2* ⍴ = -0.32). Both placental and fetal brain T2* values were significantly reduced in CHD, after adjusting for GA (placental T2*: control = 97 [±24] msec, CHD = 83 [±23] msec; brain T2*: control = 218 [±26] msec, CHD = 202 [±25] msec). Placental texture and morphology were also significantly altered in CHD (Texture: control = 0.84 [0.83-0.87], CHD = 0.80 [0.78-0.84]; Morphology: control = 9.9 [±2.2], CHD = 10.8 [±2.0]). For all fetuses, there was a significant positive association between placental T2* and placental texture (⍴ = 0.46).
Placental and fetal brain T2* values are associated in healthy fetuses and those with CHD. Placental and fetal brain oxygenation are reduced in CHD. Placental appearance is significantly altered in CHD and shows associations with placental oxygenation, suggesting altered placental development and function may be related.
3 TECHNICAL EFFICACY: Stage 3.
先天性心脏病（CHD）与胎盘及胎儿大脑发育受损有关。同时评估胎盘和胎儿大脑可能有助于我们进一步了解这些器官发育之间的关系。
1）胎盘和胎儿大脑的氧合作用相关；2）与健康对照组相比，先天性心脏病患者这些器官的氧合作用降低；3）先天性心脏病患者胎盘结构改变。
回顾性病例对照研究。
51例患有先天性心脏病的人类胎儿（32例男性；中位[四分位间距]孕周[GA]=32.0[30.9 - 32.9]周）和30例妊娠结局正常且无并发症的胎儿（18例男性；中位[四分位间距]GA = 34.5[31.9 - 36.7]周）。
场强/序列：1.5T单次激发多回波梯度回波平面成像。
使用自动化nnUnet模型进行掩膜处理。计算大脑和胎盘的平均T2*以及胎盘纹理、体积和形态的定量指标。
采用Spearman相关系数确定大脑与胎盘T2之间以及大脑和胎盘特征与孕周之间的关联。通过方差分析比较两组之间大脑T2、胎盘T2*和胎盘特征的P值。显著性水平P < 0.05。
胎盘和胎儿大脑T2之间存在显著正相关（⍴ = 0.46）。胎盘和胎儿大脑T2与孕周呈显著负相关（胎盘T2*⍴ = -0.65；胎儿大脑T2*⍴ = -0.32）。在调整孕周后，先天性心脏病患者的胎盘和胎儿大脑T2值均显著降低（胎盘T2：对照组 = 97[±24]毫秒，先天性心脏病组 = 83[±23]毫秒；大脑T2*：对照组 = 218[±26]毫秒，先天性心脏病组 = 202[±25]毫秒）。先天性心脏病患者的胎盘纹理和形态也有显著改变（纹理：对照组 = 0.84[0.83 - 0.87]，先天性心脏病组 = 0.80[0.78 - 0.84]；形态：对照组 = 9.9[±2.2]，先天性心脏病组 = 10.8[±2.0]）。对于所有胎儿，胎盘T2*与胎盘纹理之间存在显著正相关（⍴ = 0.46）。
健康胎儿和患有先天性心脏病的胎儿中，胎盘和胎儿大脑T2*值相关。先天性心脏病患者胎盘和胎儿大脑的氧合作用降低。先天性心脏病患者胎盘外观显著改变，且与胎盘氧合作用相关，提示胎盘发育和功能改变可能有关联。
3 技术效能：3级
