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T2* placental MRI in pregnancies complicated with fetal congenital heart disease

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
Pages (from-to)23-31
Number of pages9
Accepted/In press25 Feb 2021
PublishedMay 2021

Bibliographical note

Funding Information: This work was supported by the UKRI Future Leaders Fellowship [ MR/T018119/1 ], the Wellcome / EPSRC Centre for Medical Engineering [ WT 203148/Z/16/Z ], the Wellcome Trust IEH Award 102431 (iFIND project), the NIH Human Placenta Project grant 1U01HD087202-01 ( Placenta Imaging Project (PIP) ), the Wellcome Trust Sir Henry Wellcome Fellowship [ 201374/Z/16/Z ] and by the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Publisher Copyright: © 2021 Copyright: Copyright 2021 Elsevier B.V., All rights reserved.


King's Authors


Background: Congenital heart disease (CHD) is one of the most important and common group of congenital malformations in humans. Concurrent development and close functional links between the fetal heart and placenta emphasise the importance of understanding placental function and its influence in pregnancy outcomes. The aim of this study was to evaluate placental oxygenation by relaxometry (T2*) to assess differences in placental phenotype and function in CHD. Methods: In this prospective cross-sectional observational study, 69 women with a fetus affected with CHD and 37 controls, whole placental T2* was acquired using a 1.5-Tesla MRI scanner. Gaussian Process Regression was used to assess differences in placental phenotype in CHD cohorts compared to our controls. Results: Placental T2* maps demonstrated significant differences in CHD compared to controls at equivalent gestational age. Mean T2* values over the entire placental volume were lowest compared to predicted normal in right sided obstructive lesions (RSOL) (Z-Score 2.30). This cohort also showed highest lacunarity indices (Z-score −1.7), as a marker of lobule size. Distribution patterns of T2* values over the entire placental volume were positively skewed in RSOL (Z-score −4.69) and suspected, not confirmed coarctation of the aorta (CoA-) (Z-score −3.83). Deviations were also reflected in positive kurtosis in RSOL (Z-score −3.47) and CoA- (Z-score −2.86). Conclusion: Placental structure and function appear to deviate from normal development in pregnancies with fetal CHD. Specific patterns of altered placental function assessed by T2* deliver crucial complementary information to antenatal assessments in the presence of fetal CHD.

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