Abstract

Placental dysfunction is a common obstetric problem that complicates 5 - 10% of all pregnancies (1). It is a progressive condition, in which the fetal supply of oxygen and nutrients is insufficient to maintain normal fetal growth and organ development. The association between low birth weight and adverse neonatal outcome is well described (2). Moreover, there is evidence to support the hypothesis that common adult diseases such as metabolic syndrome and cardiovascular disease originate from abnormal fetal programming due to placental dysfunction - also known as Barker's Hypothesis (3). Currently, there is no available treatment to improve placental function. However, correct antenatal identification of placental dysfunction leads to a four-fold improvement in the neonatal outcome, as it allows for timely delivery and thereby reduces the risk of irreversible fetal organ damage (4). Current antenatal screening of placental dysfunction focuses on fetal weight estimates and fetal and umbilical Doppler flow measurements. However, fetal size does not exactly reflect placental function. In addition, in late onset placental dysfunction, Doppler flows usually remain normal (5).Therefore, additional markers that directly reflect placental function have the potential to considerably improve the antenatal screening of placental dysfunction. There is increasing interest in placental MRI, due to its potential to detect placental dysfunction in vivo. In particular, T2* weighted MRI has proven to be a simple and useful method to assess placental health, either studying the quantitative T2* relaxation time or the relative change in the raw T2* weighted signal in response to a given challenge (the BOLD response). T2* depends primarily on oxygenation but also on other tissue factors, including villous density, inhomogeneities in the distribution of oxygenated blood, magnetic field inhomogeneities, and the presence of other paramagnetic molecules (6). This paper aims to explain the physiological basis for changes in T2* weighted signal intensity in the placenta. Previous literature on T2* weighted placental MR is reviewed and reference values are provided for 1.5 and 3 T. Practical guidance on how to optimize the T2* weighted scans is included, and the clinical potential of T2* weighted imaging as an antenatal test of placental dysfunction is outlined. This article is protected by copyright. All rights reserved.

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