Marianne Munk Sinding

Reduced placental oxygenation during subclinical uterine contractions as assessed by BOLD MRI.

OBJECTIVES During placental Blood Oxygen Level Dependent (BOLD) Magnetic Resonance Imaging (MRI), we have observed spontaneous reductions in placental oxygenation lasting 2-4 min. We hypothesize, that these reductions in placental oxygenation are caused by subclinical uterine contractions. METHODS We evaluated placental oxygenation during a five-minute placental BOLD MRI in 56 normal pregnancies (gestational week 23-40) and observed a spontaneous reduction in eight cases. The 56 BOLD MRIs were systematically analyzed for signs of uterine contractions, i.e. visual changes in uterus shape and reductions in the number of pixels within Regions of interest (ROI) covering the outline of the entire uterus. RESULTS The eight reductions in the BOLD signal lasted for 217 ± 51 (mean ± SD) seconds with an average signal loss of 17 ± 5%. They were all associated with a contraction, which started 43 ± 21 s prior to the start of the reduction and ended 71 ± 30 s prior to the end of the reduction. In the remaining 48 MRIs, we observed no contraction. CONCLUSION We suggest that the observed spontaneous reductions in placental oxygenation are caused by uterine contractions. According to our data, subclinical uterine contractions occur regularly and have a markedly impact on placental oxygenation. Therefore, uterine contractions need to be considered in the interpretation of placental MRI as they may interfere with the MRI results.

Placental magnetic resonance imaging T2* measurements in normal pregnancies and in those complicated by fetal growth restriction

The magnetic resonance imaging (MRI) variable transverse relaxation time (T2*) depends on multiple factors, one important one being the presence of deoxyhemoglobin. We aimed to describe placental T2* measurements in normal pregnancies and in those with fetal growth restriction (FGR).

Placental T2* measurements in normal pregnancies and in pregnancies complicated by fetal growth restriction

The magnetic resonance imaging (MRI) variable transverse relaxation time (T2*) depends on multiple factors, one important one being the presence of deoxyhemoglobin. We aimed to describe placental T2* measurements in normal pregnancies and in those with fetal growth restriction (FGR).

Placental oxygen transport estimated by the hyperoxic placental BOLD MRI response.

Estimating placental oxygen transport capacity is highly desirable, as impaired placental function is associated with fetal growth restriction (FGR) and poor neonatal outcome. In clinical obstetrics, a noninvasive method to estimate the placental oxygen transport is not available, and the current methods focus on fetal well‐being rather than on direct assessment of placental function. In this article, we aim to estimate the placental oxygen transport using the hyperoxic placental blood oxygen level‐dependent (BOLD) magnetic resonance imaging (MRI) response. In 21 normal pregnancies and in four cases of severe early onset FGR, placental BOLD MRI was performed in a 1.5 Tesla MRI system (TR:8000 msec, TE:50 msec, Flip angle:90). Placental histological examination was performed in the FGR cases. In normal pregnancies, the average hyperoxic placental BOLD response was 12.6 ± 5.4% (mean ± SD). In the FGR cases, the hyperoxic BOLD response was abnormal only in cases with histological signs of maternal hypoperfusion of the placenta. The hyperoxic placental BOLD response is mainly derived from an increase in the saturation of maternal venous blood. In the normal placenta, the pO2 of the umbilical vein is closely related to the pO2 of the uterine vein. Therefore, the hyperoxic placental BOLD response may reflect the placental oxygen supply to the fetus. In early onset FGR, the placental oxygen transport is reduced mainly because of the maternal hypoperfusion, and in these cases the placental BOLD response might be altered. Thus, the placental BOLD MRI might provide direct noninvasive assessment of placental oxygen transport.

Postpartum computed tomography angiography of the fetoplacental macrovasculature in normal pregnancies and in those complicated by fetal growth restriction

Current knowledge of the fetoplacental vasculature in fetal growth restriction (FGR) due to placental dysfunction focuses on the microvasculature rather than the macrovasculature. The aim of this study was to investigate the feasibility of computed tomography angiography to analyze the fetoplacental macrovasculature in normal and FGR pregnancies.

Postpartum placental CT angiography in normal pregnancies and in those complicated by diabetes mellitus

INTRODUCTION Pregnancy complicated by diabetes mellitus (DM) is a central obstetric problem often complicated by fetal macrosomia and increased risk of intrapartum asphyxia. This risk might be explained by fetoplacental vascular abnormalities. This study aimed to investigate the fetoplacental vascular volume by placental CT angiography in normal pregnancies and in pregnancies complicated by type 1 DM (T1DM), diet controlled gestational DM (GDMd), and insulin treated gestational DM (GDMi). METHODS Postpartum, barium contrast enhanced placental CT angiography was performed in 27 normal pregnancies and 25 DM pregnancies (8 T1DM, 8 GDMd, and 9 GDMi). The fetoplacental vascular volume/placenta weight (FVV/PW)-ratio and fetoplacental vascular volume/birth weight (FVV/BW)-ratio of each diabetic group were compared to the normal group with multiple regression analysis adjusted for GA. In all pregnancies a standardized histopathological placental examination was performed postpartum. RESULTS In normal pregnancies, the fetoplacental vascular volume increased with GA (p < 0.001), placental weight (p < 0.001), and birth weight (p < 0.001). In T1DM and GDMi pregnancies, the gestational age adjusted placental weight and the birth weight were increased when compared to normal pregnancies (p < 0.05). The FVV/BW-ratio was significantly reduced in both T1DM and GDMi pregnancies when compared to normal pregnancies (p = 0.003 and p = 0.009, respectively). DISCUSSION This study demonstrates, that in insulin treated DM pregnancies the fetus as well as the placenta is larger than normal. However, despite a large placenta, a relatively smaller fetoplacental vascular volume supplies the macrosomic fetus. This finding might explain why fetuses from insulin treated DM pregnancies have high vulnerability to intrauterine and intrapartum asphyxia.