Placental Flow Research Articles

Machine learning from fetal flow waveforms to predict adverse perinatal outcomes: a study protocol.

Background: In Pakistan, stillbirth rates and early neonatal mortality rates are amongst the highest in the world. The aim of this study is to provide proof of concept for using a computational model of fetal haemodynamics, combined with machine learning. This model will be based on Doppler patterns of the fetal cardiovascular, cerebral and placental flows with the goal to identify those fetuses at increased risk of adverse perinatal outcomes such as stillbirth, perinatal mortality and other neonatal morbidities. Methods: This will be prospective one group cohort study which will be conducted in Ibrahim Hyderi, a peri-urban settlement in south east of Karachi. The eligibility criteria include pregnant women between 22-34 weeks who reside in the study area. Once enrolled, in addition to the performing fetal ultrasound to obtain Dopplers, data on socio-demographic, maternal anthropometry, haemoglobin and cardiotocography will be obtained on the pregnant women. Discussion: The machine learning approach for predicting adverse perinatal outcomes obtained from the current study will be validated in a larger population at the next stage. The data will allow for early interventions to improve perinatal outcomes.

First-trimester prediction of preterm labor using disintegrin and metalloprotease 12, uterine artery Doppler, and maternal characteristics

Background A disintegrin and metalloprotease 12 (ADAM12) is a complex placenta-derived protein with proteolytic activity that may serve as a marker of placental dysfunction for the identification of preterm birth. This has benefits of an early intervention and increased antenatal surveillance. In addition, uterine artery Doppler studies are noninvasive measurements of placental vascular flow with increased resistance reflecting impaired trophoblastic invasion. Objectives The objective of this study is to estimate the efficiency of first-trimester maternal serum ADAM12, uterine artery Doppler, and maternal characteristics in the early prediction of preterm birth. Patients and methods This cohort study was conducted on 90 pregnant women in their first trimesters with selection criteria. All patients were investigated for ADAM12 protein level, uterine artery Doppler, and maternal characteristics. They were followed up for screening of preterm birth (before 37 weeks). Results Uterine artery Doppler pulsatility index and maternal serum ADAM12 level either individually or combined are not statistically significant predictors of spontaneous preterm birth. The combination of maternal ADAM12 and BMI with cutoff levels of 162 pg/ml and 32 kg/m2, respectively, was a highly significant effective predictor of preterm birth. Advancing maternal age, increasing parity, increased BMI, and hypertension were maternal characteristics that correlated significantly with preterm birth. Conclusion Uterine artery Doppler pulsatility index and maternal serum ADAM12 level are not statistically significant predictors of spontaneous preterm birth, but ‘combined’ ADAM12 and BMI can do it significantly.

Aortic isthmus shunt dynamics in normal and complicated monochorionic pregnancies.

To study fetal aortic isthmus (AoI) shunt dynamics in monochorionic (MC) twins. Normal and complicated MC pregnancies were prospectively enrolled. The relationship of isthmus flow index (IFI) with Doppler parameters of umbilical artery (UA), descending aorta, middle cerebral artery, and ductus venosus and with left and right ventricular cardiac output and stroke volume was studied. The IFI was obtained in 180 examinations from 48 pregnancies (24 twin-twin transfusion syndrome, TTTS; 4 selective intrauterine growth restriction, sIUGR; 12 TTTS+sIUGR; and 8 uncomplicated). Median gestational age was 20.9weeks. AoI diastolic flow was reversed in three cases. UA pulsatility index (PI) and ductus venosus-PI z-scores were negatively correlated with the IFI (rs -0.40 and -0.26, respectively, p<0.001). Regression analysis identified only UA-PI as a determinant of the IFI (p<0.001). The IFI was significantly correlated with left ventricular cardiac output and stroke volume. It did not differ between TTTS donors and recipients. sIUGR fetuses had significantly lower IFI compared with normal-grown counterparts (p<0.001). In MC gestations, AoI shunting is predominantly determined by placental flow resistance, while cerebral impedance and volume status have no impact. In MC twins, the relationship between AoI flow and outcome deserves further study in the setting of sIUGR. © 2017 John Wiley & Sons, Ltd.

First-trimester placental vascular development in multiparous women differs from that in nulliparous women

Objective: Multiparas differ from nulliparas by delivering larger babies with larger placentas and by having a lower risk of developing placental syndromes. We postulate that these differences result from a different initial course of placental vascular development.Study design: We measured placental flow index (FI), vascularization index (VI) and placental volume by 3D power Doppler and obtained blood samples at 8, 10 and 12 weeks pregnancy in 34 healthy nulliparous and 16 multiparous women with an uneventful pregnancy.Results: Between 8 and 12 weeks multiparas differed from nulliparas in a more rapid initial rise in FI, a higher angiopoietin-2 (ang2) level at eight weeks and no decline in the VEGF/sVEGF-R ratio. Nevertheless, at 12 weeks the FI and placental volume were indistinguishable between both study groups.Conclusions: These results combining serially measured placental vascularization, placental volume and circulating angiogenetic factors show initial differences in placental development, that howeve, did not maintain till the end of first trimester. The results support the concept that early placental vascular development differs between nulliparas and multiparas. Nevertheless, it is unclear whether these differences contribute to the development later on in pregnancy of intergroup differences in birthweight and incidence of placental syndromes.

Влияние бета-блокаторов на плацентарный и плодовый кровоток у беременных группы высокого риска

Влияние бета-блокаторов на плацентарный и плодовый кровоток у беременных группы высокого риска

Abstract P318: miR-155 Induces Inflammation by Polarizing M1 Macrophages in a TLR3-induced Preeclamptic Mouse Model

Placental microRNA (miRNA) expression is known to be dysregulated during preeclampsia (PE), a hypertensive pregnancy disorder but the role it plays in the pathogenesis of PE is currently unknown. We have previously demonstrated that placental miR-155 expression is upregulated (P-PIC: 3.15 fold, p&lt;0.05 vs. controls) in a TLR3-induced PE mouse model similar to PE patients. In addition, poly I:C (PIC) treatment significantly increased systolic blood pressure (SBP) at gestational day 17 in P-PIC WT (147±4.5 mmHg) compared to P WT mice (103±2.7 mmHg), but did not have any effect in P-PIC miR-155 KO mice (101±2 mmHg). In PE there is an increase in the number of total and activated macrophages. M1 macrophages display the capacity to shift T cell responses toward a TH1 while M2 macrophages promote a TH2 response. We hypothesized that TLR3-induced upregulation of miR-155 contributes to hypertension in part by polarizing the macrophages to a M1 phenotype and these effects will be attenuated in P-PIC miR-155 KO mice. Placental flow cytometry analyses demonstrate that administration of poly I:C induced CD45(+) CD11b(+) macrophages in P-PIC WT mice which is attenuated in P-PIC miR-155 KO mice. In addition, placental classical ‘M1’ macrophages CD45(+) CD11b(+) CD86(+) CD206(-) were increased and alternate ‘M2’ macrophages CD45(+) CD11b(+) CD206(+) CD86(-) were decreased in P-PIC WT mice compared to controls. Interestingly, administration of poly I:C did not change M1 macrophages but increased M2 macrophages in P-PIC miR-155 KO mice. P-PIC WT mice exhibited increased placental expression of additional M1 markers (NOS2, IFNg) and decreased expression of M2 markers (Arg1, IL-10) compared to controls by qRTPCR but not in P-PIC miR-155 KO mice. The above observations are also consistent with our splenic flow cytometry and qRTPCR studies. Based on our results, miR-155 activation induces inflammation in part by increasing M1 macrophages thus contributing to hypertension. Targeting the innate immune system by inhibition of monocyte/macrophages may have beneficial cardiovascular effects in women with PE.

79 Renal and cardiac disturbances 8 weeks after exposure to placental ischemia in rat dams

Introduction Women with a history of preeclampsia (PE) have an increased risk to develop cardiovascular and renal disease later in life. Pre-existing cardiovascular risk factors may play an important role, on the other hand the transient presence of placenta ischemia might induce persistent changes in the maternal cardiovascular system. Objective We aimed to assess whether exposure to placental ischemia during pregnancy enhances long-term effects on the maternal cardiovascular and renal systems in rats using the Reduced Uterine Perfusion Pressure (RUPP) model for PE. Methods At gestational day (gd) 14, Sprague Dawley rats were randomized to two groups: SHAM (n = 12) or RUPP (n = 21). The RUPP procedure involved partial clipping of the lower abdominal aorta and both ovarian arteries to reduce placental flow. Post delivery, rats were followed for 8 weeks after which we measured mean arterial pressure (MAP, carotid), GFR (transcutaneous, sinistrin), albuminuria (24-h) and cardiac function (cardiac ultrasound). All rats were sacrificed for tissue collection and mesenteric arteries were used for reactivity experiments to assess peripheral arterial function. Parametric data are presented as mean ± SD and non-parametric data as median (25–75 percentile), and were respectively analyzed with student T-test or Mann–Whitney U-test. Morphologic and transcriptional analyses are ongoing. Results The mean weight gain of the RUPP rats during pregnancy (gd13–gd19) was significantly lower compared to the SHAM operated rats [30 ± 18 g vs 63 ± 12; p Conclusions We show that exposure to experimental placenta ischemia is accompanied by subtle disturbances in maternal cardiac and renal function after recovery from PE. Our results indicate that placental ischemia itself can result in persistent changes in the cardiac and renal systems, although at this early stage no differences in vascular reactivity or blood pressure regulation were observed. Future studies should elucidate whether aging, a second hit or underlying disease aggravate target organ dysfunction after placental ischemia. Results Despite being all followed up for 27.5 yrs, the exposed women were older when they had their first pregnancy with and median age of 24.9 yrs ((5th;95th percentiles) (19.5;27.3)) vs. 24.6 yrs (19.4;27.3), p Conclusion A small extra vitamin D in fetal life from food fortification reduced risk of PE later in life. The effect was mainly seen among current smokers.

OP20.01: Nulliparous and multiparous women differ in placental vascular development

Nulliparas differ from multiparas by giving birth to smaller babies and being at higher risk of developing pre-eclampsia. We tested the hypothesis that nulliparas and multiparas differ in their first-trimester development of placental vascularisation and volume. We measured placental flow index (FI), vascularisation index (VI) and placental volume (PV) by 3D power Doppler and VOCAL at 2 week intervals between 8 and 12 weeks pregnancy in 34 apparently healthy nulliparous and 16 multiparous, with normal pregnancy outcome. FI increased between 8 and 10 weeks in both nulliparous (p = 0.006) and multiparous women (p = 0.009) see figure 1. Between 10 and 12 weeks, the FI continued to increase significantly in nulliparas (p = 0.017) together with VI (p = 0.002), but not in multiparas. At 12 weeks, FI was indistinguishable between both groups. FI and VI varied markedly at all measurement points. The altered placental blood flow was not accompanied by a difference in placental volume growth. The placental vascularisation of multiparous women differs from nulliparous women. Multiparous women have an earlier development of first-trimester placental flow, without difference in the concomitant growth in placental volume. Supporting information can be found in the online version of this abstract Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Intraplacental villous artery resistance indices and identification of placenta-mediated diseases

Placenta-mediated diseases (PMDs) including preeclampsia and fetal growth restriction are often characterized by shallow trophoblast invasion and incomplete spiral artery remodeling leading to impaired placental perfusion. In this context, umbilical artery (UA) Doppler can be used to detect high resistance to flow characteristic of very late-stage placental disease. We propose that evaluation of intraplacental villous artery (IPVA) resistance can provide earlier detection of increased resistance in placental flow. Seventy-five patients were recruited from the Ottawa Hospital. All had scans at 18 to 20, 28 and 34 weeks of gestation. IPVAs arising perpendicular to the chorionic plate in three regions (placental tips 4 cm away from cord insertion and within 1 cm from cord insertion) were sampled at each gestational age for resistance index (RI) and pulsatility index (PI). UA Doppler was also obtained from a free loop of cord. Pregnancy outcomes were collected from a chart review. Data were analyzed using SAS version 9.4 and standard statistic tests (mean±s.d., Student's t-test, mixed-effects modeling). A total of 53 patients completed the study. Of these, 38 had normal pregnancy outcomes (controls) and 15 (cases) developed PMD (preeclampsia, n=8 and low birth weight/intrauterine growth restriction, n=7). Mean birth weight in the study group was 2482.1±518.85 g. At 18 to 20, 28 and 34 weeks gestation, the mean IPVA resistance indices in the control group were 0.86±0.16, 0.81±0.12 and 0.71±0.12 for PI and 0.57±0.07, 0.55±0.06 and 0.49±0.06 for RI, respectively. However, in the cases developing PMDs, the PIs were 1.09±0.17, 0.95±0.21 and 0.78±0.07 and RIs 0.66±0.07, 0.60±0.07 and 0.54±0.04, respectively (P<0.05). UA PI and RI Doppler did not differ between the groups as early as 18 to 20 weeks gestation. Doppler measures of IPVA appear superior to UA in detecting early changes related to PMD. IPVA PI and RI Doppler may be useful in the early identification of patients at risk of PMD.

Hipertensión inducida por el Embarazo Nuevos Conceptos.

La hipertensión inducida por el embarazo es una enfermedad que complica el embarazo progresiva y solapadamente, acarreando con frecuencia graves consecuencias maternas y perinatales. Conocemos que es una alteración bioquímica y orgánica del endotelio vascular, con predominio de sustancias contráctiles sobre las relajantes, –lo que lo hace lábil a las sustancias vasopresoras–, así como incremento de la actividad mitogénica y anormalidades de los mecanismos de coagulación. Hay disminución del volumen plasmático en relación directa con la hipertensión, disminución de la deformabilidad del eritrocito, placentación defectuosa, todo lo cual sugiere un fondo inmunológico y genético, que empieza con el inicio del embarazo. No existen análisis premonitorios, salvo los que indican gravedad de la enfermedad. Es preferible considerar la presión diastólica =80mm de Hg como hipertensión. La madre puede colaborar en vigilar el crecimiento y movilidad de su bebé mientras está en el útero. La ecografía establece el desarrollo y el bienestar fetal. El sulfato de magnesio y la nifedipina, en nuestro medio, son las drogas de elección para tratar las crisis hipertensivas, recomendaciones no bajar la presión diastólica por debajo de 100 mm de Hg para evitar empeorar el flujo placentario. El tratamiento de la hipertensión inducida por el embarazo consiste en el nacimiento de feto y placenta, existiendo en el periodo posterior inmediato al parto riesgo de convulsiones y shock hipovolémico, así como de coagulación intravascular diseminada. La prolongación del embarazo puede dejar secuela hipertensiva materna pocos años más tarde y, en el feto, hipertensiva y secuelas neurológicas. El manejo de la enfermedad requiere atención especializada del ginecoobstetra, con amplio conocimiento de su fisiopatología y las modificaciones maternas y fetales. Se explica las razones por las que se hace necesaria una modificación de la clasificación de las enfermedades hipertensivas que complican el embarazo.

A “cure” for preeclampsia: Improving neonatal outcomes by overcoming excess fetal placental vascular resistance

From a broad perspective there are only three arterial systems that respond to relative hypoxia with vasoconstriction. They are the placental, the pulmonic and the renal vascular beds. The renal system’s adaptation to hypoxia is markedly different from the other two circulatory beds and will not be further considered here. Regional vasoconstriction is adaptive in the placenta and lung because it redirects red blood cells from areas of relative hypoxia to more oxygenated areas thereby maximizing oxygen uptake for a given cardiac output. The fetal placental and pulmonary vascular systems are unique because their smooth muscle cells have a unique and possibly identical potassium channel that responds to hypoxia by closing, thereby depolarizing the cell membrane allowing calcium ion influx and muscle contraction. It may be that a variety of initial causes of temporary or local placental hypoxia initiate a cascade of first fetal placental then maternal vasoconstriction and endothelial activation leading to the clinical syndrome we call preeclampsia. The response cascades seen in preeclampsia, which for purposes of this article I will abbreviate as (PECL), after development of widespread vasoconstriction, will also be seen to be identical or at least parallel in pulmonary hypertension (PAH). This means that some or all of the pharmacotherapies presently used, tested or considered in early PAH may also have a therapeutic effect in PECL by reducing fetal placental arterial resistance thereby increasing fetal placental flow. This would allow increased oxygen and other nutrient uptake and possibly increased fetal cardiac output in the face of reduced fetal cardiac work. This may allow a delay in delivery in which fetuses grow and are better oxygenated in preterm PECL, improving neonatal outcomes.

Decreased placental thickness and impaired Doppler indices in idiopathic polyhydramnios: a prospective case–control study

Objective: To evaluate placental thickness, Doppler velocimetry, biophysical profile and perinatal outcomes in pregnancies complicated by idiopathic polyhydramnios.Materials and methods: This prospective case–control study was conducted on 139 pregnant women, of these 70 patients with idiopathic polyhydramnios comprised the study group and 60 pregnant women comprised the control group. Risk factors recorded were; age, parity, body mass index (BMI), gestational weeks, amniotic fluid index (AFI), biophysical profiles (BPP), placental thickness, middle cerebral artery pulsatility index (MCA PI), umbilical artery Doppler velocimetry (Umb A S/D) values and perinatal outcomes.Results: Sixty-nine of the cases had mild-moderate (AFI: 250–450 mm) polyhydramnios (%98.5) and one of the cases had severe polyhydramnios (>450 mm) in study group. There was no statistically significant difference between the groups in terms of age, parity, BMI, gestational weeks, fetal birth weights and BPP (p > 0.05). Placental thickness, MCA PI and UA S/D values showed statistically significant difference between the groups (p < 0.05). The fetuses with lower placental thickness had lower scores of biophysical profile. There were negative correlations between placental thickness and AFI (r = −0.265), umbilical artery S/D and placental thickness (r = −0.212), MCA PI and AFI (r = −171, p = 0.44). However there was a positive correlation between AFI and umbilical artery Doppler values (r = 0.450).Conclusion: Idiopathic polyhydramnios is associated with decreased placental thickness, impaired uterine, umbilical and middle cerebral artery flow.

Three-dimensional power Doppler indices of preeclamptic placentas correlated to umbilical artery Doppler and albuminuria

Purpose: To obtain three-dimensional power Doppler (3DPD) indices of placenta in pregnancies complicated with preeclampsia compared to normal pregnancies and correlated to umbilical artery Doppler and albuminuria.Methods: A case-control study was conducted at Ain Shams University Maternity Hospital. Evaluation of placental vascular indices, vascularization index (VI), flow index (FI) and vascularization flow index (VFI), was done using 3DPD in 80 preeclampsia pregnancies compared to 80 normal controls.Results: 3DPD indices (VI, FI and VFI) of preeclampsia cases revealed lower values than controls (p < 0.001). There was a statistical inverse correlation between albuminuria versus VI (p < 0.05) and a statistical inverse correlation was found between VI, FI and VFI versus umbilical artery RI.Conclusion: 3DPD indices of placental vasculature revealed lower values in preeclamptic pregnancies than normal pregnancies. Further studies are needed to discuss the possible role of 3DPD in predicting preeclampsia.

Possible joint pathways of early pre-eclampsia and congenital heart defects via angiogenic imbalance and potential evidence for cardio-placental syndrome

This editorial refers to ‘Maternal and foetal angiogenic imbalance in congenital heart defects’, by E. Llurba et al. doi:10.1093/eurheartj/eht389 Foetal vasculogenesis and angiogenesis and maternal angiogenesis are essential requirements for a pregnancy. Decidua-associated vascular changes arise in the inner junctional zone myometrium in early pregnancy, followed by trophoblast invasion with associated remodelling.1 Decidual natural killer and dendritic cells regulate key developmental processes at the human foetal–maternal interface via human leucocyte antigen (HLA)-C, HLA-E, and HLA-G.2 Intervillous flow starts at 7–8 weeks gestation, via connecting channels between maternal myometrial spiral arteries and lacunae in the wall of the implanted cytoblast. Early trophoblast plugging might protect the embryo against high oxygen concentrations, and it has to be postulated that premature loss of those plugs could lead to early miscarriage or early-onset pre-eclampsia.3 In the past decade, extensive research has investigated the abnormalities that can occur in the first trimester of pregnancy that could lead to chorionic regression or small placenta, contributing to intrauterine growth restriction and early-onset pre-eclampsia.4 Placental flow defects can occur as early as 12 weeks in women who subsequently develop pre-eclampsia. Hypoxia and reoxygenation episodes can generate reactive oxygen species, leading to placental oxidative stress and placental dysfunction. Although the causes of pre-eclampsia, defined as new hypertension (diastolic blood pressure >90 mmHg) and substantial proteinuria (>300 mg in 24 h) after 20 weeks gestation,4 remains largely unknown, the leading hypothesis strongly suggests disturbed placental function in early pregnancy, possibly due to failed interaction between two genetically different organisms.4 As a second stage of the foetal–maternal interphase, research by Levine and Karumanchi has shown an increased production of bioactive trophoblast debris, including an excess of syncytiotrophoblast-derived antiangiogenic factors, such as soluble forms of vascular endothelial growth factor (VEGF) receptors, including the VEGF receptor-1, also …

Porous media flow models for maternal placental circulation

s / Placenta 34 (2013) A1–A99 A15 Conclusion: Detailed placental measures collected by simple imaging methods illuminate placental functional efficiency, a key factor in gestational life that is likely important in fetal programming. PCA demonstrates the complex interactions between lateral expansion of the chorionic plate surface, branching growth of chorionic surface vessels, and arborisation of the fetal stem villi to create the placental surface exchange area that makes up disk thickness. Measurement of any single dimension can lead to misleading conclusions because in different combinations, specific measures may have opposite effects on beta. http://dx.doi.org/10.1016/j.placenta.2013.06.044 P1.8. POROUS MEDIA FLOW MODELS FOR MATERNAL PLACENTAL CIRCULATION Christopher Ball , David Grynspan , Andree Gruslin 3,4 Department of Pathology and Laboratory Medicine, The Ottawa Hospital, Ottawa, Ontario, Canada; Department of Pathology and Laboratory Medicine, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada; Department of Obstetrics and Gynecology, The Ottawa Hospital, Ottawa, Ontario, Canada; Department of Cellular Molecular Medicine, The Ottawa Hospital, Ottawa, Ontario, Canada Introduction: It is reasonable to believe that the presence of abnormal flow patterns in the chorionic vessels is an earlier and more sensitive predictor of IUGR than altered end diastolic flow in the umbilical artery. It furthermore appears that the prediction of IUGR becomes increasingly sensitive as predictive flowmeasurements are taken increasingly distal (to the fetus) in the umbilical cord. This, we hypothesize, results from remodelling of the villous circulatory beddthe most proximate correlate of the factors that lead to IUGR. The effect of lacunar blood flow, the intimately connected maternal side of placental flow, cannot be ignored. Aim:Our aim is tomodel the fluidmechanics of the normalmaternal lacunar blood flows in order to assess its influence on flow within the measurable parts of the fetal arterial tree. In view of the placental structure, we aim to apply a model of flow through porous media to the maternal flow bed. Methods: Preliminary inquiry has lead us to suspect that this flowproblem is analogous to the problem of laminar flow through a porous medium (such as in models of fuel cells, ground water, etc.). Here we will illustrate application of this canonical flow model to that of the maternal placenta. Discussion: The problem of modelling EDFR provides an example where interdisciplinary collaboration between medicine and engineering hopefully will permit rapid progress through novel application to one field of established constructs from another. http://dx.doi.org/10.1016/j.placenta.2013.06.045 P1.9. ECHOCARDIOGRAPHIC ANALYSES OF PREGNANCIES IN THE PLACENTAL GROWTH FACTOR KNOCKOUT MOUSE Kristiina Aasa , Bruno Zavan , Philip Wong , Yat Tse , Stephen Pang , B. Anne Croy 1 Queen's University, Kingston, ON, Canada; UNIFAL-MG, Alfenas, Minas

Utero-placental expression of angiotensin-(1–7) and ACE2 in the pregnant guinea-pig

BackgroundIn humans, trophoblast invasion, vascular remodeling and placental development are critical to determine the fate of pregnancy. Since guinea-pigs (GP) and humans share common pregnancy features including extensive trophoblast invasion, transformation of the uterine spiral arteries and a haemomonochorial placenta, the GP animal model was deemed suitable to extend our knowledge on the spatio-temporal immunoreactive expression of the vasodilator arpeptide of the renin-angiotensin system, angiotensin-(1–7) [Ang-(1–7)] and its main generating enzyme, angiotensin converting enzyme 2 (ACE2).MethodsUtero-placental units were collected in days 15, 20, 40 and 60 of a 64–67 day long pregnancy in 25 Pirbright GP. Ang-(1–7) and ACE2 expression in utero-placental units were evaluated by immunohistochemistry.ResultsAng-(1–7) and ACE2 were detected in the endothelium and syncytiotrophoblast of the labyrinthine placenta, interlobium, subplacenta, giant cells, syncytial sprouts, syncytial streamers, and myometrium throughout pregnancy. In late pregnancy, perivascular or intramural trophoblasts in spiral and mesometrial arteries expressed both factors. Immunoreactive Ang-(1–7) and ACE2 were present in decidua and in the vascular smooth muscle of spiral, myometrial and mesometrial arteries, which also express kallikrein (Kal), the bradykinin receptor 2 (B2R), vascular endothelial growth factor (VEGF) and its type 2 receptor (KDR), but no endothelial nitric oxide synthase (eNOS). In addition, the signal of Ang-(1–7) and ACE2 was especially remarkable in giant cells, which also show Kal, B2R. eNOS, VEGF and KDR.ConclusionsThe spatio-temporal expression of Ang-(1–7) and ACE2 in GP, similar to that of humans, supports a relevant evolutionary conserved function of Ang-(1–7) and ACE2 in decidualization, trophoblast invasion, vascular remodeling and placental flow regulation, as well as the validity of the GP model to understand the local adaptations of pregnancy. It also integrates Ang-(1–7) to the utero-placental vasodilatory network. However, its antiangiogenic effect may counterbalance the proangiogenic activity of some of the other vasodilator components.

Corrección intrauterina de mielomeningocele: experiencia del programa de medicina y terapia fetal del Hospital Universitario Virgen del Rocío

The most frequent form of spina bifida is myelomeningocele. There is no optimal postnatal treatment for this defect. In addition to the motor or sensory deficits, which depend on the location of the lesion, the defect is usually associated with Chiari ii malformation in affected children. Myelomeningocele has high mortality and, in up to 80% to 90% of patients, can be accompanied by hydrocephalus, which causes severe neurocognitive impairment and requires the patient to be shunted for survival. Intrauterine repair of fetal malformations employing open access through hysterotomy has become a therapeutic option due to improved anesthetic and surgical techniques and instrumentation, which have allowed this type of intervention to become relatively frequent. Anesthetic treatment should focus on both the mother and fetus and the hemodynamic factors regulating placental flow, uterine dynamics, blood loss and fetal well-being must remain well-controlled. Within our Program for Fetal Medicine and Therapy, 21 open fetal interventions have been performed: 17 EXIT procedures and 4 procedures for the intrauterine correction of fetal myelomeningocele. We describe our experience of the intrauterine repair of fetal myelomeningocele through open fetal surgery.

OP25.09: Early fetal growth in malaria infected pregnancies

pregnancy outcomes. The current sensitivity and positive predictive value of this association has, however, not yet justified initiation of increased antenatal surveillance in these patients. This study was carried out to identify if 3D placental evaluation enhances the performance of this serum marker as a predictor of adverse pregnancy outcomes. Methods: 62 patients with PAPP-A levels lower than 0.4 multiples of median (MoM) were evaluated between 11 weeks to 13 weeks 6 days of gestation with 3D power Doppler studies in this prospective study. Placental volume, Vascularisation Index (VI), Flow Index and Vascularisation Flow Index (VFI) were computed with standardised equipment settings and correlated with pregnancy outcomes. Results: 38 patients had an uneventful pregnancy outcome. 29 of these had normal 3D placental parameters. Of the 24 patients with adverse outcomes 19 had a small volume placenta, impaired 3D placental vascularisation indices or both. Conclusions: 3D and 3D power Doppler evaluation of the placenta in the late first trimester improves the prediction of adverse outcomes in patients with low PAPP-A levels.

OP09.06: First trimester uterine artery Doppler and placental 3D power Doppler vascular flow in the prediction of Preeclampsia

OP09.06: First trimester uterine artery Doppler and placental 3D power Doppler vascular flow in the prediction of Preeclampsia

Placental Vascular Flow Velocity is Correlated with Fetus Body Weight at Birth

Placental Vascular Flow Velocity is Correlated with Fetus Body Weight at Birth