Long-term maternal morbidity and mortality associated with ischemic placental disease

Adams, Tracy; Yeh, Corinne; Bennett-Kunzier, Nadia; Kinzler, Wendy L.

doi:10.1053/j.semperi.2014.03.003

Cited by 40 publications

(29 citation statements)

References 34 publications

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“…The role of the placenta in the pathogenesis of FGR as well as in PE is well established [Palloto and Kilbride, 2006;Adams et al, 2014;Friedman and Cleary, 2014]. Therefore, placenta-based investigation of CNVs is crucial for understanding FGR, PE and their related genes and pathways.…”

Section: Discussionmentioning

confidence: 99%

Genomic Alterations Are Enhanced in Placentas from Pregnancies with Fetal Growth Restriction and Preeclampsia: Preliminary Results

et al. 2015

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Fetal growth restriction (FGR) secondary to placental insufficiency and preeclampsia (PE) are associated with substantially increased childhood and adult morbidity and mortality. The long-term outcomes are related to placental aberrations and intrauterine programming. Advances in microarray technology allow high-resolution, genome-wide evaluation for DNA copy number variations - deletions and duplications. The aim of our study was to demonstrate the usefulness of microarray testing in FGR placentas. Using Affymetrix GeneChip for chromosomal microarray (CMA), we analyzed 10 placentas from pregnancies with FGR attributed to placental insufficiency; 5 with FGR below the 5th percentile and 5 from the 5th to <10th percentiles. All fetuses had normal anomaly scans and karyotypes. We also analyzed 5 third-trimester placentas from pregnancies complicated by PE with severe features and 5 from PE without severe features, all with appropriately grown fetuses. The results were compared to 10 placentas from uncomplicated pregnancies with healthy neonates. CMA analysis identified more genomic alterations in FGR (p < 0.05) and in PE (p < 0.05) placentas than in healthy controls. There was a correlation to the severity of FGR and PE. The genomic alterations were below the resolution of normal karyotyping. The altered genes are related to adult human height, stress reactions and to cellular migration, differentiation and adhesion. Though very preliminary, our data support evaluating FGR and PE placentas using CMA. Larger data sets are needed for further evaluation of the findings and their clinical implications.

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Section: Discussionmentioning

confidence: 99%

Genomic Alterations Are Enhanced in Placentas from Pregnancies with Fetal Growth Restriction and Preeclampsia: Preliminary Results

et al. 2015

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“…These are (i) turbulent flow conditions, particularly vortices at the arterial openings, which are an equivalent of functional “dead volumes” with suboptimal exchange capacity, and (ii) elevated blood pressure in the IVS, which could potentially become a risk for fetoplacental perfusion as soon as fetal capillaries become compressed or even collapse. In view of the concept of ischemic placental disease, the present study demonstrates possible pathogenetic mechanisms that are capable of linking the early origins (insufficient arterial remodeling) to the considerably later development of clinically symptomatic placental disease13536.…”

Section: Resultsmentioning

confidence: 80%

Dynamic modeling of uteroplacental blood flow in IUGR indicates vortices and elevated pressure in the intervillous space – a pilot study

Roth

Haeussner

Ruebelmann

et al. 2017

Sci Rep

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Ischemic placental disease is a concept that links intrauterine growth retardation (IUGR) and preeclampsia (PE) back to insufficient remodeling of uterine spiral arteries. The rheological consequences of insufficient remodeling of uterine spiral arteries were hypothesized to mediate the considerably later manifestation of obstetric disease. However, the micro-rheology in the intervillous space (IVS) cannot be examined clinically and rheological animal models of the human IVS do not exist. Thus, an in silico approach was implemented to provide in vivo inaccessible data. The morphology of a spiral artery and the inflow region of the IVS were three-dimensionally reconstructed to provide a morphological stage for the simulations. Advanced high-end supercomputing resources were used to provide blood flow simulations at high spatial resolution. Our simulations revealed turbulent blood flow (high-velocity jets and vortices) combined with elevated blood pressure in the IVS and increased wall shear stress at the villous surface in conjunction with insufficient spiral artery remodeling only. Post-hoc histological analysis of uterine veins showed evidence of increased trophoblast shedding in an IUGR placenta. Our data support that rheological alteration in the IVS is a relevant mechanism linking ischemic placental disease to altered structural integrity and function of the placenta.

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“…Previous knowledge indicates that ischemic placental disease may be linked to both low BW and an increased venous thrombotic risk. 3,16 Other conditions of ischemic placental disease, preeclampsia and placental abruption, are also consistently documented risk factors for maternal postpartum VTE. 3,5 Furthermore, histological placental examinations of women with growth restriction provide evidence of both maternal and fetal vascular obstruction.…”

Section: Discussionmentioning

confidence: 99%

Association Between Newborn Birth Weight and the Risk of Postpartum Maternal Venous Thromboembolism

et al. 2015

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Background-Postpartum venous thromboembolism (VTE) is a potentially fatal and preventable event leading to substantial short-and long-term morbidity. We sought to evaluate whether the delivery of term newborns of low or high birth weight was associated with greater risks of VTE. Methods and Results-In a population-based case-control study conducted in Washington State from 1987 through 2011, cases of hospitalized VTE within 3 months of delivery were identified by using selected International Classification of Diseases, Ninth Revision, Clinical Modification codes. Controls were randomly selected postpartum women without VTE, matched on birth year. Birth weight and other maternal and pregnancy characteristics were extracted from birth certificate data. Among term live singleton deliveries, we compared the risk of VTE for mothers of newborns of low and high birth weights (<2500 g and >4000 g, respectively) versus mothers of newborns of normal birth weight (2500-4000 g). Logistic regression models were adjusted for maternal age, race, education, body mass index, parity, delivery methods, gestational length, smoking, gestational diabetes mellitus, and preeclampsia. Patients with VTE (n=547) were older, had a higher body mass index, and experienced more pregnancy-related complications than controls (n=9482).In comparison with mothers of newborns with normal birth weight, mothers of newborns with low birth weight had a 3-fold increased risk of VTE, which persisted after multivariable adjustment (odds ratio, 2.98; 95% confidence interval, 1.80-4.93). Mothers of newborns with high birth weight had only a slightly increased risk of VTE, which was attenuated after multivariable adjustment (odds ratio, 1.26; 95% confidence interval, 0.99-1.61). Conclusions-The delivery of a newborn with low birth weight is associated with a 3-fold increased risk of maternal postpartum VTE. This should be considered when assessing VTE risk at delivery.

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Long-term maternal morbidity and mortality associated with ischemic placental disease

Cited by 40 publications

References 34 publications

Genomic Alterations Are Enhanced in Placentas from Pregnancies with Fetal Growth Restriction and Preeclampsia: Preliminary Results

Genomic Alterations Are Enhanced in Placentas from Pregnancies with Fetal Growth Restriction and Preeclampsia: Preliminary Results

Dynamic modeling of uteroplacental blood flow in IUGR indicates vortices and elevated pressure in the intervillous space – a pilot study

Association Between Newborn Birth Weight and the Risk of Postpartum Maternal Venous Thromboembolism

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