Placental bed vascular disorders

Brosens, Ivo; Khong, T. Y.

doi:10.1017/cbo9780511750847.004

Cited by 6 publications

(5 citation statements)

References 87 publications

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“…The capacity of the uteroplacental circulation to deliver nutrients near term is determined, in large part, by the extent of vascular remodelling in the first trimester, particularly the number of spiral arteries modified and how deeply their modification extends into the myometrium. Pregnancies in which remodelling is shallow, or affects few arteries, are associated with high resistance to flow in the placental bed and reduced perfusion of the intervillous space [52,53]. Although mothers and fetuses have a mutual interest in placental perfusion once a mother is 'committed' to carrying a fetus to term, fetuses favour the uterus receiving a larger share of maternal cardiac output, especially near term when fetal needs are greatest [48].…”

Section: Trophoblast and The Subversion Of Extrinsic Defencesmentioning

confidence: 99%

Maternal–fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

Haig

2015

Phil. Trans. R. Soc. B

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Antagonistic coevolution between maternal and fetal genes, and between maternally and paternally derived genes may have increased mammalian vulnerability to cancer. Placental trophoblast has evolved to invade maternal tissues and evade structural and immunological constraints on its invasion. These adaptations can be co-opted by cancer in intrasomatic selection. Imprinted genes of maternal and paternal origin favour different degrees of proliferation of particular cell types in which they reside. As a result, the set of genes favouring greater proliferation will be selected to evade controls on cell-cycle progression imposed by the set of genes favouring lesser proliferation. The dynamics of stem cell populations will be a particular focus of this intragenomic conflict. Gene networks that are battlegrounds of intragenomic conflict are expected to be less robust than networks that evolve in the absence of conflict. By these processes, maternal–fetal and intragenomic conflicts may undermine evolved defences against cancer.

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Section: Trophoblast and The Subversion Of Extrinsic Defencesmentioning

confidence: 99%

Maternal–fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

Haig

2015

Phil. Trans. R. Soc. B

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“…Initially, physiologic transformation of the spiral arteries includes endothelial vacuolation and smooth muscle swelling [8–11], and it has been attributed in part to immune processes within the decidua [4,12–18]. Subsequently, trophoblasts invading the spiral arteries destroy the smooth muscle in the media, which is replaced by fibrinoid material [1,3,19–21]. …”

Section: Introductionmentioning

confidence: 99%

“…Such deep placentation can be defective when remodeling of the junctional zone of the spiral arteries (arterial segments in the inner third of the myometrium and overlying endometrium) is absent or incomplete [21,24–26]. Insufficient physiologic transformation of the spiral arteries is associated with adverse pregnancy outcomes [3,21,27], including second-trimester spontaneous abortion [28–30], fetal death [30], abruptio placentae [31], preeclampsia [1,32–34], small for gestational age [32–35], preterm labor [36], preterm prelabor rupture of membranes [37,38], and maternal autoimmune diseases [39]. …”

Section: Introductionmentioning

confidence: 99%

Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta

Labarrere

DiCarlo

Bammerlin

et al. 2017

American Journal of Obstetrics and Gynecology

131

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Background Failure of physiologic transformation of spiral arteries has been reported in preeclampsia, fetal growth restriction, fetal death, and spontaneous preterm labor with intact or ruptured membranes. Spiral arteries with failure of physiologic transformation are prone to develop atherosclerotic-like lesions of atherosis. There are striking parallels between preeclampsia and atherosclerotic disease, and between lesions of atherosis and atherosclerosis. Endothelial activation, identified by intercellular adhesion molecule-1 expression, is present in atherosclerotic-like lesions of heart transplantation and considered a manifestation of rejection. Similarly, endothelial activation/dysfunction has been implicated in the pathophysiology of atherosclerosis and preeclampsia. Intercellular adhesion molecule-1-overexpressing-activated endothelial cells are more resistant to trophoblast displacement than nonactivated endothelium and may contribute to shallow spiral artery trophoblastic invasion in obstetrical syndromes having failure of physiologic transformation. Objective To determine whether failure of spiral artery physiologic transformation was associated with activation of interstitial extravillous trophoblasts and/or spiral artery endothelium and presence of acute atherosis in the placental basal plate. Study Design A cross-sectional study of 123 placentas (19-42 weeks’ gestation) obtained from normal pregnancies (n = 22), preterm prelabor rupture of membranes (n = 26), preterm labor (n = 23), preeclampsia (n = 27), intrauterine fetal death (n = 15), and small for gestational age (n = 10) was performed. Failure of spiral artery physiologic transformation and presence of cell activation was determined using immunohistochemistry of placental basal plates containing a median of 4 (minimum: 1; maximum: 9) vessels per placenta. Endothelial/trophoblast cell activation was defined by the expression of intercellular adhesion molecule-1 (ICAM-1). Investigators examining microscopic sections were blinded to clinical diagnosis. Pairwise comparisons among placenta groups were performed with the Fisher’s exact and Wilcoxon rank sum tests using a Bonferroni-adjusted level of significance (.025). Results 87% (94/108) of placentas having spiral arteries with failure of physiologic transformation (actin-positive and cytokeratin-negative) in the basal plate, and 0% (0/15) of placentas having only spiral arteries with complete physiologic transformation (cytokeratin-positive and actin-negative), had arterial endothelial and/or interstitial extravillous trophoblasts reactive with the ICAM-1 activation marker (P < .001). A significant correlation (R2 = 0.84) was found between expression of spiral artery endothelial and interstitial extravillous trophoblast ICAM-1 (P < .001) in activated placentas. Lesions of atherosis were found in 31.9% (30/94) of placentas with complete and/or partial failure of physiologic transformation of spiral arteries that were ICAM-1-positive, in none of the 14 placentas with failure of physiolog...

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“…Although acute atherosis was originally described in the spiral arteries of patients with preeclampsia [2–4,6–12,15–18,20,22,23,25–30,39–41,43–47], this lesion is not specific, and has been reported in normal pregnancy [3,4,21,30,41], as well as those complicated by diabetes mellitus [5,15,24], gestational and chronic hypertension [15,24,27,28], systemic lupus erythematosus, and antiphospholipid antibody syndrome [14,24,31,34,37], as well as intrauterine fetal growth restriction (IUGR) [13,16,19,20,22,32]. The prevalence of acute atherosis in spontaneous midtrimester abortion, spontaneous preterm labor, preterm prelabor rupture of membranes (PPROM), and unexplained fetal death, however, is unknown.…”

Section: Introductionmentioning

confidence: 99%

The frequency of acute atherosis in normal pregnancy and preterm labor, preeclampsia, small-for-gestational age, fetal death and midtrimester spontaneous abortion*

Kim

Chaemsaithong

Romero

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Acute atherosis is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis and perivascular lymphocytic infiltration. This lesion is generally confined to non-transformed spiral arteries and is frequently observed in patients with preeclampsia. However, the frequency of acute atherosis in the great obstetrical syndromes is unknown. The purpose of this study was to determine the frequency and topographic distribution of acute atherosis in placentas and placental bed biopsy samples obtained from women with normal pregnancy and those affected by the “great obstetrical syndromes”. We also examined the relationship between acute atherosis and pregnancy outcome in patients with preeclampsia. Material and methods A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted to examine 16,345 placentas. Patients were classified into the following groups: 1) uncomplicated pregnancy; 2) spontaneous preterm labor and preterm prelabor rupture of membranes (PPROM); 3) preeclampsia; 4) gestational hypertension; 5) small for gestational age; 6) chronic hypertension; 5) fetal death; 6) spontaneous abortion; and 7) others. A subset of patients had placental bed biopsy. The incidence of acute atherosis was compared among the different groups. Results 1) The prevalence of acute atherosis in uncomplicated pregnancies was 0.4% (29/6,961) based upon examination of nearly 7,000 placentas; 2) the frequency of acute atherosis was 10.2% (181/1,779) in preeclampsia, 9% (26/292) in fetal death, 2.5% (3/120) in midtrimester spontaneous abortion, 1.7% (22/1,298) in small for gestational age neonates, and 1.2% (23/1,841) in spontaneous preterm labor and PPROM; 3) among patients with preeclampsia, those with acute atherosis had significantly more severe disease, earlier onset, and a greater frequency of small-for-gestational age neonates than in those without the lesion (p < 0.05 all); 4) the lesion was more frequently observed in the decidua (parietalis or basalis) than in the decidual segment of the spiral arteries in patients with placental bed biopsies. Conclusions Acute atherosis is rare in normal pregnancy, and occurs more frequently in patients with pregnancy complications, including preeclampsia, spontaneous preterm labor, preterm PROM, midtrimester spontaneous abortion, fetal death, and SGA.

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Placental bed vascular disorders

Cited by 6 publications

References 87 publications

Maternal–fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

Maternal–fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta

The frequency of acute atherosis in normal pregnancy and preterm labor, preeclampsia, small-for-gestational age, fetal death and midtrimester spontaneous abortion*

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