Placental lesions associated with acute atherosis

Abstract

Objective Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age (SGA), spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion, amniotic fluid infection, fetal vascular thrombo-occlusive disease or chronic inflammation. 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 examine 16,457 placentas. The frequency of placenta lesions (diagnosed using the criteria of the Perinatal Section of the Society for Pediatric Pathology) was compared between pregnancies with and without atherosis. Results Among 16,457 women who were enrolled, 10.2% (1,671/16,457) were excluded, leaving 14,786 women who contributed data for analysis. Among them, the prevalence of acute atherosis was 2.2% (326/14,786). Women with acute atherosis were more than six times as likely as those without to have placental lesions consistent with maternal underperfusion (adjusted odds ratio- aOR: 6.7; 95% CI 5.2–8.6). To a lesser degree, acute atherosis was also associated with greater risks of having either lesions consistent with fetal vascular thrombo-occlusive disease (aOR 1.7; 95% CI 1.2–2.3) or chronic chorioamnionitis (aOR 1.9; 95% CI 1.3–3), but not with other chronic inflammatory lesions, after adjusting for gestational age at delivery. In contrast, women with acute atherosis were 60% less likely to have lesions consistent with amniotic fluid infecition, adjusting for gestational age at delivery (aOR 0.4; 95% CI 0.3–0.5). Conclusions Acute atherosis is associated with increased risks of having placental lesions consistent with maternal vascular underperfusion, and to a lesser extent, chronic chorioamnionitis and those consistent with fetal vascular thrombo-occlusive disease.

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

“…The identification of failure of spiral artery physiologic transformation in multiple pregnancy complications in general and not only in malperfusion pathologies of the placenta in particular, suggests that inflammation leading to cell activation may be the trigger for an abnormal placentation that expresses as different pathologies of pregnancy. Finally, the frequency of atherosis in our study was higher than the frequency recently described in a large population of placentas from normal and abnormal pregnancies [159,162]. We believe this is due to the high sensitivity of triple-antibody immunohistochemistry when compared with hematoxylin-eosin used to detect failure of physiologic transformation of the spiral arteries and placental atherosis [44].…”

Distinctive patterns of placental lesions in pre‐eclampsia vs small‐for‐gestational age and their association with fetoplacental Doppler

“…The prevalence of developmental lesions was also higher in pregnancies with both PE and SGA. Our data suggest that decidual arteriopathy (the most common developmental finding) could represent a key insult in this subgroup of PE, causing maternal malperfusion that mediates uteroplacental ischemia 50 . However, malperfusion could also originate from placental hypoperfusion due to maternal hemodynamic maladaptation, which is most probably the mechanism underlying placental involvement in PE without SGA 51 .…”

The prediction of fetal death with a simple maternal blood test at 24-28 weeks: a role for angiogenic index-1 (PlGF/sVEGFR-1 ratio)

“…The pathologic processes implicated in fetal death include: infection 65–84 , placental abruption, 5, 37, 70, 85–92 vascular lesions of the placenta, 28, 35, 93–100 preeclampsia, 41, 101–105 fetal growth restriction 9, 106–114 , maternal anti-fetal rejection, 35, 115–120 metabolic disorders, 121–133 genetic disorders, 80, 131, 134–137 umbilical cord accident, 97, 138–145 trauma 146–148 , and placental senescence 22 ; however, most of the 47,000 stillbirths reported from developed countries in 2015 149 were classified as unknown etiology. It is currently believed that the causes of fetal loss change with gestational age: chromosomal abnormalities 150–153 and infection 75 are the most common causes during the first half of pregnancy, placental causes (abruption or vascular abnormalities) 154–156 , and maternal anti-fetal rejection 118 become the most common causes after 26 weeks until term 14 , after which the etiology of in most cases, especially after 40 weeks, is unknown 14 .…”