Acute Atherosis of the Uterine Spiral Arteries: Clinicopathologic Implications

Abstract

Acute atherosis is unique vascular changes of the placenta associated with poor placentation. It is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis of the arterial wall, perivascular lymphocytic infiltration, and it is histologically similar to early-stage atherosclerosis. Acute atherosis is rare in normal pregnancies, but is frequently observed in non- transformed spiral arteries in abnormal pregnancies, such as preeclampsia, small for gestational age (SGA), fetal death, spontaneous preterm labor and preterm premature rupture of membranes. In preeclampsia, spiral arteries fail to develop physiologic transformation and retain thick walls and a narrow lumen. Failure of physiologic transformation of spiral arteries is believed to be the main cause of uteroplacental ischemia, which can lead to the production of anti-angiogenic factors and induce endothelial dysfunction and eventually predispose the pregnancy to preeclampsia. Acute atherosis is more frequently observed in the spiral arteries of the decidua of the placenta (parietalis or basalis) than in the decidual or myometrial segments of the placental bed. The presence and deeper location of acute atherosis is associated with poorer pregnancy outcomes, more severe disease, earlier onset of preeclampsia, and a greater frequency of SGA neonates in patients with preeclampsia. Moreover, the idea that the presence of acute atherosis in the placenta may increase the risk of future cardiovascular disease in women with a history of preeclampsia is of growing concern. Therefore, placental examination is crucial for retrospective investigation of pregnancy complications and outcomes, and accurate placental pathology based on universal diagnostic criteria in patients with abnormal pregnancies is essential for clinicopathologic correlation.

Is an episode of suspected preterm labor that subsequently leads to a term delivery benign?

“…However, this was interpreted as a potential etiology for spontaneous preterm delivery. The specific lesions, found in excess in placentas delivered after spontaneous preterm labor, were diagnosed as maternal decidual vasculopathy (defined as the presence of failure of physiological transformation of the decidual portion of the spiral arteries and organized thrombi and multiple placental infarcts) (35–38). The proposed operative mechanism of disease responsible for preterm labor in these cases is utero-placental ischemia (39).…”

The immunophenotype of decidual macrophages in acute atherosis

“…Acute atherosis has been described in the spiral arteries of the decidua underlying the placenta, termed the decidua basalis, and in the decidua parietalis (underlying the fetal chorioamniotic membranes), as well as in myometrial tissues . Such lesions are characterized by the presence of (a) fibrinoid necrosis of the vessel wall, (b) perivascular lymphocytic infiltration, and (c) accumulation of foam cells . The foam cells detected in the decidual tissues from women with acute atherosis are described as lipid‐laden macrophages; however, other non‐foamy macrophages are detected in and around these vessels.…”

HMOX1 is partly responsible for phenotypic and functional abnormalities in mesenchymal stem cells/stromal cells from placenta of preeclampsia (PE) patients

“…Another characteristic change in the untransformed spiral arteries in PE is acute atherosis. It has been compared to the vascular lesion of atherosclerosis and is claimed to be similar to changes in vessels of tissues undergoing rejection [37]. Atherosis found in disorders other than PE is observed in decidual vessels beyond the site of placental implantation [38].…”