Abstract
Decidua basalis, the endometrium of pregnancy, is an important interface between maternal and fetal tissues, made up of both maternal and fetal cells. Acute atherosis is a uteroplacental spiral artery lesion. These patchy arterial wall lesions containing foam cells are predominantly found in the decidua basalis, at the tips of the maternal arteries, where they feed into the placental intervillous space. Acute atherosis is prevalent in preeclampsia and other obstetric syndromes such as fetal growth restriction. Causal factors and effects of acute atherosis remain uncertain. This is in part because decidua basalis is challenging to sample systematically and in large amounts following delivery. We summarize our decidua basalis vacuum suction method, which facilitates tissue-based studies of acute atherosis. We also describe our evidence-based research definition of acute atherosis. Here, we comprehensively review the existing literature on acute atherosis, its underlying mechanisms and possible short- and long-term effects. We propose that multiple pathways leading to decidual vascular inflammation may promote acute atherosis formation, with or without poor spiral artery remodeling and/or preeclampsia. These include maternal alloreactivity, ischemia-reperfusion injury, preexisting systemic inflammation, and microbial infection. The concept of acute atherosis as an inflammatory lesion is not novel. The lesions themselves have an inflammatory phenotype and resemble other arterial lesions of more extensively studied etiology. We discuss findings of concurrently dysregulated proteins involved in immune regulation and cardiovascular function in women with acute atherosis. We also propose a novel hypothesis linking cellular fetal microchimerism, which is prevalent in women with preeclampsia, with acute atherosis in pregnancy and future cardiovascular and neurovascular disease. Finally, women with a history of preeclampsia have an increased risk of premature cardiovascular disease. We review whether presence of acute atherosis may identify women at especially high risk for premature cardiovascular disease.
Highlights
Arterial lesions specific to the spiral arteries at the fetal-maternal border were first reported in 1945 [1]
We showed that higher rates of acute atherosis detection was achieved using vacuum suction samples, as compared to routinely sampled basal surface placental tissue and fetal membrane roll biopsies from the same pregnancies [33]
Our large Oslo Pregnancy Biobank, consisting of decidual tissue collected during elective cesarean section, along with placental tissue biopsies, fetal and maternal blood samples, amniotic fluid, and maternal muscle and fat tissue biopsies, has enabled multiple studies comparing the presence of decidual acute atherosis and dysregulated features of other anatomical compartments [20,21,22,23,24,25,26, 31, 33, 35,36,37,38,39,40,41]
Summary
Arterial lesions specific to the spiral arteries at the fetal-maternal border were first reported in 1945 [1] These lesions were later termed acute atherosis, described as lipid-laden foam cells within the intima, surrounded by fibrinoid necrosis and perivascular immune cell infiltrate [2, 3]. Systematic sampling of the decidua in large amounts following delivery is quite difficult, and a uniform, evidence-based research definition of acute atherosis lesions is historically lacking. As discussed below, both issues have been addressed by us [22, 26]. Even when these constraints are overcome, only a subset of the decidua can realistically be evaluated in any morphological tissue study, one can only with certainty determine the presence of acute atherosis, and never the definitive absence
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