Acute Atherosis Lesions at the Fetal-Maternal Border: Current Knowledge and Implications for Maternal Cardiovascular Health

• Published in: Frontiers in immunology 2021-12, Vol.12, p.791606-791606
• Main Authors: Pitz Jacobsen, Daniel, Fjeldstad, Heidi Elisabeth, Johnsen, Guro Mørk, Fosheim, Ingrid Knutsdotter, Moe, Kjartan, Alnæs-Katjavivi, Patji, Dechend, Ralf, Sugulle, Meryam, Staff, Anne Cathrine
• Format: Article
• Language: English
• Subjects: acute atherosis; Arteries - metabolism; Arteries - pathology; Atherosclerosis - etiology; Atherosclerosis - pathology; Biomarkers; Biopsy; cardiovascular disease; Cardiovascular Diseases - diagnosis; Cardiovascular Diseases - etiology; Cardiovascular Diseases - metabolism; Decidua - blood supply; Decidua - metabolism; Decidua - pathology; decidua basalis; Disease Susceptibility - immunology; Endometritis - genetics; Endometritis - metabolism; Endometritis - pathology; Female; Humans; Immunohistochemistry; Immunology; inflammation; Isoantigens - immunology; Organ Specificity; Placenta - immunology; Placenta - metabolism; Placenta - pathology; Postpartum Period; preeclampsia; Pregnancy; tolerance; Translational Research, Biomedical
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2021.791606

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.