Abstract
Physiological transformation with remodeling of the uteroplacental spiral arteries is key to a successful placentation and normal placental function. It is an intricate process that involves, but is not restricted to, complex interactions between maternal decidual immune cells and invasive trophoblasts in the uterine wall. In normal pregnancy, the smooth muscle cells of the arterial tunica media of uteroplacental spiral arteries are replaced by invading trophoblasts and fibrinoid, and the arterial diameter increases 5- to 10-fold. Poor remodeling of the uteroplacental spiral arteries is linked to early-onset preeclampsia and several other major obstetrical syndromes, including fetal growth restriction, placental abruption, and spontaneous preterm premature rupture of membranes. Extravillous endoglandular and endovenous trophoblast invasions have recently been put forth as potential contributors to these syndromes as well. The well-acknowledged disturbed extravillous invasion of maternal spiral arteries in preeclampsia is summarized, as are briefly novel concepts of disturbed extravillous endoglandular and endovenous trophoblast invasions. Acute atherosis is a foam cell lesion of the uteroplacental spiral arteries associated with poor remodeling. It shares some morphologic features with early stages of atherosclerosis, but several molecular differences between these lesions have also recently been revealed. Acute atherosis is most prevalent at the maternal-fetal interface, at the tip of the spiral arteries. The localization of acute atherosis downstream of poorly remodeled arteries suggests that alterations in blood flow may trigger inflammation and foam cell development. Acute atherosis within the decidua basalis is not, however, confined to unremodeled areas of spiral arteries or to hypertensive disorders of pregnancy and may even be present in some clinically uneventful pregnancies. Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia. Furthermore, we propose that acute atherosis may develop at different gestational ages, depending on the type and degree of the inflammatory insult. This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia. Some controversies will be presented, including endovascular and interstitial trophoblast invasion depths, the concept of 2-stage trophoblast invasion, and whether the replacement of maternal spiral artery endothelium by fetal endovascular trophoblasts is permanent. We will discuss the role of acute atherosis in the pathophysiology of preeclampsia and short- and long-term health correlates. Finally, we suggest future opportunities for research on this intriguing uteroplacental interface between the mother and fetus.
Highlights
From the Division of Obstetrics and Gynaecology, Oslo University Hospital, Oslo, Norway (Drs Staff and Fjeldstad, Ms Fosheim, and Drs Moe, Johnsen, Alnaes-Katjavivi, and Sugulle); Faculty of Medicine, University of Oslo, Oslo, Norway (Drs Staff and Fjeldstad, Ms Fosheim, and Drs Moe, Turowski, and Sugulle); Department of Obstetrics and Gynaecology, Baerum Hospital, Vestre Viken Hospital Trust, Drammen, Norway (Dr Moe); and Department of Pathology, Oslo University Hospital, Oslo, Norway (Dr Turowski)
Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia
This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia
Summary
This integrative concept takes into account that all pathways trigger placental (syncytiotrophoblast) stress and similar maternal responses but that FGR is more prevalent in early-onset preeclampsia as this preeclampsia form results mainly from early placental dysfunction with severe adverse effects on fetal growth.[44,45] Our revised 2-stage model of preeclampsia accommodates most known risk factors, including chronic prepregnancy disease, primiparity, and other pregnancy-related risk factors (including multiples).[17] First, maternal obesity, for instance, is a well-known risk factor for both preeclampsia and gestational hypertension,[52] a finding that fits ajog.org well with our concept of these hypertensive disorders representing a spectrum of disease, rather than distinct entities.[17] Second, maternal obesity causes chronic inflammation, which may contribute to reduced periconceptional endometrial function and dysfunctional spiral artery remodeling, in turn resulting in increased earlyonset preeclampsia risk.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
