Learning from the placenta: acute atherosis and vascular remodeling in preeclampsia-novel aspects for atherosclerosis and future cardiovascular health.
Preeclampsia is a common and potentially lethal pregnancy complication for women and offspring. Women who develop preeclampsia also run a long-term augmented risk of cardiovascular disease and premature death, and two theories are discussed. Women developing preeclampsia and persons developing cardiovascular disease may have common risk factors, which are unmasked by the "stress" of pregnancy. Alternatively, a new risk factor might occur de novo during the preeclamptic pregnancy. In preeclampsia, lipid deposition in walls of the maternal uterine arteries leading to the placenta, named spiral arteries, regularly occurs. These vascular lesions resemble early stages of atherosclerosis and are named "acute atherosis" and is thought to regress after delivery. The mechanisms that contribute to acute atherosis in preeclampsia are largely unknown, but are related to the impaired vascular remodeling of the spiral arteries in the first half of pregnancy. One striking feature is that the development of these "atherosclerosis-like" lesions requires a few months in pregnancy and may be partly linked to invasion of trophoblasts (specialized fetally derived placenta cells). We summarize normal and pathological vessel remodeling in pregnancy and discuss similarities and differences between preeclampsia and arteriosclerosis. The transient appearance of acute atherosis of uterine wall spiral arteries seen in pregnancy complications and the molecular interaction between trophoblast, smooth muscle and vascular cells could add important elements to explain arteriosclerosis and stenosis in cardiovascular disease. Further understanding of the process underlying spiral artery atherosis in the months of pregnancy may cast light on development of cardiovascular disease later in life.
Staff
Anne Cathrine
AC
Department of Obstetrics and Gynaecology, Oslo University Hospital, Ullevål, Kirkeveien, Oslo, Norway. annetine.staff@uus.no
Dechend
Ralf
R
Pijnenborg
Robert
R
D050197:Atherosclerosis / Q000097:blood / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000473:pathology*; D005260:Female; D006801:Humans; D009389:Neovascularization, Pathologic / Q000473:pathology*; D018919:Neovascularization, Physiologic; D010920:Placenta / Q000098:blood supply* / Q000473:pathology; D058226:Plaque, Atherosclerotic / Q000473:pathology*; D011225:Pre-Eclampsia / Q000473:pathology*; D011247:Pregnancy; D014327:Trophoblasts / Q000473:pathology; D055988:Uterine Artery / Q000473:pathology; D014599:Uterus / Q000098:blood supply / Q000473:pathology