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Preeclampsia is a serious complication of pregnancy, potentially lethal for women and offspring. Affected women have an augmented risk of later cardiovascular disease and premature death and may have risk factors in common with older persons developing cardiovascular disease. In some cases of preeclampsia, lipid-filled foam cells accumulate in the walls of the spiral arteries of the uteroplacental circulation (acute atherosis). These lesions resemble the early stages of atherosclerosis and are thought to regress after delivery. The mechanisms that contribute to acute atherosis are largely unknown, but are related to defective vascular remodeling of the spiral arteries in the first half of pregnancy. Spiral artery lipid deposition may also occur in normal pregnancies, which suggests that it may not be confined exclusively to maladapted spiral arteries or caused by hypertension. Our first hypothesis is that there are several pathways to the development of acute atherosis, which converge at the point of excessive decidual inflammation in the final common pathway. Our second hypothesis is that acute atherosis, evolving during the short time of pregnancy, identifies a subset of women at augmented risk for atherosclerosis and later chronic arterial disease better than the diagnosis of preeclampsia itself. If confirmed, this may enable better preventive management for the affected women.

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Conference paper

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