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There are three types of decidual vasculopathy at term, acute atherosis, fibrinoid medial necrosis, and mural arterial hypertrophy with two separate mechanisms. Acute atherosis and fibrinoid medial necrosis demonstrate the replacement of the muscular wall by the fibrinoid material and “foamy cells”, whereas mural arterial hypertrophy depicts thickened hypertrophic muscular wall with a narrowed lumen. In this review, decidual vasculopathy is reexamined using the knowledge of CD56 expression on endovascular trophoblasts (EVTs) at term with perspective in diagnosis and pathogenesis. All three types of vasculopathy can be identified in both decidua basalis and decidua vera (capsularis/parietalis) at term. Decidual vasculopathy at basalis is related to the persistence of EVTs in spiral artery remodeling at implantation and phenotypic switch to express CD56. However, no trophoblastic invasion of spiral artery is present at decidua vera. At implantation, the spiral artery undergoes a trophoblastic-dependent remodeling in decidua basalis whereas the spiral artery undergoes trophoblastic-independent remodeling in decidual vera. Decidual vasculopathy at term is related to spiral artery remodeling at implantation and this is associated with factors other than trophoblastic invasion alone. The spiral artery remodeling at implantation and pathogenesis of decidual vasculopathy at term is likely through circulating factors in relation to complex physiological and pathological conditions in pregnancy.

Decidual vasculopathy and spiral artery remodeling revisited II: relations to trophoblastic dependent and independent vascular transformation