Decidual Vasculopathy in Preeclampsia and Spiral Artery Remodeling Revisited: Shallow Invasion versus Failure of Involution

Abstract

Decidual vasculopathy is commonly associated with preeclampsia and develops in the late pregnancy in the uterine spiral arteries, which were previously remodeled by the extravillous trophoblasts. In normal early pregnancy, trophoblasts invade into the spiral artery, leading to vascular transformation, and this transformation is found to be associated with phenotypic switch of the endovascular trophoblasts to express CD56, a maternal protein likely from the natural killer (NK) cells. These endovascular trophoblasts are diminished at term. The decidual vessels are also returned to near normal at the delivery. Both the uterus and the uterine spiral arteries undergo involution after delivery. In preeclampsia, the endovascular trophoblasts are present within the vessel wall associated with the persistence of switched phenotype similar to those seen in the early implantation. The persistence of the endovascular trophoblasts in decidual vasculopathy indicates a failure to return to normal vessels in preeclampsia, thus suggesting a potential mechanism of pathogenesis. NK cells seem critical not only for early implantation and spiral artery remodeling but also for the development of decidual vasculopathy in preeclampsia. In this short review, some critical aspects of decidual vasculopathy in normal pregnancy and preeclampsia are reexamined and a new hypothesis is proposed.

Decidual Vasculopathy and Spiral Artery Remodeling Revisited III: Hypoxia and Re-oxygenation Sequence with Vascular Regeneration

“…These data suggest that the placental lateral growth occurs in a spatiotemporal manner, with asynchronous vascular recovery taking place after the initial vascular transformation [56]. We have noticed the vascular recovery/regeneration at the end of the second trimester, with markedly diminished endovascular and intramural trophoblasts, similar to those identified by the early investigators [12,59], and we felt that the abnormal vascular recovery/regeneration and failure of death of the endovascular trophoblasts (failure to die) both play a central role in the pathogenesis of decidual vasculopathy in late gestation [3].…”

“…Similar observations were also made by other investigators many decades ago [59]. Naturally, the presence of endovascular trophoblasts within the lumen or wall of the vessels in the third trimester, regardless of clinical manifestations, raised the question of the abnormal cell death process of endovascular trophoblasts (failure to die) [3]. A large spectrum of the "failure to die" manifestations of endovascular trophoblasts can be correlated with a large spectrum of clinically important pregnancy complications, including preeclampsia, and various degrees of maternal vascular malperfusion (ischemia).…”

“…Decidual vasculopathy is classified into three morphologic variants, namely acute atherosis, fibrinoid medial necrosis and mural arteriole hypertrophy/hyperplasia [2]. Acute atherosis and fibrinoid medial necrosis are considered the two morphologic variants of the same disease spectrum, which was therefore considered "classic type vasculopathy" [1,[3][4][5]. The pathogenesis of classic type vasculopathy was shown to be related to direct trophoblastic invasion of the spiral artery in early pregnancy (named "physiologic changes") and the persistence of these changes up to late gestation [4].…”

Cushing’s syndrome during pregnancy with different clinical courses: Two case reports

“…Specifically, the small-sized placenta was related to FGR, and decidual vasculopathy, increased syncytial knots, and matured villi were associated with the placental ischaemic changes of early onset preeclampsia. 6) For Patient 2, the placenta was extremely small for the gestational age of 39 weeks, even though the state of CS and maternal blood pressure were well controlled and foetal growth was acceptable after surgical treatment. In fact, the pathological findings of Patient 2 reflected this favourable progress after surgery.…”

Overlapping Pathogenic Signalling Pathways and Biomarkers in Preeclampsia and Cardiovascular Disease

“…However, the development of preeclampsia has been closely associated with abnormal placentation occurring in the early stages of pregnancy where impaired spiral uterine artery (SUA) remodelling plays a significant role (2). The lack of the SUA remodelling represents an initial step leading to vascular changes and hypertension (3).…”