Patterns of trophoblast migration in deep uterine arteries in accreta placentation

During normal placentation, extravillous trophoblast (EVT) colonises and, in synergy with maternal leukocytes, transforms the walls of uterine spiral arteries in the decidua and inner myometrium. In placenta accreta spectrum (PAS), migration of extravillous trophoblasts (EVT) is abnormally deep, reaching larger upstream arteries in myometrium. As little is known about their interactions in accreta areas, scar tissue and deeper arteries were examined for colonisation and remodelling by trophoblast and maternal inflammatory cells.

Samples (n = 79) were fresh hysterectomy specimens taken immediately after surgery in 11 patients presenting with placenta previa accreta at birth, at term or near term. They were obtained from accreta areas, non-accreta areas and, in cases of associated dehiscence of the lower uterine segment, from the adjacent shell (uterine boundary membrane). Samples were stained using antibodies to EVT (cytokeratin) or inflammatory cells (CD45). Arterial profiles positioned within 5 mm of villous placenta at scar sites were included in the analysis (54 lumina).

EVT colonisation of scar tissue was much more extensive than in adjacent myometrium (p < 0.001). Large arteries were remodelled (20.3 %), partially remodelled (22.2 %) or unremodelled (29.6 %). Unremodelled arteries were present in 10/11 specimens while 6/11 had one or more fully remodelled. Leucocytes/inflammatory cells were frequently associated with arteries undergoing remodelling. EVT also accumulated beneath the serosa but were not found to cross it.

Some remodelling of deep arteries occurs in most samples from accreta areas, but persistence of unremodelled arteries in distal segments with abnormally high velocity intraplacental blood flow is probably the main mechanism leading to lacuna formation.