Spiral artery remodeling and trophoblast invasion in preeclampsia and fetal growth restriction: relationship to clinical outcome.
Failure to transform uteroplacental spiral arteries is thought to underpin disorders of pregnancy, including preeclampsia and fetal growth restriction (FGR). In this study, spiral artery remodeling and extravillous-cytotrophoblast were examined in placental bed biopsies from normal pregnancy (n = 25), preeclampsia (n = 22), and severe FGR (n = 10) and then compared with clinical parameters. Biopsies were immunostained to determine vessel wall integrity, extravillous-cytotrophoblast location/density, periarterial fibrinoid, and endothelium. Muscle disruption was reduced in myometrial spiral arteries in preeclampsia (P = 0.0001) and FGR (P = 0.0001) compared with controls. Myometrial vessels from cases with birth weight <5th percentile (P<0.001), abnormal uterine Doppler (P<0.01), abnormal umbilical artery Doppler (P<0.001), and preterm delivery (P<0.001) had less muscle destruction compared with >5th percentile. Fewer extravillous-cytotrophoblast surrounded both decidual and myometrial vessels in the normal group and preeclampsia group compared with the FGR group (P = 0.001). For myometrial vessels, the normal group contained more intramural extravillous-cytotrophoblast than in preeclampsia (P = 0.015). Decidual vessels in the FGR group had less fibrinoid deposition compared with controls (P = 0.013). For myometrial vessels, less fibrinoid was deposited in both the preeclampsia group (P = 0.0001) and the FGR group (P = 0.01) when compared with controls, and less fibrinoid was deposited in the preeclampsia group when compared with FGR group (P<0.001). Myometrial vessels obtained from birth weights <5th percentile had less periarterial fibrinoid than those with >5th percentile (P<0.02). A major defect in myometrial spiral artery remodeling occurs in preeclampsia and FGR that is linked to clinical parameters. Interstitial extravillous-cytotrophoblast is not reduced in preeclampsia but is increased in FGR.
Institute of Medical Genetics, College of Medicine, Veterinary and Life Sciences, University of Glasgow School of Medicine, Yorkhill, Glasgow G38SJ, United Kingdom. Fiona.lyall@glasgow.ac.uk.
Fiona
F
Lyall
Stephen C
SC
Robson
Judith N
JN
Bulmer
D000328:Adult; D001158:Arteries / Q000473:pathology*; D001724:Birth Weight; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000473:pathology*; D006801:Humans; D007231:Infant, Newborn; D009215:Myometrium / Q000098:blood supply* / Q000473:pathology; D010920:Placenta / Q000098:blood supply* / Q000473:pathology; D011225:Pre-Eclampsia / Q000473:pathology*; D011247:Pregnancy; D011256:Pregnancy Outcome; D014327:Trophoblasts / Q000473:pathology*
Doppler ultrasonography; decidua; intrauterine growth retardation; myometrium; preeclampsia; pregnancy; spiral artery; trophoblasts