title: A high uterine artery pulsatility index reflects a defective development of placental bed spiral arteries in pregnancies complicated by hypertension and fetal growth retardation.
abstract: BACKGROUND
  The development of PIH is associated with a defective trophoblast invasion and conversion of spiral arteries into low-resistance uteroplacental arteries. Hypertension may then be a compensatory response to a defective uteroplacental perfusion. Similar mechanisms may operate in IUGR.
  
  
  OBJECTIVE
  To compare uterine artery Doppler blood flow measurements with placental bed histology. The hypothesis was that placental bed vessel pathology plays a role for a raised flow resistance.
  
  
  METHODS
  After blood flow measurements, a placental bed biopsy was taken at CS in 26 complicated (study group) and 29 uncomplicated pregnancies (control group).
  
  
  RESULTS
  The uterine artery PI was significantly more often abnormally high in the study group compared with the control group, and also in hypertensive pregnancies compared with normotensive IUGR pregnancies. Physiological vessel changes were found in all controls but were absent in 76% of study cases. Physiological changes were significantly more often absent in SGA than in AGA newborns. Absence of physiological changes were significantly more often found in cases with an abnormally high PI.
  
  
  CONCLUSIONS
  The results link together circulatory and structural pathophysiological changes of the uteroplacental unit. A defective physiological conversion of the spiral arteries was associated with an increased uterine flow resistance.
  
  
  CONCLUSIONS
  This study gave further support for the existence of a triad of defective placental bed vessel maturation, increased uteroplacental flow resistance, and hypertension.
authors.affiliation: Department of Obstetrics and Gynecology, University of Lund, Malmö General Hospital, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Olofsson
authors.forename: R N
authors.initials: RN
authors.lastname: Laurini
authors.forename: K
authors.initials: K
authors.lastname: Marsál
mesh_terms: D000293:Adolescent; D000328:Adult; D001158:Arteries; D001724:Birth Weight; D002585:Cesarean Section; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D010920:Placenta / Q000098:blood supply*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011254:Pregnancy in Diabetics / Q000473:pathology / Q000503:physiopathology; D011673:Pulsatile Flow / Q000502:physiology*; D014463:Ultrasonography; D014599:Uterus / Q000098:blood supply*