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A high uterine artery pulsatility index reflects a defective development of placental bed spiral arteries in pregnancies complicated by hypertension and fetal growth retardation

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Abstract

Introduction: 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. Aim: 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. Materials and 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. Discussion: 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. Conclusion: This study gave further support for the existence of a triad of defective placental bed vessel maturation, increased uteroplacental flow resistance, and hypertension.

References (32)

  • I Brosens et al.

    The physiological response of the vessels of the placental bed to normal pregnancy

    J Pathol Bacteriol

    (1967)
  • R Pijnenborg et al.

    Review article: Trophoblast invasion and the establishment of haemochorial placentation in man and laboratory animals

    Placenta

    (1981)
  • W Moll et al.

    The hemodynamic implications of hemochorial placentation

    Eur J Obstet Gynecol Reprod Biol

    (1975)
  • E Jauniaux et al.

    In vivo investigations of the anatomy and the physiology of early human placental circulations

    Ultrasound Obstet Gynecol

    (1991)
  • HG Dixon et al.

    A study of the vessels of the placental bed in normotensive and hypertensive women

    J Obstet Gynaecol Br Emp

    (1958)
  • WB Robertson et al.

    The pathological response of the vessels of the placental bed to hypertensive pregnancy

    J Pathol Bacteriol

    (1967)
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      Citation Excerpt :

      It is generally accepted that placental dysfunction among other causes is related to abnormal transformation of the spiral arteries into low resistance vessels in early pregnancy [7,8]. The vascular resistance of the uterine arteries can be assessed by the pulsatility index (UtA PI) estimated by Doppler sonography [9]. The association between high UtA PI and pregnancy complications related to placental dysfunction such as preeclampsia (PE) and IUGR is well described [10].

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