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

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.