Abstract

To compare first-trimester uterine artery pulsatility index (UtA-PI) and three-dimensional (3D) placental volume in pregnancies conceived through in-vitro fertilization (IVF) using autologous or donor oocytes and pregnancies conceived naturally, and to relate these measurements to the development of pre-eclampsia (PE). UtA-PI and placental volume were measured at 11 + 0 to 13 + 6 weeks of gestation in 416 IVF pregnancies (307 with autologous and 109 with donor oocytes) and in 498 spontaneously conceived pregnancies. We recruited nulliparous women with singleton pregnancy. The measured mean UtA-PI and placental volume values were converted to multiples of the expected normal median (MoM), adjusted for gestational age. MoM values of IVF pregnancies were compared with MoM values of the naturally conceived pregnancies and related to PE development. Placental volume was significantly reduced in IVF pregnancies (K = 169.3; P < 0.0001) compared with natural pregnancies. No difference was found in UtA-PI MoM between the two groups. Among IVF pregnancies, significantly lower placental volumes were seen in those that received donor oocytes when compared with those with autologous oocytes (z = 3.89; P < 0.001). In IVF pregnancies that developed PE, lower values of placental volume were demonstrated with respect to normotensive pregnancies (donor: U = 6.8; P = 0.009; autologous: U = 5.1; P = 0.023), whereas no difference was found in UtA-PI. Multivariate logistic regression analysis demonstrated that placental volume (odds ratio (OR), 1.97 (95% CI, 1.33-2.27)) and donor oocytes in IVF pregnancy (OR, 2.24 (95% CI, 1.5-2.83)) were independent predictors of PE, whereas autologous oocytes in IVF pregnancy were not found to be significant in the model. First-trimester placental volume, as assessed by 3D ultrasound, is reduced in IVF pregnancies and this reduction is more marked in those involving donor oocyte recipients. The relative decrease in placental volume in IVF pregnancies that developed PE suggests an etiological mechanism different from uterine perfusion in such patients. Copyright © 2015 ISUOG. Published by John Wiley & Sons Ltd.

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