The underlying pathophysiology of preeclampsia is thought to be abnormal trophoblast invasion of the spiral arteries leading to maldevelopment of uteroplacental perfusion. We estimated whether uterine artery Doppler measurements made in the early second trimester would predict the subsequent development of preeclampsia.
Uterine artery Doppler measurements before 21 weeks of gestation (median 16.6 weeks) were correlated with subsequent development of preeclampsia in a cohort of 2,188 low-risk nulliparous women in a randomized control trial of antioxidant supplementation for prevention of preeclampsia. Preeclampsia developed in 165 (7.5%) women.
Development of preeclampsia overall was associated with increased resistance index, pulsatility index, a pulsatility index or resistance index multiple of the median at or above the 75th percentile but not the presence of a notch or a bilateral notch before 21 weeks of gestation. The sensitivity was 43% (95% confidence interval [CI] 35–51) and specificity 67% (95% CI 65–69) for prediction of preeclampsia overall. The presence of a notch or bilateral notch, resistance index, and pulsatility index multiple of the median was significantly associated with early onset (before 34 weeks of gestation) compared with late onset or no preeclampsia (odds ratio [OR] 6.9, 95% CI 2.3–20.9; sensitivity 78%, 95% CI 52–94; specificity 66%, 95% CI 64–68). The presence of a notch or resistance index multiple of the median at or above the 75th percentile increased the odds of developing severe compared with mild or no preeclampsia (OR 2.2, 95% CI 1.4–3.7; sensitivity 53%, 95% CI 40–65; specificity 66%, 95% CI 64–68).
Our data show poor sensitivity of second-trimester Doppler ultrasound measurements for prediction of preeclampsia overall in a well-characterized, low-risk, nulliparous population. The technique has utility in identifying poor trophoblast invasion of spiral arteries of a magnitude that severely compromises uteroplacental blood flow and gives early-onset disease.
Second-trimester Doppler ultrasound measurements have poor sensitivity for prediction of preeclampsia in a well-characterized, low-risk, nulliparous population.
From the Departments of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio, University of Pittsburgh, Pittsburgh, Pennsylvania, University of Alabama at Birmingham, Birmingham, Alabama, University of Utah, Salt Lake City, Utah, Columbia University, New York, New York, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, Case Western Reserve University-MetroHealth Medical Center, Cleveland, Ohio, Northwestern University, Chicago, Illinois, University of Texas Health Science Center at Houston, Houston, Texas, Brown University, Providence, Rhode Island, Ohio State University, Columbus, Ohio, Drexel University, Philadelphia, Pennsylvania, Wake Forest University Health Sciences, Winston-Salem, North Carolina, Oregon Health & Science University, Portland, Oregon, the University of Texas Medical Branch, Galveston, Texas, Wayne State University, Detroit, Michigan, and George Washington University Biostatistics Center, Washington, DC; and the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland.
* For a list of other members of the NICHD MFMU, see the Appendix online at http://links.lww.com/AOG/A319.
The project described was supported by grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) (HD34208, HD27869, HD40485, HD40560, HD40544, HD34116, HD40512, HD21410, HD40545, HD40500, HD27915, HD34136, HD27860, HD53118, HD53097, HD27917, and HD36801); the National Heart, Lung, and Blood Institute; and the National Center for Research Resources (M01 RR00080, UL1 RR024153, UL1 RR024989) and its contents do not necessarily represent the official view of NICHD, National Heart, Lung and Blood Institute, National Center for Research Resources, or the National Institutes of Health.
The authors thank Sabine Bousleiman, RNC, MSN, and Margaret Cotroneo, RN, for participating in protocol development and coordination between clinical research centers; Elizabeth Thom, PhD, for protocol and data management and statistical analysis; and Jay D. Iams, MD, Alan M. Peaceman, MD, and Gail D. Pearson, MD, ScD, for protocol development and oversight.
Dr. Spong, Associate Editor of Obstetrics & Gynecology, was not involved in the review or decision to publish this article.
Corresponding author: Leslie Myatt, PhD, University of Texas Health Science Center San Antonio, Mail Code 7836, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900; e-mail Myattl@uthscsa.edu.
Financial Disclosure The authors did not report any potential conflicts of interest.