In women with chronic hypertension, does fetal growth restriction increase progression to maternal preeclampsia?

Among women with chronic hypertension, it is unclear whether uteroplacental dysfunction should be classified as indicating superimposed preeclampsia or be considered a direct complication of chronic hypertension.

To evaluate whether fetal growth concerns at a routine fetal ultrasound at 35+0 to 36+6 weeks of gestation were related to progression to preeclampsia.

We undertook a secondary analysis of a prospectively evaluated cohort of women with chronic hypertension and singleton pregnancies who underwent routine fetal ultrasound at 35⁺⁰-36⁺⁶ weeks' gestation. We compared the incidence of preeclampsia and other adverse pregnancy outcomes between cases and propensity score-matched controls; cases had an estimated fetal weight <10th percentile, with and without fetal growth restriction, defined as abnormal fetal Dopplers (uterine artery pulsatility index >95th percentile, umbilical artery pulsatility index >95th percentile, or middle cerebral artery pulsatility index <5th percentile), and controls had estimated fetal weight ≥10th percentile. Superimposed preeclampsia was defined by maternal criteria, either traditionally by the development of new-onset proteinuria at ≥20 weeks or by additional maternal criteria according to the 2019 American College of Obstetricians and Gynecologists or 2021 International Society for the Study of Hypertension in Pregnancy guidance. Covariates included in propensity score-matched were maternal race/ethnicity, mode of conception, smoking status, systemic lupus erythematosus, parity, history of preeclampsia, history of a baby with birthweight <10th percentile, maternal age, body mass index, and gestational weight gain in kilograms. Matching was conducted using a nearest-neighbor algorithm without replacement, a ratio of 1 case to 2 controls, and a caliper width of 0.2 standard deviation of the logit of the propensity score. Balance between groups after matching was assessed using standardized mean differences, with values <0.1 considered indicative of adequate balance.

Of the 1258 included pregnancies with chronic hypertension, there were 167 (13.3%) cases (64, 38.3% of which were designated as fetal growth restriction cases with abnormal fetal Dopplers), and 1091 (86.7%) controls. Of 1258 women, 234 (18.6%) went on to develop preeclampsia. After propensity score matching analysis, there were no differences between the 167 cases and 334 propensity score-matched controls in baseline maternal or 35-36 weeks' characteristics. Cases with fetal growth restriction (vs propensity score-matched controls) more often developed preeclampsia (regardless of definition), underwent labor induction, had a cesarean delivery, and had a shorter ultrasound-to-birth interval by 1.8 weeks; they also delivered 1.7 weeks earlier and more often had babies with birthweight <10th percentile for gestational age or those admitted to the neonatal unit. There was no difference between groups in the composite neonatal outcome. Cases without fetal growth restriction (vs propensity score-matched controls) did not differ with regard to the development of preeclampsia, but they did have a shorter ultrasound-to-birth interval (by 0.8 weeks), delivered 0.7 weeks earlier, and more often had babies with birthweight <10th percentile.

Our findings suggest that women with chronic hypertension who have evidence of fetal growth restriction at 35-36 weeks' gestation (but not those with only an estimated fetal weight <10th percentile) more frequently develop maternal manifestations of superimposed preeclampsia and should be considered for enhanced maternal and fetal surveillance. These findings should be replicated at earlier gestational ages.