Aspirin Discontinuation at 24-28 Weeks and Placental Biomarker Trajectories: Post Hoc Analysis of a Randomised Trial.

Abstract

To compare the trajectories of placental biomarkers throughout pregnancy after aspirin discontinuation at 24-28 weeks with those of a cohort treated until 36 weeks of gestation. A longitudinal secondary analysis of the StopPRE trial, using repeated measures of soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and their ratio. Nine maternity hospitals across Spain. The original StopPRE trial included 936 women at high risk for preterm preeclampsia based on first-trimester screening. All participants received aspirin 150 mg daily until randomisation at 24-28 weeks. At that point, 463 women were assigned to continue aspirin until 36 weeks, while 473 were assigned to discontinue it. sFlt-1, PlGF, sFlt-1/PlGF were measured at baseline (24-28 weeks) and during follow-up visits at 28-32, 32-36, and after 36 weeks of gestation. Linear mixed-effects models (LMM) with treatment-by-gestational age interaction were used to analyze biomarker trajectories over time. Differences in trajectories of raw values and multiples of the median for sFlt-1, PlGF, sFlt-1/PlGF between groups. Among 463 participants in the aspirin continuation group and 473 in the discontinuation group, 3483 measurements of each biomarker were analysed. There were no significant differences in the trajectories of sFlt-1, PlGF, or sFlt-1/PlGF between groups (p-values for raw analysis: 0.662, 0.728 and 0.979, respectively). In women at high risk of preterm preeclampsia, discontinuing aspirin at 24-28 weeks did not alter the trajectories of placental biomarkers. This may explain why stopping aspirin did not increase preterm PE risk in the StopPRE trial.