OP13.06: StopPRE trial: effect of aspirin discontinuation at 24–28 weeks on the trajectories of biophysical and biochemical markers

Discontinuation of aspirin in women at an increased risk of pre-eclampsia (PE) during first trimester screening, with normal angiogenic factors at 24-28 weeks of gestation, does not heighten the risk of preterm PE. Moreover, aspirin does not affect mean arterial blood pressure (MAP), mean uterine artery pulsatility index (UtAPI), or biomarkers trajectories after 20 weeks of gestation. Our aim was to investigate the impact of aspirin discontinuation at 24-28 weeks on the trajectories of biophysical and biochemical markers. This is a longitudinal secondary analysis of the Detection of False Positives From First trimester Pre-eclampsia Screening at the Second trimester of Pregnancy (StopPRE) trial, using repeated measures of MAP, UtAPI, placental growth factor (PlGF), and soluble fms-like tyrosine kinase-1 (sFlt-1). In the trial, 936 women at high risk for PE during the first trimester screening received aspirin 150mg daily from screening to randomisation. At 24-28 weeks, 463 women were randomly allocated to continue aspirin until 36 weeks, while 473 were assigned to discontinue aspirin. All markers were assessed at baseline (24-28 weeks) and follow-up visits at 28-32, 32-36, and after 36 weeks. Generalised estimating equations procedure with treatment by gestational age interaction were used to explore the effect of aspirin on markers' trajectories over time. Among all participants, there were 3,193 MAP, 2,954 UtAPI, and 3,437 biomarker measurements. Trajectories of MAP, UtAPI, PlGF, sFlt-1, and sFlt-1/PlGF raw values and percentiles or multiples of the median (MoM) showed no significant differences between the groups (p-values for raw analysis: 0.804, 0.353, 0.211, 0.852, and 0.802, respectively). In women at an increased risk of preterm PE, discontinuation of aspirin at 24-28 weeks of gestation does not affect the trajectories of MAP, UtAPI, PlGF, sFlt-1, and sFlt-1/PlGF. This finding may help explain why discontinuing aspirin did not lead to an increased risk of preterm PE in the StopPRE trial.