Preeclampsia (PE) is a pregnancy disease that affects 2%–4% of gestations and is one of the leading causes of maternal and fetal morbidity and mortality in the world. Its aetiology is multifactorial, with abnormal placentation being a significant contributing factor to its onset. Given the absence of a curative treatment beyond elective delivery, considerable efforts within the scientific community have been directed towards developing strategies for preventing PE. In the last decade, different sophisticated first-trimester screening programmes have been developed, with the use of algorithms that combine maternal characteristics and medical and obstetric history with mean arterial blood pressure (MAP), mean Uterine Artery Pulsatility Index (UtAPI) by Doppler ultrasound, pregnancy-associated plasma protein-A (PAPP-A) and placental growth factor (PlGF).
In high-risk pregnancies, administration of low-dose aspirin has been shown to reduce the risk of developing preterm PE by 62%. However, the precise mechanism by which aspirin prevents PE remains unclear. One proposed mechanism suggests that aspirin promotes placental development by enhancing trophoblastic invasion, stabilising endothelial function, and reducing inflammation. The greater effectiveness of aspirin in preventing PE when initiated before 16weeks of gestation provides support for this hypothesis.
However, aspirin has not shown significant benefits on biomarkers indicative of appropriate trophoblastic invasion and placental function—such as MAP, UtAPI [16] or biochemical marker trajectories beyond 20weeks of gestation. This could indicate that aspirin's preventive effects may be most pronounced during the first half of pregnancy. In line with this hypothesis, the StopPRE trial demonstrated that stopping aspirin in women at increased risk for PE, based on first-trimester screening but with normal angiogenic factors at 24–28weeks, did not increase the incidence of preterm PE. No previous studies have assessed the impact of aspirin discontinuation on placental biomarkers, which could offer further insight into its mechanism of action to prevent PE. This longitudinal secondary analysis of the StopPRE trial aimed to advance understanding in this area by evaluating the effects of discontinuing aspirin between 24 and 28weeks on the progression of biochemical markers.
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. The original StopPRE trial included 936 women at high risk for preterm preeclampsia based on first-trimester screening. All participants received aspirin 150mg daily until randomisation at 24–28weeks. At that point, 463 women were assigned to continue aspirin until 36weeks, while 473 were assigned to discontinue it. sFlt-1, PlGF, sFlt-1/PlGF were measured at baseline (24–28weeks) and during follow-up visits at 28–32, 32–36, and after 36weeks of gestation. Linear mixed-effects models (LMM) with treatment-by-gestational age interaction were used to analyze biomarker trajectories over time.
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 this secondary analysis of the StopPRE trial, authors analysed the evolution of 3483 measurements of sFlt-1, PlGF and sFlt-1/ PlGF throughout gestation in women who were at high risk of preterm PE and received treatment with aspirin from the first trimester. They compared those who continued treatment from 24 to 28weeks until week 36 and those who discontinued aspirin treatment at week 24–28. Study found no evidence that the suspension of aspirin treatment modified the evolution of placental biomarkers in these patients.
In women at increased risk of preterm PE who are treated with daily 150mg aspirin, discontinuing treatment between 24 and 28weeks of gestation does not affect the trajectories of PlGF, sFlt-1, or the sFlt-1/PlGF ratio. This finding helps explain why discontinuing aspirin treatment did not lead to a higher incidence of preterm PE in the StopPRE trial.
Source: Erika Bonacina1 | Mireia Armengol-Alsina1 | Pablo Garcia-Manau1; BJOG: An International Journal of Obstetrics & Gynaecology, 2025
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