Abstract
The road to low-dose aspirin therapy for the prevention of preeclampsia began in the 1980s with the discovery that there was increased thromboxane and decreased prostacyclin production in placentas of preeclamptic women. At the time, low-dose aspirin therapy was being used to prevent recurrent myocardial infarction and other thrombotic events based on its ability to selectively inhibit thromboxane synthesis without affecting prostacyclin synthesis. With the discovery that thromboxane was increased in preeclamptic women, it was reasonable to evaluate whether low-dose aspirin would be effective for preeclampsia prevention. The first clinical trials were very promising, but then two large multi-center trials dampened enthusiasm until meta-analysis studies showed aspirin was effective, but with caveats. Low-dose aspirin was most effective when started <16 weeks of gestation and at doses >100 mg/day. It was effective in reducing preterm preeclampsia, but not term preeclampsia, and patient compliance and patient weight were important variables. Despite the effectiveness of low-dose aspirin therapy in correcting the placental imbalance between thromboxane and prostacyclin and reducing oxidative stress, some aspirin-treated women still develop preeclampsia. Alterations in placental sphingolipids and hydroxyeicosatetraenoic acids not affected by aspirin, but with biologic actions that could cause preeclampsia, may explain treatment failures. Consideration should be given to aspirin’s effect on neutrophils and pregnancy-specific expression of protease-activated receptor 1, as well as additional mechanisms of action to prevent preeclampsia.
Highlights
Accepted: 23 June 2021The rationale for low-dose aspirin therapy began in the 1970s with the discovery of thromboxane and prostacyclin [1,2]
Hauth et al reanalyzed the MFM Network data based on compliance [24,25]. They found that women who were more than 75% compliant in taking their aspirin had a sigfound that women who were more than 75% compliant in taking their aspirin had a signifinificant decrease in the incidence of preeclampsia, from 5.7% to 2.7%, as well as significant cant decrease in the incidence of preeclampsia, from 5.7% to 2.7%, as well as significant decreases in the incidence of low birth weight, preterm birth, and adverse pregnancy outdecreases in the incidence of low birth weight, preterm birth, and adverse pregnancy comes (Figure 4)
The actions of low-dose aspirin are generally attributed to selective inhibition of maternal platelet thromboxane; beneficial effects must extend to the placenta, which is a major source of eicosanoids
Summary
The rationale for low-dose aspirin therapy began in the 1970s with the discovery of thromboxane and prostacyclin [1,2]. In the 1980s, low-dose aspirin was being used to prevent recurrent myocardial infarction and other thrombotic events based on its ability to selectively inhibit thromboxane synthesis without affecting prostacyclin synthesis [3,4,5,6]. The reason this is possible is because the synthesis of thromboxane and prostacyclin is compartmentalized in different cell types. Endothelial cells do have nuclei and can regenerate cyclooxygenase, so prostacyclin production is minimally affected by low-dose aspirin.
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