from Pre-Eclampsia Placentas Differentially Affect Platelet Function

Pre-eclampsia (PE) complicates around 3 % of all pregnancies and is one of the most com-mon causes of maternal mortality worldwide. The pathophysiology of PE remains unclear however its underlying cause originates from the placenta and manifests as raised blood pressure, proteinuria, vascular or systemic inflammation and hypercoagulation in the mother. Women who develop PE are also at significantly higher risk of subsequently devel-oping cardiovascular (CV) disease. In PE, the failing endoplasmic reticulum, oxidative and inflammatory stressed syncytiotrophoblast layer of the placenta sheds increased numbers of syncytiotrophoblast extracellular vesicles (STBEV) into the maternal circulation. Platelet reactivity, size and concentration are also known to be altered in some women who develop PE, although the underlying reasons for this have not been determined. In this study we show that STBEV from disease free placenta isolated ex vivo by dual placental perfusion associate rapidly with platelets. We provide evidence that STBEV isolated from normal pla-centas cause platelet activation and that this is increased with STBEV from PE pregnan-cies. Furthermore, treatment of platelets with aspirin, currently prescribed for women at hig