Which mechanism best explains why low-dose aspirin (75–150 mg/day) initiated before 16 weeks reduces the risk of pre-eclampsia in high-risk women?

• A Inhibits COX-2 in endothelium, increasing prostacyclin and causing vasodilation
• B Reduces placental sFlt-1 production by inhibiting prostaglandin E2 synthesis
• C Improves trophoblast invasion by inhibiting thromboxane-mediated spiral artery vasoconstriction
• D Preferentially inhibits platelet COX-1, shifting the TXA2:prostacyclin ratio in favour of prostacyclin ✓

Explanation

Low-dose aspirin irreversibly acetylates platelet COX-1, blocking thromboxane A2 (TXA2) synthesis. Because platelets lack nuclei and cannot regenerate COX, the inhibition is permanent for platelet lifespan. Endothelial cells can regenerate COX-2 and continue producing prostacyclin (PGI2). This shifts the balance toward vasodilation and anti-aggregation. Early initiation before 16 weeks improves trophoblast invasion during the critical window of placentation, accounting for the reduced pre-eclampsia risk.

Reference: Williams Obstetrics, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.