aspirin and prasugrel

Aspirin irreversibly inhibits cyclo-oxygenase-1, decreasing thromboxane A2 production, while prasugrel irreversibly blocks the P2Y12 ADP receptor. Both pathways are required for full platelet activation; combined use produces additive antiplatelet effects, significantly increasing bleeding risk.

Enhanced bleeding risk, including gastrointestinal and intracranial haemorrhage. However, this combination is beneficial in reducing thrombotic events in patients with acute coronary syndromes or after coronary stenting, so the prescribing context determines net effect. Bleeding is the primary adverse outcome.

Use dual antiplatelet therapy only when clearly indicated, such as acute coronary syndrome or drug-eluting stent placement. Monitor for signs of bleeding, including occult blood loss. Consider gastroprotection with a proton pump inhibitor where appropriate. The duration of dual therapy should be guided by current cardiology guidelines and individual thrombotic versus bleeding risk.

This interaction is well established in randomised controlled trials and clinical guidelines for dual antiplatelet therapy. The additive bleeding risk is a recognised feature of all combinations of aspirin with P2Y12 inhibitors.