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Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1) enzymes in platelets, blocking thromboxane A2 production. This impairs platelet aggregation and prolongs bleeding time for the platelet's lifespan (7-10 days), even after a single dose. Effects peak within hours and persist, raising risks for gastrointestinal, intracranial, and surgical bleeding.[1][2]
Low-dose aspirin (75-325 mg daily) for cardiovascular prevention mildly elevates risk (1.5-2x baseline) but benefits often outweigh harms in secondary prevention. Higher doses (>325 mg) or long-term use amplify risks exponentially. Enteric-coated forms reduce GI irritation but not systemic bleeding effects.[1][6]
Platelet transfusion restores function (1-2 units for urgent cases). Desmopressin shortens bleeding time in mild cases. Avoid PPIs alone for GI protection—combine with dose minimization. Effects wane as new platelets form (full recovery in 5-7 days).[5][8]
ACCP and AHA recommend low-dose aspirin for high CV risk but advise against primary prevention in low-risk adults over 70 due to bleed outweighing benefits. Screen for H. pylori and use PPIs in at-risk groups.[6][9] Sources [1]: NEJM: Aspirin and Platelet Function [2]: PubMed: Aspirin and Bleeding Risks [3]: Lancet: GI Bleeding with Aspirin [4]: Stroke: Aspirin and Hemorrhagic Risk [5]: AABB Platelet Guidelines [6]: USPSTF Aspirin Recommendations [7]: NEJM: Anticoagulants + Aspirin [8]: Blood: Managing Aspirin Bleeding [9]: AHA/ACC Guidelines
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