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Aspirin inhibits platelet aggregation by irreversible acetylation of the cyclo-oxygenase-1 (COX-1) enzyme, resulting in almost complete inhibition of thromboxane production by platelets.1 However, aspirin yields only modest long-term reductions in vascular events,2, 3 which has led investigators to develop alternative antiplatelet drugs and to study the effects of their combination with aspirin and of dual treatment with anticoagulant drugs. Yet the disparity between the effect of aspirin on thromboxane production and its clinical benefits might be due, at least in part, to the one-dose-fits-all approach used in trials and clinical practice, particularly the use of low doses in individuals with higher bodyweight. Obesity and increased body-mass index (BMI) are associated with reduced inhibition of COX-1 by…….. see more https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31133-4/fulltext