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The anti\u2010platelet effects of aspirin and a P2Y<jats:sub>12<\/jats:sub>antagonist are often considered to be separately additive. However, there is evidence of an overlap in effects, in that a high level of P2Y<jats:sub>12<\/jats:sub>receptor inhibition can blunt TXA<jats:sub>2<\/jats:sub>receptor signalling in platelets and reduce platelet production of TXA<jats:sub>2<\/jats:sub>. Against this background, the addition of aspirin, particularly at higher doses, could cause significant reductions in the production of prostanoids in other tissues, e.g. prostaglandin I<jats:sub>2<\/jats:sub>from the blood vessel wall. This review summarizes the data from clinical studies in which dose\u2010dependent effects of aspirin on prostanoid production have been evaluated by both plasma and urinary measures. It also addresses the biology underlying the cardiovascular effects of aspirin and its influences upon prostanoid production throughout the body. 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