Anti-inflammatory effect thromboxane production

Mode of action. Acetylsalicylic acid is unique among NSAIDs in that it also irreversibly inhibits COX by acylating the active site of the enzyme, so preventing the formation of products including thromboxane, prostacyclin and other prostaglandins, imtil more COX is synthesised. Acetylsalicylic acid is rapidly hydrolysed to salicylic acid in the plasma. Salicylic acid also has an anti-inflammatory action but additionally exerts important effects on respiration, intermediary metabolism and acid-base balance, and it is highly irritant to the stomach. 

Based on several randomized trials, aspirin has become the preferred antiplatelet agent in the treatment of aU ACSs. Early aspirin administration to all patients without contraindications within the first 24 hours of hospital admission is a quality care indicator (see Table 16-3). The antiplatelet effects of aspirin are mediated by inhibiting the synthesis of thromboxane A2 through an irreversible inhibition of platelet cyclooxygenase-1. Following the administration of a non-enteric-coated formulation, aspirin rapidly (<10 minutes) inhibits thromboxane A2 production in the platelets. Aspirin also has anti-inflammatory actions, which decrease C-reactive protein and also may contribute to its effectiveness in ACS. In patients undergoing PCI, aspirin prevents acute thrombotic occlusion during the procedure. 

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