Lowdose aspirin remains the gold standard therapy in the prevention of myocardial infarction, ischaemic stroke, and vascular death among patients at high and low risk of these events. . In aspirin ‘resistance’ the change is not in the drug target, and the effects can fluctuate over time and are at least partly reversible by increasing the dose. Biochemical Endpoints for in Vivo and ex Vivo Tests were done. Aspirin dose 325 to 1,300 mg daily were administered to previous ischaemic stoke patients to investigate the extent of inhibition of platelet aggregation. Signaldependent de novo synthesis of COX1 occuring over time in aspirin-treated platelets after persistent activation has been suggested to provide an additional source of aspirin-insensitive thromboxane biosynthesis.
