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Aspirin reduces the odds of serious atherothrombotic vascular events and death in a broad category of high risk patients by about one quarter. (1) The primary antithrombotic mechanism is believed to be inhibition of the biosynthesis of thromboxane (and thus platelet activation) by inactivation of platelet cyclo-oxygenase-1. However, aspirin is not that effective. It still fails to prevent most (at least 75%) serious vascular events in patients with symptomatic atherothrombosis. (1) Recurrent vascular events in patients taking aspirin ("aspirin treatment failures") have many possible causes (box), and aspirin resistance has emerged as an additional contender. (2,3)
But what is aspirin resistance? Aspirin resistance has been used to describe several different phenomena. One is the inability of aspirin to protect patients from ischaemic vascular events. This has also been called clinical aspirin resistance. (4) However, this definition is non-specific and could apply to any of the conditions listed in the box. Furthermore, it is not realistic to expect that all vascular complications can be prevented by any single preventive strategy. (5) Aspirin resistance has also been used to describe an inability of aspirin to produce an anticipated effect on one or more tests of platelet function, such as inhibiting biosynthesis of thromboxane, (6) inhibiting platelet aggregation, (7) and causing a prolongation of the bleeding time. (5,8) This has been caned biochemical aspirin resistance. (4) However, the precise qualitative and quantitative abnormalities of platelet function which define biochemical aspirin resistance have not been established, let alone their clinical relevance. As shown in the table, there are several different laboratory tests of platelet function which are being …