Aspirin resistance refers to less than expected suppression of
thromboxane A(2) production by
aspirin and has been reported to be independently associated with an increased risk of adverse cardiovascular events. Possible causes of
aspirin resistance include poor compliance, drug interaction, inadequate
aspirin dose, increase turnover of platelets, genetic polymorphisms of cyclo-oxygenase-1, and upregulation of alternate (non-platelet) pathways of
thromboxane production. Laboratory methods used to detect
aspirin resistance include those that measure
thromboxane A(2) production and
thromboxane A(2)-dependent platelet function. However, since there is currently no standardised approach to the diagnosis and there are no proven effective treatments for
aspirin resistance that improve outcome, patients with
cardiovascular disease receiving
aspirin should not be routinely tested for
aspirin resistance. Instead physicians should be aware of the factors that may impair
aspirin function, ensure that they use an appropriate dose of
aspirin and optimise compliance with
aspirin therapy. Further research exploring the mechanisms of
aspirin resistance is needed in order to better define and develop a standardised test for
aspirin resistance that is specific, reliable, can be readily applied in routine laboratories and correlate with an increased risk of cardiovascular events.