Abstract
Low dose aspirin is an efficient antiplatelet agent to decrease the risk of occlusive arterial events, however it is not infallible. Aspirin resistance describe its inability to block the formation of thromboxane A2 in platelets and/or to produce an inhibitory effect on platelet aggregation. Detection of aspirin resistance relies on the results of various platelet function tests or on blood and urinary thromboxane metabolites concentrations, but these methods show very low correlation and reproducibility. Moreover, light-transmission aggregometry using arachidonic acid, known as the reference functional assay, requires technical expertise. The incidence rate of aspirin resistance amoung populations suffering from cardiovascular diseases is about 25%, however there is a wide variability depending on the specificity of the used test and the clinical features of the considered population.Aspirin resistance is associated with the recurrence of arterial occlusive events: the odds ratio is about 4 all tests combined, therefore it could be considered as a risk marker. Evidence is lacking regarding the relevance of these tests to resort an intensification of the antithrombotic treatment, and experts recommend to reserve their use for high-risk situations. Nevertheless several studies have explored the effect of dose increases or intake frequency increases, and revealed encouraging results regarding pharmacodynamic endpoints. The reasons for aspirin resistance are numerous, often remain debate, and can accumulate to result in poor response to aspirin.
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