The antiplatelet effect of aspirin is mostly explained by the irreversible cyclooxygenase-1 inhibition resulting in the suppression of thromboxane A2 synthesis. The benefit of aspirin was proved in various cardiovascular diseases. However, the inter- and intraindividual variability of its antiplatelet effect is well known. Aspirin resistance can be understood from the clinical point of view--as a failure of the protective effect of aspirin from thrombotic complication or can be defined from the laboratory aspect--as an inability to cause in vitro detectable platelet function inhibition. The cause of this phenomenon has not been completely explained yet and more mechanisms have been proposed, incomplete suppression of thromboxane A2 generation being one of them. Laboratory diagnostics of aspirin resistance is based on the demonstration of the insufficient inhibition of platelet aggregation or the incomplete suppression of thromboxane A2 synthesis (assay for its metabolite, 11-dehydrothromboxane B2 in urine). The results of some trials raise the possibility that aspirin resistance could be a new independent predictor of cardiovascular events.

Keywords: Aspirin /pharmacology/; Cardiovascular Diseases /prevention & control/; Drug Resistance; Humans; Platelet Aggregation /drug effects/; Platelet Aggregation Inhibitors /pharmacology/