[Therapy with aspirin: a new look at the old problem].

Aspirin is known to be efficient in secondary prevention of atherothrombosis. However, a considerable number of patients despite daily doses of aspirin still experience and suffer from various cardiovascular complications. In the medical literature this phenomenon was described as <<aspirin resistance>>, however, no well-defined criteria for this notion have been developed as yet. The overwhelming majority of researchers take the term <<aspirin resistance>> to mean both inability of the drug to prevent development of secondary thrombotic events, and its failure to adequately inhibit the function of blood platelets according to the findings of various laboratory tests. The incidence of detecting <<aspirin resistance>> varies considerably depending on the pathology involved and the method(s) used, amounting to from 5 to 70% of the cases. Amongst possible mechanisms capable of influencing the aspirin's clinical effect considered (herein, are the following aspects: polymorphism and/or mutation of the cyclooxigenese-1gene, production of thromboxane A2 in macrophages and endothelial cells via cyclooxigenese-2 polymorphism of Ilb/IIIa platelet receptors, competitive interaction with non-steroidal anti-inflammatory drugs for binding with the cyclooxigenese-1 of blood platelets, and platelet activation via other pathways which are not blocked by aspirin.