ASPIRIN RESISTANCE: MOLECULAR MECHANISMS & TECHNIQUES

Aspirin became a cornerstone in the treatment of coronary artery disease and widely used in the secondary prevention of vascular events. Aspirin resistance remains a poorly defined term though clinical definition is failure of the drug to prevent an atherothrombotic event despite the regular intake of appropriate doses is a relatively common problem. Various laboratory parameters assessing its efficacy, like bleeding time, platelet reactivity, thromboxane A2 (TXA2) production and measurement of platelet aggregation have confirmed the lack of its uniform effect on the platelets. Various molecular mechanism responsible for Aspirin resistance include  Insufficient suppression of COX-1, over- expression of COX-2 mRNA, Erythrocyte induced platelet activation, Genetic polymorphism of enzymes like COX-1, COX-2 or thromboxane A2 synthase. Clinical factor like non compliance of patient is also responsible for Aspirin resistance. The limitations in understanding Aspirin resistance include difficulties in assessing platelet function and aspirin resistance and contributed to variable reporting of Aspirin resistance. Therefore, the definition of Aspirin resistance requires refinement to include genetic polymorphism of various enzymes responsible for Aspirin resistance. However, various techniques for platelet analysis also require modification to understand Aspirin resistance.