Abstract— Its antithrombotic mechanism is believed to be inhibition of the biosynthesis of thromboxane (and thus palatelet activation) by inactivation of platelet cyclooxygenase-1 (COX-1). But in significant number of patients clotting occurs despite of taking regular Aspirin resulting in Aspirin resistance. Aspirin resistance in different studies varied from 8% to 45%. This Aspirin resistance is either of due to inadequate intake of Aspirin, Concurrent intake of certain NSAIDS, Concurrent cigarette smoking, certain diseases like Diabetes and Arteritis, Increased platelet sensitivity to collagen and ADP, Biosynthesis of thromboxane, Increased turnover and vascular endothelial cells, Over expression of COX-2 in RNA, Generation of β2-iso PGF2 alpha binds to thromboxane receptors, Polymorphism in Ia/IIa, Ib/V/IX and IIb/IIIa receptors, COX-1, COX-2 thromboxane-A2 synthatase or other arachiodonate metabolism enzymes, Factor XIII etc. It can be diagnosed by Bleeding time, Selection-P. over expression, measurement of urinary concentration of the metabolite II-dehydrothromboxane B2 indicate the level indicate the level of TXA2 generation etc. Its resistance may lead to acute coronary syndrome, Acute Myocardial Infraction and/ or cardiovascular death in these coronary artery disease patients. Combining with other antiplatelet agents with other precautions like avoid concurrent use of NSAIDS, avoid cigarette smoking, taking proper dose of aspirin etc may prevent Aspirin resistance.
Keywords— Aspirin Resistance, Atherothrombotic vascular event, Acute Myocardial Infraction
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