Review

The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?

Raul Altman^1,2 , Héctor L Luciardi² , Juan Muntaner² and Ramón N Herrera²

¹  Centro de Trombosis de Buenos Aires, Universidad Nacional de Tucumán, Argentina

²  Magíster on Thrombosis, Facultad de Medicina, Universidad Nacional de Tucumán, Argentina

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Thrombosis Journal 2004, 2:1doi:10.1186/1477-9560-2-1

Published:	14 January 2004

First paragraph (this article has no abstract)

Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH₂. Subsequently, thromboxane synthase acts on PGH₂ to form TXA₂, a transient biological product that induces platelet aggregation and is a powerful vasoconstrictor. Aspirin acts primarily by interfering with the biosynthesis of cyclic prostanoids: TXA₂, prostacyclin, and other prostaglandins. It irreversibly inhibits COX-1 by acetylation of serine-530 and induces a long-lasting functional defect in the platelets. The resultant decrease in production of prostaglandins and TXA₂ probably accounts for much of aspirin's antithrombotic effect [1,2]. The plasma half-life of aspirin is only 20 min in circulating blood. It is rapidly deacetylated and converted to salicylate in vivo. Salicylate does not affect COX-1 or COX-2 activity [3].