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Molecular Diagnosis & Therapy

, Volume 12, Issue 1, pp 55–56 | Cite as

Diagnostics for Aspirin Resistance

  • Paul A. Gurbel
  • Kevin P. Bilden
  • Udaya S. Tantry
Commentary
  • 17 Downloads

The clinical efficacy of aspirin therapy in preventing thrombotic events that has been observed in major clinical trials has mainly been attributed to the inhibition of the platelet cyclo-oxygenase (COX)-1 enzyme. Based on the measurement of stable thromboxane derivatives, it was suggested that more than 95% inhibition of platelet COX-1 is required to observe any clinical efficacy of aspirin therapy.[1] Recently, reports of ‘aspirin resistance’ have emerged and its association with adverse clinical event occurrence has attracted major interest among clinicians as well as the general public.[2]

Laboratory methods that isolate the primary target of aspirin in platelets (i.e. inhibition of COX-1 by using arachidonic acid as an agonist in platelet aggregation measurements), have demonstrated that aspirin is highly effective in inhibiting platelet COX-1. However, the estimation of the prevalence of ‘aspirin resistance’ is highly assay-specific, and higher prevalence is significantly...

Keywords

Aspirin Thromboxane Aspirin Therapy Aspirin Resistance Heart Outcome Prevention Evaluation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgments

Dr Gurbel has received research grant and honoraria from Bayer, Astrazeneca, Schering Plough, Eli Lily, and Daiichi/Sankyo.

Drs Bilden and Tantry have no conflicts of interest that are directly relevant to the content of this commentary.

References

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Copyright information

© Adis Data Information BV 2008

Authors and Affiliations

  • Paul A. Gurbel
    • 1
  • Kevin P. Bilden
    • 1
  • Udaya S. Tantry
    • 1
  1. 1.Sinai Center for Thrombosis ResearchBaltimoreUSA

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