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J Am Coll Cardiol, 2006; 48:847, doi:10.1016/j.jacc.2006.05.023 (Published online 21 July 2006).
© 2006 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Reply

Peter J. Mason, MD, MPH*, Alice K. Jacobs, MD and Jane E. Freedman, MD

* Brigham and Women’s Hospital, Division of Cardiology, 75 Francis Street, Boston, Massachusetts 02115 (Email: pjmason{at}partners.org).

We appreciate the comments and criticisms voiced by Dr. Maree and colleagues. With respect to pharmacodynamic heterogeneity and genotypic variation in cyclooxygenase (COX)-1, we applaud the investigators’ work and agree that the single haplotype identified may contribute to, but not entirely explain, the phenomenon of "aspirin resistance." As suggested in our study (1), variation in aspirin responsiveness is most likely explained by a combination of several processes. If true, however, that 12% of the investigators’ cohort with stable coronary artery disease carried the specific COX-1 haplotype, it may prove interesting to study this population in greater detail. We also find interesting the observation by Dr. Maree et al. that low-dose (75 mg) enteric-coated aspirin failed to inhibit platelet COX in certain individuals. Although previously studied in some detail, the effects of aspirin dose and formulation are still worthy of further investigation. Finally, we agree that the biological validity and clinical relevance of "aspirin resistance" remains somewhat unproven.


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  1. Mason PJ, Jacobs AK, Freedman JE. Aspirin resistance and atherothrombotic disease J Am Coll Cardiol 2005;46:986-993.[Abstract/Free Full Text]

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Aspirin Resistance and Atherothrombotic Disease
Andrew O. Maree, Hani Jneid, and Desmond J. Fitzgerald
JACC 2006 48: 846-847. [Full Text]  




This Article
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j.jacc.2006.05.023v1
48/4/847    most recent
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