doi: 10.1161/CIRCULATIONAHA.106.661462
(Circulation. 2007;115:e46.)
© 2007 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article, "Residual Arachidonic Acid–Induced Platelet Activation via an Adenosine Diphosphate–Dependent but Cyclooxygenase-1– and Cyclooxygenase-2–Independent Pathway: A 700-Patient Study of Aspirin Resistance"
Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass
We thank Dr Kronish and his colleagues for their interest in our work.1 Kronish et al suggest that because of the patient population we studied, our work underestimates the role of noncompliance in aspirin resistance if applied to all patients taking aspirin.1 However, we did not suggest that the high compliance rate in our study was representative of all patients taking aspirin. The precise incidence of patient noncompliance with aspirin will, of course, vary according to the patient setting. Kronish et al reference their own work and the findings of Cotter et al,2 who have reported a relatively high (16%) incidence of aspirin noncompliance, but Kronish et al do not reference the findings of Tantry et al,3 who have reported a low (0.4%) incidence of aspirin noncompliance. Kronish et al acknowledge that, irrespective of the precise incidence of patient noncompliance with aspirin, the novel finding of our study1 is that there is a residual arachidonic acid–induced platelet activation via an adenosine diphosphate–dependent but cyclooxygenase-1– and cyclooxygenase-2–independent pathway in aspirin-compliant patients.
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Acknowledgments |
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Disclosures
Dr Frelinger has received research grant support from BioCytex, Dade Behring, Eli Lilly, and the TIMI Study Group. Dr Furman has received research grant support from Dade Behring and Eli Lilly and speaking honoraria from Sanofi Aventis. Dr Michelson has received research grant support from Accumetrics, BioCytex, Dade Behring, Eli Lilly, McNeil, and the TIMI Study Group, and honoraria from Eli Lilly, Sanofi Aventis/Bristol-Myers Squibb, and Dade Behring. The remaining authors report no conflicts.
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References |
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 Top References |
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1. Frelinger AL III, Furman MI, Linden MD, Li Y, Fox ML, Barnard MR, Michelson AD. Residual arachidonic acid–induced platelet activation via an adenosine diphosphate–dependent but cyclooxygenase-1– and cyclooxygenase-2–independent pathway: a 700-patient study of aspirin resistance. Circulation. 2006; 113: 2888–2896.
2. Cotter G, Shemesh E, Zehavi M, Dinur I, Rudnick A, Milo O, Vered Z, Krakover R, Kaluski E, Kornberg A. Lack of aspirin effect: aspirin resistance or resistance to taking aspirin? Am Heart J. 2004; 147: 293–300.[CrossRef][Medline] [Order article via Infotrieve]
3. Tantry US, Bliden KP, Gurbel PA. Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation. J Am Coll Cardiol. 2005; 46: 1705–1709.
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