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”

Abstract

HomeCirculationVol. 115, No. 3Response 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” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse 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” Andrew L. FrelingerIII, Mark I. Furman, Matthew D. Linden, Youfu Li, Marsha L. Fox, Marc R. Barnard and Alan D. Michelson Andrew L. FrelingerIIIAndrew L. FrelingerIII Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author , Mark I. FurmanMark I. Furman Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author , Matthew D. LindenMatthew D. Linden Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author , Youfu LiYoufu Li Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author , Marsha L. FoxMarsha L. Fox Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author , Marc R. BarnardMarc R. Barnard Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author and Alan D. MichelsonAlan D. Michelson Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, Mass Search for more papers by this author Originally published23 Jan 2007https://doi.org/10.1161/CIRCULATIONAHA.106.661462Circulation. 2007;115:e46We 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.DisclosuresDr 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.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.LinkGoogle Scholar2 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.CrossrefMedlineGoogle Scholar3 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.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails January 23, 2007Vol 115, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.106.661462 Originally publishedJanuary 23, 2007 PDF download Advertisement SubjectsAcute Coronary SyndromesChronic Ischemic Heart DiseasePlateletsPrimary PreventionSecondary PreventionThrombosis